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        <title>Frontiers in Immunology | Immunological Memory section | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/immunology/sections/immunological-memory</link>
        <description>RSS Feed for Immunological Memory section in the Frontiers in Immunology journal | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-05-13T12:32:07.346+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2026.1809241</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2026.1809241</link>
        <title><![CDATA[Not all plasma cells are made equal: well-hidden layers of heterogeneity]]></title>
        <pubdate>2026-05-11T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Audrey Anoh Akessé</author><author>Amélie Bonaud</author>
        <description><![CDATA[Plasma cells (PCs) are the final stage of B cell development and sustain long-term humoral immunity by continuously secreting antibodies. Once considered a homogeneous population defined by a short-lived versus long-lived dichotomy, PCs are now recognised as highly heterogeneous. Recent advances have overturned several dogmas, revealing that long-lived plasma cells (LLPCs) can arise from diverse B cell precursors, and persist in tissues beyond the bone marrow. PC heterogeneity is shaped by intrinsic factors, including B cell origin, antigen affinity, BCR signalling strength and immunoglobulin isotype, as well as extrinsic factors such as tissue-specific microenvironments, cytokines and cellular interactions at induction and maintenance sites. Furthermore, temporal variables, termed “Moment”, including age, sex, and inflammatory status, modulate PC fate throughout their maturation. This process also plays a central role in the emergence of heterogeneity within these LLPCs. Together, these parameters define a dynamic, context-dependent PC landscape with significant implications for immune regulation and vaccine design.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2026.1785563</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2026.1785563</link>
        <title><![CDATA[Why are long-lived plasma cells long-lived?]]></title>
        <pubdate>2026-05-07T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Julia Grace Reinke</author><author>Christopher Schorr</author><author>Kelvin Paul Lee</author>
        <description><![CDATA[Long-Lived Plasma Cells (LLPCs) are an integral part of long-term protective humoral immunity. They can live for decades, unlike Short-Lived Plasma Cells (SLPCs), and continuously produce antibody regardless of antigen stimulation, unlike Memory B Cells (MBCs). LLPCs are critical for the sustained protective immunity against pathogens that are only intermittently present in a population but can cause significant morbidity/mortality when active—such as epidemic diseases. What drives B cell differentiation specifically to the LLPC lineage is still not fully understood; there is conflicting information on what drives the fate decisions for MBCs vs. SLPCs vs. LLPCs. Evidence suggests that although LLPC and SLPC have similar gene transcriptional profiles they differ significantly in their metabolic profiles–likely due to the demands of prolonged continuous antibody production in LLPC. These metabolic changes include increased uptake of metabolic substrates, increased mitochondrial mass/function and enhanced fuel availability via lipophagy, and enhanced proteostasis to remove misfolded proteins. However, the possibility of repeated antigen-driven generation of a large number of highly metabolically active long-lived cells is problematic for a resource-constrained organism, and it is now clear that LLPC numbers are constrained by a limited number of specialized LLPC niches in the bone marrow and other tissues. LLPCs are not intrinsically long-lived but rely on interactions with the LLPC niche to maintain their longevity. For example, activation of the CD28 receptor on LLPC by its ligands CD80/CD86 on dendritic cells (DC) in the LLPC niche results in augmented metabolism through enhanced lipophagy, intracellular long chain fatty acid availability, oxidative phosphorylation, increased mitochondrial mass and function that are necessary for LLPC survival. CD28 activation is essential for the survival of LLPC but not for SLPC, supporting the concept that enhancement of LLPC metabolic capacity by interactions with its niche plays a key role in LLPC longevity. In human health, new insights into how LLPCs survive and differentiate will impact the development of robust and long-lasting vaccinations, as well as with treatment of autoantibody-mediate autoimmune diseases and PC malignancies such as multiple myeloma (MM)—as these malignancies remain dependent on many of the same survival pathways as their nonmalignant LLPC counterparts.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2026.1822561</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2026.1822561</link>
        <title><![CDATA[Exercise and tissue-resident memory T cells: from circulating numbers to spatial immune remodeling]]></title>
        <pubdate>2026-05-07T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Enli Xie</author><author>Yushan He</author><author>Tainan Cao</author><author>Changchun Li</author><author>Zhiming Wang</author>
        <description><![CDATA[Tissue-resident memory T (TRM) cells have become a paradigm shift in the field of immunology and have changed our view of local immune surveillance at barrier surfaces. In contrast to circulating memory T cells, TRM cells are fixed in non-lymphoid organs like lungs, intestine and skin to act as the first line of defense against reinfection and malignant conversion. The finding contradicts the conventional emphasis on exercise immunology on the number of circulating lymphocytes and requires a new conceptual framework of the so-called quantitative to spatial immune remodeling. This review summarizes the current developments in the TRM cell biology and its relevance to exercise immunology and answer the main question of the review: will endurance training, like a vaccine, elevate the density of both TRM cells in non-lymphoid tissues and their functional capacity? To begin with, we define the molecular basis of TRM cells, their differentiation routes, storage processes (CD69, CD103), and tissue-specific diversity. Then, we explore the possible ways in which exercise might be able to change the establishment of TRM cells and their functions, namely exercise related adrenergic signaling, thermoregulatory shifts, and hemodynamic forces regulating the T cell homing receptor and tissue resident program. The traditional finding of decreased upper respiratory tract infection risk in athletes is reevaluated based on the perspective of increased respiratory mucosal TRM cell immunity. We then elaborate on the biphasic J-shaped relationship between exercise intensity and immunoprotection, and elucidate how optimal training levels are achieved at lower intensities whereas higher intensities can undermine the level of TRM cell-mediated immunity. Lastly, we have identified key knowledge gaps and research directions that are needed in the future, namely, the mechanistic analysis of β2-adrenergic receptor signaling in TRM cell biology, the creation of tissue-specific exercise prescription strategies and the translation of these findings into practice as a way to prevent infections and treat cancer immunotherapy. Incorporating basic immunology with exercise physiology, the review is intended to trigger a paradigm shift in exercise immunology shifting away the circulating numbers toward the spatially-resolved insight of how exercise alters the immune picture of the tissues.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2026.1787641</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2026.1787641</link>
        <title><![CDATA[Single-cell CyTOF profiling reveals alterations in B, T and macrophage subsets during murine hepatic aging]]></title>
        <pubdate>2026-04-28T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Zheng Ding</author><author>Bing Fang</author><author>Jing Peng</author><author>Siyu Wang</author><author>Xiaomin Tian</author><author>Guixi Chen</author><author>Yuqiu Wei</author><author>Yuebin Gao</author><author>Yixuan Li</author><author>Jiazeng Sun</author>
        <description><![CDATA[IntroductionPopulation aging is a global demographic shift closely associated with immune dysregulation, which significantly increases the risk of chronic liver diseases. As a crucial immune and metabolic organ, the liver relies on a complex immune network consisting of innate and adaptive cell subsets to maintain homeostasis and defend against invading pathogens. However, the remodeling mechanism of the hepatic immune landscape with aging remains incompletely understood.MethodsWe investigated the changes in hepatic immune cell subsets and related molecular profiles during aging, focusing on the identification and characterization of key immune cell populations and their associated gene expression patterns in aged livers.ResultsWe identified Igd+ B cells in the hepatic immune compartment, which showed a significant reduction in aged livers. This reduction was accompanied by the enrichment of B cell signal transduction pathways and downregulation of genes related to cell migration and receptor binding. Meanwhile, aged livers exhibited selective expansion of multiple CD4+ T cell subsets (Th1, Th2, Th17, Treg) and an increase in resident-derived pro-inflammatory M1 macrophages, whereas CD8+ T cells, double-negative T cells, and most innate lymphoid cell subsets remained stable. Our study delineated age-associated alterations in hepatic B, T, and macrophage subsets as a characteristic feature of murine hepatic immune aging.DiscussionThese findings clarify the characteristics of the hepatic immune landscape during aging, providing a valuable reference for future studies on liver aging and the development of strategies to address age-related liver immune dysregulation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2026.1758356</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2026.1758356</link>
        <title><![CDATA[Resveratrol and the neuroinflammation axis in Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and cerebral ischemia]]></title>
        <pubdate>2026-04-21T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Haoyu Wang</author><author>Fei Li</author><author>Haifan Wang</author><author>Zenan Tian</author><author>Hong Fan</author><author>Zhibin Shi</author>
        <description><![CDATA[Resveratrol (RES), a naturally occurring polyphenolic compound found in grapes, berries, and peanuts, has attracted considerable interest because of its antioxidant, anti−inflammatory, and neuroprotective properties. This narrative review examines the current evidence regarding the potential effects of RES on memory−related processes and neuroinflammatory biomarkers in major neurological disorders, including Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis (MS), and cerebral ischemia. Relevant literature was identified through searches of major scientific databases, and studies addressing the molecular mechanisms, experimental outcomes, and therapeutic implications of RES in these conditions were evaluated. The available evidence indicates that RES can modulate several biological pathways associated with neurodegeneration, including oxidative stress, inflammatory signaling, mitochondrial dysfunction, and neuronal survival. Experimental studies suggest that RES may influence key molecular mediators such as pro−inflammatory cytokines, nitric oxide (NO) signaling, and matrix metalloproteinases, which are implicated in neuronal damage and blood–brain barrier disruption. In preclinical models of AD and PD, RES has been associated with improvements in cognitive performance, reduction of neuroinflammatory markers, and attenuation of neuronal loss. Similarly, studies in MS and cerebral ischemia models indicate that RES may modulate immune responses, reduce oxidative damage, and limit ischemia−related neuronal injury. However, most of the current evidence derives from in vitro and animal studies, and clinical data remain limited. Moreover, the low bioavailability of RES and variability in dosing regimens represent important challenges for clinical translation. Therefore, although experimental findings support the potential neuroprotective role of RES, further well−designed clinical studies are required to determine its therapeutic relevance and safety in human neurological disorders. This narrative review was developed through a structured search of PubMed, Scopus, and Web of Science for articles published between 2000 and 2024, focusing on mechanistic, preclinical, and clinical investigations of RES in neurological disorders. This review synthesizes current evidence on the molecular and cellular mechanisms underlying the neuroprotective effects of RES, with particular emphasis on its antioxidant, anti-inflammatory, and immunomodulatory activities. By integrating findings from experimental and clinical research, the review highlights the potential of RES to modulate key pathways involved in neurodegeneration and neuroinflammation. Although further well-designed clinical studies are required to clarify its therapeutic efficacy and translational relevance, the available evidence supports continued investigation of RES as a promising candidate for neuroprotective strategies in neurological disorders.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2026.1734384</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2026.1734384</link>
        <title><![CDATA[B-cell DNA methylation signature in response to hepatitis B virus vaccination in females and males]]></title>
        <pubdate>2026-04-10T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Katarzyna Malgorzata Kwiatkowska</author><author>Simona Anticoli</author><author>Stefano Salvioli</author><author>Luciano Calzari</author><author>Davide Gentilini</author><author>Claudia Sala</author><author>Gastone Castellani</author><author>Christian Albano</author><author>Nicoletta Vonesch</author><author>Paola Tomao</author><author>Rita Carsetti</author><author>Paolo Garagnani</author><author>Anna Ruggieri</author>
        <description><![CDATA[IntroductionSex-based differences in immune responses to vaccination are well-documented, yet the underlying epigenetic mechanisms remain poorly understood. This study investigates DNA methylation profiles in B cells following hepatitis B virus (HBV) vaccination, with a focus on sex-specific patterns.MethodsUsing high-resolution genome-wide methylation analysis, we examined post-vaccination samples from healthy male and female health care workers.ResultsOur results reveal distinct methylation signatures associated with vaccine response, with several loci showing sex-dependent differential methylation. Pathway analysis identified immune-related genes and regulatory elements potentially involved in B cell activation and memory formation. Our findings show that DNA methylation levels differ between responders versus non-responders to HBV vaccination and these alterations vary with biological sex.DiscussionUnderstanding these epigenetic variations may open new perspective on vaccination practice. Collecting data on B cell epigenetics in different vaccination protocols could improve our knowledge on immunization function and contribute to more personalized vaccination strategies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2026.1707427</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2026.1707427</link>
        <title><![CDATA[Vitiligo secondary to immunosuppressants: a pharmacovigilance study of the FDA Adverse Event Reporting System]]></title>
        <pubdate>2026-03-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ying Jia</author><author>Hanzhang Xie</author><author>Yixuan Yang</author><author>Bingnan Cui</author><author>Junhui Wang</author><author>Zhanshuo Xiao</author>
        <description><![CDATA[BackgroundVitiligo is an acquired depigmentation disorder affecting individuals worldwide. The potential link between immunosuppressants and the onset or exacerbation of vitiligo remains a topic of clinical concern.ObjectiveThis study aims to evaluate the association between various immunosuppressants and vitiligo using data from the FDA Adverse Event Reporting System (FAERS).MethodsA retrospective pharmacovigilance analysis was conducted using FAERS data from January 2004 to June 2024. Vitiligo cases were identified through the Medical Dictionary for Regulatory Activities (MedDRA) terminology. Disproportionality analysis was performed using the Reporting Odds Ratio (ROR), Proportional Reporting Ratio (PRR), Bayesian Confidence Propagation Neural Network (BCPNN), and Empirical Bayes Geometric Mean (EBGM) to detect significant drug-event associations.ResultsA total of 435 vitiligo-related adverse event (AE) reports were identified. The United States, Canada, France, Germany, and Brazil contributed the most reports. Vitiligo reports were more frequent in female patients, particularly within the 18–65 age group. The primary indications for immunosuppressant use included psoriasis, rheumatoid arthritis, psoriatic arthropathy, Crohn’s disease, and ulcerative colitis. Adalimumab (74 cases) and secukinumab (52 cases) accounted for the highest number of reports. Significant signals were detected for alemtuzumab, ixekizumab, ustekinumab, secukinumab, guselkumab, and risankizumab.ConclusionThis study highlights the importance of continuous pharmacovigilance in monitoring potential adverse events associated with immunosuppressants. The observed association between specific immunosuppressants and vitiligo suggests a need for further research to elucidate underlying mechanisms and develop strategies to mitigate these potential AEs.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2026.1722621</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2026.1722621</link>
        <title><![CDATA[Tuberculosis preventive therapy in postpartum women with HIV modifies M. tuberculosis-specific and nonspecific immune responses]]></title>
        <pubdate>2026-03-11T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Damayanti Yengkhom</author><author>Grace Montepiedra</author><author>Gaerolwe Masheto</author><author>Deo Wabwire</author><author>Lynda Stranix-Chibanda</author><author>Allen Matubu</author><author>Avy Violari</author><author>Gerhard Theron</author><author>Amita Gupta</author><author>Adriana Weinberg</author>
        <description><![CDATA[BackgroundTuberculosis (TB) has significant morbidity in pregnant and postpartum women with HIV (pregnant and PPWWHIV). TB preventive therapy (TPT) is recommended in pregnant and PPWWHIV with documented or presumed latent TB infection (LTBI). TB-stimulated IFNγ release assay and skin test positivity decline after TPT, but the underlying mechanisms and relationship with TB-specific immunologic memory are incompletely understood. We investigated this aspect in PPWWHIV.MethodsPPWWHIV with LTBI received isoniazid TPT between 12 and 40 weeks postpartum. Blood obtained at 12 and 44 weeks postpartum was used to compare functional and phenotypic characteristics of unstimulated and TB-stimulated CD4+ and CD8+ conventional T cells (Tconv); unconventional T cells, including γδ, iNKT, MR1+ and MR1- MAIT, and NKT; NK; and antigen presenting cells (APC) pre- and post-TPT.ResultsIn 45 participants with medians of 477 CD4+ T cells/µL and <50 HIV RNA copies/mL of plasma on antiretroviral therapy, both Tconv and innate immune cells responded to TB antigenic stimulation in vitro with an increase in functional markers. TPT was associated with a pronounced decrease in the proportions of granzyme B-expressing Tconv and unconventional T cell subsets both in TB-stimulated and unstimulated conditions. TB-stimulated Th1- and Th17-like responses in unconventional T cells also decreased from pre- to post-TPT. TB-stimulated conventional and unconventional regulatory T cells mostly decreased after TPT with a few exceptions. Very few changes were observed in circulating or TB-stimulated APC in response to TPT.ConclusionsTPT was associated with a significant decrease in TB-specific T cell responses, including Tconv but mostly unconventional T cells, suggesting an important role of unconventional T cell memory in the control of TB infection. The prominent decrease of granzyme B-expressing T cells in response to TPT highlighted the importance of granzyme B in the maintenance of LTBI.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2026.1760904</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2026.1760904</link>
        <title><![CDATA[Case Report: Rapid recurrence of psoriasiform dermatitis upon sequential anti-PD-1 therapy with pembrolizumab and tislelizumab with 3-year follow-up]]></title>
        <pubdate>2026-03-04T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Chao-Cheng Chi</author><author>Zi-Yun Li</author><author>Sui-Qing Cai</author><author>Zhuang-Li Tang</author>
        <description><![CDATA[Psoriasiform eruption is an uncommon cutaneous immune-related adverse event (irAE) associated with anti-PD-1 therapy, and its rapid recurrence upon switching to a different anti-PD-1 agent is a scarcely documented phenomenon. We report the case of a 59-year-old man with stage IIB lung adenocarcinoma who developed a pruritic, scaly eruption after his fourth cycle of pembrolizumab. Histopathological examination confirmed a diagnosis of grade 2 psoriasiform dermatitis according to the Common Terminology Criteria for Adverse Events (CTCAE) version 5.0. The initial episode was resolved with systemic corticosteroids. However, upon switching anti-PD-1 therapy to tislelizumab, a similar but more widespread eruption recurred rapidly within a week. The recurrence was successfully managed with topical corticosteroid and antihistamines, and the anti-PD-1 therapy was subsequently discontinued. During the 3-year follow-up after discontinuation, the patient’s skin lesions resolved completely with no recurrence, and no tumor progression was observed. The reduced latency of psoriasiform dermatitis recurrence upon anti-PD-1 inhibitor rechallenge suggests a memory T cell–driven immune response. It also highlights that such irAEs were observed with the two PD-1 inhibitors pembrolizumab and tislelizumab used in this case and can be effectively managed. In this case, tumor progression was not observed after treatment cessation, although causality cannot be inferred.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2026.1735878</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2026.1735878</link>
        <title><![CDATA[ACK2 antibody conditioning enhances adoptive transfer of hematopoietic progenitors to study central trained immunity in mice]]></title>
        <pubdate>2026-03-04T00:00:00Z</pubdate>
        <category>Methods</category>
        <author>Andrea Guiu</author><author>Paula Guerrero</author><author>María Sobén</author><author>Daniel Gozalbo</author><author>M. Luisa Gil</author><author>Alberto Yáñez</author>
        <description><![CDATA[Hematopoietic stem and progenitor cell (HSPC) transplantation is a cornerstone for studying hematopoiesis. However, classical conditioning regimens such as irradiation or chemotherapy induce strong inflammation, alter the bone marrow (BM) microenvironment, and severely limit the interpretation of differentiation processes. Moreover, donor HSPC engraftment efficiency in immunocompetent recipients without conditioning is usually very low. In this work, we produced and purified the monoclonal anti-c-Kit antibody ACK2 and tested its capacity to transiently deplete HSPCs in immunocompetent C57BL/6 mice. We defined the in vivo clearance kinetics of the ACK2 antibody from serum, identified the optimal transplantation window, and evaluated donor engraftment efficiency. Intraperitoneal injection of ACK2 induced transient HSPC depletion in the BM, with maximal depletion and complete clearance of circulating antibody at day 4 post-injection. Transplantation of donor HSPCs in ACK2-conditioned recipients at this time point resulted in significantly improved engraftment compared to PBS-treated recipients, particularly in the BM. As a proof of concept, we applied this mouse model to investigate properties of innate immune memory in HSPCs exposed to Candida albicans in vivo. For this, we adoptively transferred HSPCs from infected mice with a non-virulent C. albicans strain and assessed the functional properties of their derived neutrophils in vivo. We found that neutrophils derived from C. albicans-exposed HSPCs displayed an enhanced recruitment to the peritoneal cavity during a secondary C. albicans infection compared to control HSPC-derived neutrophils. In conclusion, here we describe a non-inflammatory, antibody-based conditioning method that enhances adoptive transfer of HSPCs in immunocompetent mice. Consistent with previous reports, ACK2-based conditioning alone does not enable permanent hematopoietic engraftment, but rather facilitates transient donor cell engraftment which provides a versatile methodological tool to study the biology and functional programming of exogenous HSPCs in vivo, including their contribution to trained immunity.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2026.1809363</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2026.1809363</link>
        <title><![CDATA[Correction: Long non-coding RNAs in response to Ebola virus vaccine-induced immunity]]></title>
        <pubdate>2026-03-03T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Izabela Mamede</author><author>Thomaz Luschër-Dias</author><author>Isabelle Franco Moscardini</author><author>Patrícia Gonzales-Dias</author><author>Bárbara Marinho</author><author>Fernando Marcon</author><author>Thiago Dominguez Crespo Hirata</author><author>Michael Eichberg</author><author>Donata Medaglini</author><author>Ali M. Harandi</author><author>Claire-Anne Siegrist</author><author>Tom H. M. Ottenhoff</author><author>Francesco Santoro</author><author>Marylyn M. Addo</author><author>André Gonçalves</author><author>Daniela M. Ferreira</author><author>Rafael Polidoro</author><author>Glória R. Franco</author><author>Paulo P. Amaral</author><author>Helder Nakaya</author><author>VSV-EBOPLUS Consortium

 </author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2025.1695514</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2025.1695514</link>
        <title><![CDATA[Long non-coding RNAs in response to Ebola virus vaccine-induced immunity]]></title>
        <pubdate>2026-02-10T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Izabela Mamede</author><author>Thomaz Luschër-Dias</author><author>Isabelle Franco Moscardini</author><author>Patrícia Gonzales-Dias</author><author>Bárbara Marinho</author><author>Fernando Marcon</author><author>Thiago Dominguez Crespo Hirata</author><author>Michael Eichberg</author><author>Donata Medaglini</author><author>Ali M. Harandi</author><author>Claire-Anne Siegrist</author><author>Tom H. M. Ottenhoff</author><author>Francesco Santoro</author><author>Marylyn M. Addo</author><author>André Gonçalves</author><author>Daniela M. Ferreira</author><author>Rafael Polidoro</author><author>Glória R. Franco</author><author>Paulo P. Amaral</author><author>Helder Nakaya</author>
        <description><![CDATA[Long noncoding RNAs (lncRNAs) have emerged as critical regulators of gene expression, yet their role in shaping human responses to vaccination remains largely uncharacterized. Here, we analyzed RNA-sequencing data from three independent human cohorts vaccinated with the rVSVΔG-ZEBOV-GP Ebola vaccine to profile lncRNA expression dynamics. Using differential expression analysis and correlation meta-analysis across cohorts, we identified an expression signature with several lncRNAs, including LEF1-AS1 and DOCK8-AS1, that exhibit conserved transcriptional activation following vaccination. Correlation of lncRNA expression with gene targets and IgG titers revealed putative roles for lncRNAs in regulating and/or participate in both innate immune responses and adaptive antibody production. Functional enrichment of lncRNA co-expressed protein-coding genes highlighted involvement in T-cell differentiation, interferon signaling, and leukocyte activation. Integrating global run-on sequencing data and comparative transcriptomic analysis across other vaccine studies suggests that LEF1-AS1 modulation is distinctively associated with Ebola vaccination. Our findings demonstrate that lncRNAs are potential integral components of the human vaccine response and provide a foundation for future mechanistic studies targeting noncoding RNA regulation of immunity.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2026.1769061</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2026.1769061</link>
        <title><![CDATA[Editorial: Exploring immune memory dynamics in chronic antigen exposure and disease progression: implications for immunotherapy]]></title>
        <pubdate>2026-02-09T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Stefano Caserta</author><author>Alejandra Pera</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2025.1680375</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2025.1680375</link>
        <title><![CDATA[Emerging novel methodologies to understand and strategically target long-lived plasma cells in vaccine design to induce durable immunity]]></title>
        <pubdate>2026-02-06T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Gina Cusimano</author><author>Ryan P. Staupe</author><author>Nicole L. Sullivan</author>
        <description><![CDATA[Long-lived plasma cells (LLPCs) are a subset of antibody secreting cells (ASCs) that reside within lymphoid tissues, including the bone marrow (BM) and gut associated lymphoid tissues (GALT), and can secrete antigen-specific antibodies for up to decades or longer. Due to these traits, LLPCs serve as a crucial mediator for durable protective immunity. The signals needed to control the differentiation of LLPCs from naïve B cells, however, are not well understood. Accordingly, it remains a challenge to design vaccines that specifically drive LLPC generation and subsequent antibody durability. In this review, we discuss LLPC generation and heterogeneity following vaccination, vaccine design decisions known to impact immunological memory, and how novel emerging technologies can be used to inform on LLPC biology to enable LLPC targeting vaccine design.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2025.1685796</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2025.1685796</link>
        <title><![CDATA[Active LXR signaling, coupled with elevated mitochondrial and glycolytic metabolism contributes to GM-CSF–induced trained immunity]]></title>
        <pubdate>2026-01-07T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yuanyuan Liu</author><author>Arslan Hamid</author><author>Hannah Hardege</author><author>Qian Zhang</author><author>Helena Körner</author><author>Merle Leffers</author><author>Noelia A. Gonzalez</author><author>Gerhard Liebisch</author><author>Marcus Hoering</author><author>Hannes Findeisen</author><author>Katarzyna Placek</author><author>Mihai G. Netea</author><author>Holger Reinecke</author><author>Dennis Schwarz</author><author>Yahya Sohrabi</author>
        <description><![CDATA[Granulocyte-macrophage colony-stimulating factor (GM-CSF) contributes to the host defense and the pathogenesis of inflammatory diseases at least in part through inducing trained immunity (TI), however, the mechanism remains poorly characterized. In this paper, we systematically investigated the associated metabolic and epigenetic reprogramming, with a particular focus on the role of liver X receptors (LXRs) in this process. We employed a comprehensive experimental approach, including in vitro isolation and purification of human monocytes from healthy donors, cytokine assays, quantitative PCR, Seahorse metabolic analysis, flow cytometry, and chromatin immunoprecipitation (ChIP), shotgun lipidomics, as well as transcriptomic data analysis to investigate GM-CSF–induced trained immunity. Our results demonstrate that GM-CSF induces TI by enhancing cellular metabolism, as evidenced by increased glycolysis, mitochondrial activity, fatty acid oxidation, and pyruvate metabolism. Lipidomics and RNA sequencing analyses revealed upregulation of lipid synthesis, high triglyceride storage, and acetyl-CoA–producing pathways, leading to increased histone acetylation in GM-CSF–trained cells. Furthermore, glycolysis and mitochondrial metabolism are essential for establishing TI in these cells. Notably, pharmacological inhibition of GM-CSF activated LXR signaling, which potentially mediated via PPARγ, attenuated GM-CSF–induced TI via reducing glycolytic flux and histone acetylation while activation of LXR amplified these effects. Together, these results highlight the role of LXR in linking cellular metabolism with epigenetic reprogramming and demonstrate that elevated metabolic activity and active LXR signaling both are essential for GM-CSF–induced trained immunity. Importantly, these pathways may represent therapeutic targets for modulating GM-CSF–driven maladaptive inflammation in chronic inflammatory diseases.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2025.1773368</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2025.1773368</link>
        <title><![CDATA[Correction: The role of immune cells-mediated memory in weight cycling, glucose disorders and insulin resistance]]></title>
        <pubdate>2026-01-07T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Yiding Chen</author><author>Dongqi Zhou</author><author>Lan Wang</author><author>Lisha Sun</author><author>Yun Yin</author><author>Guo Liu</author><author>Changyan Zi</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2025.1671844</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2025.1671844</link>
        <title><![CDATA[Post-translational modification of NK cell receptors offers clues to antigenic specificity riddle]]></title>
        <pubdate>2026-01-07T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Maria O. Ustiuzhanina</author><author>Elena I. Kovalenko</author><author>Dmitry M. Chudakov</author>
        <description><![CDATA[Natural killer (NK) cells protect against infections through a distinctive combination of innate and adaptive immune capabilities. They exhibit characteristics of immunological memory by enhanced secondary response to pathogen exposure. We discuss current progress in identifying long-lived NK cell clones with enhanced memory functionality and the capacity for intensive cytokine and cytotoxic granule production upon re-encountering external antigens. We examine data related to how various NK cell receptors facilitate the recognition of specific foreign peptides in particular human leukocyte antigen (HLA) contexts and may promote the formation of memory clones. Finally, we propose and substantiate a model that resolves the accumulated fundamental contradictions and explains the semi-antigen-specific nature of the NK cell response through the clonally imprinted expression patterns of enzymes involved in the post-translational modification of HLA-binding receptors.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2025.1721553</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2025.1721553</link>
        <title><![CDATA[The role of immune cells-mediated memory in weight cycling, glucose disorders and insulin resistance]]></title>
        <pubdate>2025-12-18T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Yiding Chen</author><author>Dongqi Zhou</author><author>Lan Wang</author><author>Lisha Sun</author><author>Yun Yin</author><author>Guo Liu</author><author>Changyan Zi</author>
        <description><![CDATA[Weight cycling (WC), defined as the repeated process of weight gain and loss, is one of the biggest challenges in the management of weight. It is estimated that the majority of individuals (60%) will regain their lost weight within a few years. There is a positive correlation between WC and the increased risk of metabolic diseases. Although multiple factors probably contribute to this variation, immune cells-mediated immune memory plays a key role. In this review, we showed that immune memory is one of the core mechanisms of WC, glucose and insulin disorders. Immune cells, such as macrophages, CD4+ T cells, CD8+ T cells, Treg cells and CD7+ monocytes, were included. We also exhibited potential therapies to prevent WC targeting immune memory.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2025.1666233</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2025.1666233</link>
        <title><![CDATA[Reversing inflammatory diseases via trained immunity: mechanisms, challenges, and prospects]]></title>
        <pubdate>2025-10-15T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Wanli Xu</author><author>Zhilin Guo</author><author>Tingyun Xu</author><author>Junjie Chen</author><author>Leyi Chen</author><author>Wenan Xu</author>
        <description><![CDATA[Chronic inflammatory diseases are widespread and often accompanied by comorbidities, making treatment challenging. Current immunosuppressive and anti-inflammatory therapies have limited efficacy and significant side effects, and are insufficient to address the complexity of coexisting conditions. This review explores recent advances in innate immune memory, also known as trained immunity, and its potential role in inflammatory diseases. We hypothesize that targeting the regulatory mechanisms of trained immunity may lead to novel therapeutic strategies that more effectively control inflammation and improve disease outcomes. Finally, we highlight that the interplay between trained immunity and inflammatory diseases remains incompletely understood, and further research is needed to elucidate its mechanisms and clinical translational potential.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fimmu.2025.1669796</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fimmu.2025.1669796</link>
        <title><![CDATA[Trained immunity in atherosclerosis: plasticity, metabolic-vascular axis, and AI-driven precision remodeling]]></title>
        <pubdate>2025-10-10T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Bing Zhao</author><author>Jiayang Wan</author><author>Huifen Zhou</author><author>Jiehong Yang</author><author>Haitong Wan</author>
        <description><![CDATA[Chronic inflammation linked to atherosclerosis is closely related to a trained immunoregulatory network. Traditional studies primarily focus on the pro-inflammatory memory of monocytes, they frequently neglect important aspects such as the cell’s plasticity, interactions between different organs, and the dynamic regulation of the metabolism-vascular axis. This review presents four novel frameworks, including the trained immunity plasticity spectrum model. It demonstrates how monocytes maintain a dynamic balance between pro-inflammatory, tolerogenic, and anti-inflammatory phenotypes, regulated by mTOR/AMPK signaling and competitive histone modifications. The trained immunity–metabolism–vascular axis shows that metabolic disorders can change the way immune memory is formed. They achieve this by modifying the vascular microenvironment through epigenetic changes, exosomes, and products of mitochondrial stress. The cross-organ trained immunity framework reveals how remote epigenetic communication between the bone marrow, gut, and liver influences the development of monocytes. Finally, dynamic immune reprogramming integrates CRISPR-based epigenetic editing, metabolism-focused interventions, and AI-driven multi-omics predictions. This approach signifies a major transition from simply alleviating symptoms to accurately reshaping immune memory. This review reinterprets the immunometabolic mechanisms of atherosclerosis. It also lays the foundation for personalized therapies enhanced by AI and explores new interdisciplinary research avenues.]]></description>
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