γδ T cells and innate-like lymphocytes in skin immunity and autoinflammation

γδ T cells are a specialized subset of T lymphocytes distinguished by their MHC-independent antigen recognition, enabling rapid responses to stress, infections, and cellular perturbations. In the skin, these cells act as frontline sentinels, bridging innate and adaptive immunity. Emerging evidence indicates that dysregulation of γδ T cells contributes to the pathogenesis of autoinflammatory and autoimmune skin disorders, including psoriasis, lupus, and chronic dermatitis, primarily through cytokine-driven inflammation and tissue damage. Understanding the phenotypic and functional heterogeneity of γδ T cells in these contexts is critical to elucidating disease mechanisms and informing therapeutic strategies.

This Research Topic aims to gather high-quality contributions that dissect the mechanisms through which γδ T cells—and, where relevant, other innate-like lymphocytes such as MAIT cells, NKT cells, and ILCs—modulate skin immunity in health and autoinflammatory disease. We particularly encourage studies that focus on disease-driving mechanisms, including subset-specific cytokine production (e.g., IL-17, IFN-γ), signaling pathway dysregulation, and cellular interactions that amplify or regulate skin inflammation. Investigations into tissue residency, memory-like properties, and cross-talk with other immune populations are highly relevant when connected to pathological inflammation.

We welcome submissions addressing, but not limited to:

-Phenotypic and functional characterization of γδ T cell subsets in autoinflammatory and autoimmune skin disorders
-Mechanisms by which γδ T cells contribute to cytokine-mediated tissue damage, inflammation, or disease exacerbation.
-Interactions between γδ T cells, keratinocytes, macrophages, and other innate and adaptive immune populations driving autoinflammatory pathology.
-Signaling, genetic, epigenetic, and metabolic dysregulation underlying pathogenic γδ T cell responses.
-Mechanistic and translational insights into therapeutic strategies targeting γδ T cells or related innate-like lymphocytes (MAIT, NKT, ILCs) to modulate skin inflammation.

Submissions of original research, comprehensive reviews, and mechanistic clinical studies are encouraged. Manuscripts should focus on pathogenesis, underlying mechanisms, and translational implications, emphasizing how modulation of γδ T cells or other innate-like lymphocytes can mitigate skin inflammation and improve outcomes in autoinflammatory disorders.

The topic editors declare no conflict of interest

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
• Conceptual Analysis
• Editorial
• FAIR² Data
• General Commentary
• Hypothesis and Theory
• ... View all formats

Articles that are accepted for publication by our external editors following rigorous peer review incur a publishing fee charged to Authors, institutions, or funders.

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
• Conceptual Analysis
• Editorial
• FAIR² Data
• General Commentary
• Hypothesis and Theory
• Methods
• Mini Review
• Opinion
• Original Research
• Perspective
• Review
• Study Protocol
• Systematic Review
• Technology and Code

Keywords: γδ T cells, MAIT cells, NKT cells, ILCs, skin immunity, autoinflammation, autoimmune skin disorders, IL-17, tissue residency, immune regulation

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.