Type 2 Inflammatory Diseases: specific and common mechanisms, comorbidities and lessons learned from targeted therapy

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Submission deadlines

  1. Manuscript Summary Submission Deadline 1 March 2026 | Manuscript Submission Deadline 19 June 2026

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Background

Diseases driven by type 2 inflammation at epithelial barriers include several chronic allergic and atopic disorders involving the skin, airway, and gastrointestinal tract. In general, type 2 inflammation is characterized by the presence of Th2 cells and ILC2s, which secrete the type 2 inflammatory cytokines IL-4, IL-5, IL-13, and IL-31 in response to epithelial-derived alarmins, including IL-33 and TSLP. Further, tissue infiltration of eosinophils and/or activated macrophages, accompanied by activated mast cells, often results in impaired defense against pathogens by barrier dysfunctionality and altered expression of antimicrobial peptides. Many of these conditions are also complicated by an increased risk of infections due to impaired or dysregulated epithelial immunity. Aside from that, microbial colonization or infections can alter atopic conditions, either being protective (e.g., the “hygiene hypothesis”), or provocative.

This Research Topic aims to explore the spectrum of these conditions, including:

• Skin diseases (e.g., atopic dermatitis (AD), chronic spontaneous urticaria, and prurigo nodularis);
• Diseases of the lower airways (e.g., asthma or eosinophilic/type 2 COPD);
• Conditions of the upper airways (e.g., allergic rhinitis, CRSwNP); and
• Diseases of the gastrointestinal tract (e.g., food allergy and eosinophilic esophagitis (EoE)).

The introduction of novel therapies in recent years has revolutionized our understanding of type 2 inflammatory diseases. These biologicals target specific pathways of type 2 diseases such as the IL-4R alpha chain, IL-5, IL-13, IL-31RA, TSLP, or IgE, and have proven their efficacy. Our understanding of type 2 inflammation processes has substantially grown by observing patients under these therapies (and also those clinical trials on type 2 inflammation key molecules, which failed to show improvement so far). Recent studies give rise to hope that targeted treatment leads to prevention of the development of comorbidities, and also to have a positive effect on infection risk. Whether a remission or disease modification by reprogramming of the immune system can be achieved is currently a central debate. In parallel, the impact of anti-inflammatory therapeutics interfering more broadly with immune cell activation, e.g. inhibiting janus kinases, on infection susceptibility remains to be elucidated.

These findings on barrier disturbance, comorbidities and infection susceptibility in type-2 inflammatory conditions may appear to be disease- or organ specific, but are one of a kind, since being caused by the common cytokine milieu. The important interplay of the immune system and the barrier plays an important role in the aforementioned observations and this research topic aims to connect and provide an interdisciplinary view to finally help identifying key mediators and mechanisms. This will help to answer critical questions spanning endotyping, biomarkers of response, optimal treatment selection, and risk reduction of comorbidities.

We welcome Original Research, Reviews, Perspectives, and Clinical Trial reports that provide an interdisciplinary view to identify key mediators and mechanisms. We particularly invite contributions addressing:

- Specific and common mechanisms of type 2 inflammation, particularly alarmin signaling.
- "Lessons learned" from both successful and failed clinical trials with targeted therapies.
- Real-world data comparing biologicals and JAK inhibitors regarding infection risk and comorbidities.
- Endotyping strategies and biomarkers for predicting treatment response.
- The potential for disease modification and remission through immune reprogramming.

Please note that manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation, for instance in an independent patient population or by PCR, are considered out of scope.

Topic Editor Dong-Hun Lee has served as an investigator and/or speaker and/or advisor for AbbVie, Amgen, AmorePacific, Cosmax, EHL Bio, Eli Lilly, Galderma, Incyte, Kangstem Bio, LEO Pharma, Novartis, Pfizer, and Sanofi. Topic Editor Stephan Traidl has served as a consultant and/or received lecture fees from Abbvie, Almirall, Johnson & Johnson, Lilly, LEO Pharma, La Roche-Posay, Novartis, and Sanofi, and has received research funding or grants from the Deutsche Forschungsgemeinschaft (DFG), Else Kröner Fresenius Stiftung, FreeNovation Stiftung, International Society of Atopic Dermatitis, Kanert Stiftung, and Sanofi. Topic Editor Lennart Roesner received grants to their institution by Almirall and Novartis; received personal fees from Almirall and Novartis for consulting services and holding public lectures.

Article types and fees

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

  • Brief Research Report
  • Case Report
  • Classification
  • Clinical Trial
  • Editorial
  • FAIR² Data
  • General Commentary
  • Hypothesis and Theory
  • Methods

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Article types

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

  • Brief Research Report
  • Case Report
  • Classification
  • Clinical Trial
  • Editorial
  • FAIR² Data
  • General Commentary
  • Hypothesis and Theory
  • Methods
  • Mini Review
  • Opinion
  • Original Research
  • Perspective
  • Review
  • Study Protocol
  • Systematic Review
  • Technology and Code

Keywords: Inflammation, type 2, inflammatory, disease, epithelial, immune crosstalk, infection

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