Age-associated B Cells: Central Players in Immunosenescence, Autoimmunity and Chronic Inflammation

About this Research Topic

Submission deadlines

  1. Manuscript Summary Submission Deadline 31 October 2025 | Manuscript Submission Deadline 28 February 2026

  2. This Research Topic is still accepting articles.

Background

Aging is accompanied by profound alterations in the immune system, collectively termed immunosenescence, contributing to heightened susceptibility to infections, poor vaccine responsiveness, and an increased incidence of autoimmunity and chronic inflammatory diseases. Central to the immune aging process is a distinct subset of B cells known as age-associated B cells (ABCs). These cells accumulate during aging, exhibit unique transcriptional signatures (such as T-bet expression), and demonstrate amplified responses to innate immune stimuli, notably TLR7 and TLR9 signals. ABCs have dual roles, acting both protectively in antiviral immunity and pathogenically by exacerbating autoimmunity and tissue damage. Despite rapidly growing interest, the precise mechanisms underlying their emergence, function, and interactions within the aging immune environment remain incompletely understood.

This Research Topic seeks to further our understanding of ABCs as pivotal modulators of immune aging, autoimmunity, and chronic inflammation. Current evidence increasingly highlights ABCs as essential drivers of age-related immune dysfunction; however, their developmental origins, functional diversity, and context-dependent behavior remain elusive. Recent technological advances—including single-cell RNA sequencing, lineage tracing, and systems-level immunology—are beginning to clarify ABC subset complexity and the pathways governing their interactions within the immune landscape. Expanding beyond intrinsic ABC biology, this Topic also encourages studies exploring ABC interactions with various immune cells (such as T cells, myeloid cells, and other immune subsets) and their interactions with stromal and tissue cells, thereby providing comprehensive insights into their integrated role in immune aging.

Several critical questions remain open: What molecular and cellular factors drive ABC expansion during aging? How do ABC interactions with immune and non-immune cell populations influence chronic inflammatory responses and compromise immune tolerance? Can therapeutic interventions selectively targeting ABC subsets be developed effectively without impairing beneficial immune responses?

This Research Topic aims to gather original research, reviews, and perspective articles addressing the molecular signatures, dynamic cellular networks, and immune regulatory interactions involving ABCs. By integrating findings from diverse model systems, human studies, and molecular approaches, this Topic will facilitate a holistic perspective on the contribution of ABCs to aging and autoimmune diseases and identify novel therapeutic avenues and biomarkers.

We welcome submissions addressing:

o Mechanistic insights into ABC differentiation, maintenance, and functional diversification
o Interaction of ABCs with adaptive and innate immune cells, stromal cells, or other tissue cells involved in aging and disease
o Roles of ABCs in autoimmune and chronic inflammatory disorders
o Implications of ABC-mediated interactions for impaired humoral immunity in elderly populations
o Novel therapeutic strategies selectively targeting ABC subsets and their pathways
o Utilization of ABCs as biomarkers for immune aging and disease susceptibility

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This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

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  • Mini Review

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Keywords: age-associated B cells, ABCs, immunosenescence, autoimmunity, chronic inflammation, B Lymphocytes

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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