Research Topic

Alopecia Areata

About this Research Topic

Alopecia Areata (AA) is a CD8+ T cell-mediated autoimmune disease that is directed against anagen-associated autoantigens which become exposed to the immune system following the collapse of the hair follicle’s physiological immune privilege, and presumably only when hair follicles undergo active growth, produce a hair shaft, and are engaged in pigment synthesis (anagen).

The mechanisms that contribute to the development of AA are currently under investigation. A major genome wide association study (GWAS) strongly supported the importance of NKG2D in AA, which had previously been suggested by immunohistological analyses. In a large cohort of AA patients, expression of the genes encoding the NKG2D agonists, MICA, and even more prominently so, the MICA family member ULBP3, was found to be strongly associated with AA. Members of the γc cytokine-receptor pathway have also been implicated in AA, suggesting a role for downstream signaling via JAK molecules, with increased JAK1 and JAK3 expression detected in lesional human and mouse skin. In fact, even though properly controlled, randomized, double-blind, and prospective clinical trials on these findings remain to be published, an impressive preventive and therapeutic effect of JAK inhibitors (e.g. Ruxolitinib or Tofacitinib) has been observed in AA patients. Most studies have demonstrated a key role of IFN-γ, which signals via the JAK pathway, as a major pathogenic cytokine in AA. However, other studies and preliminary clinical case reports have pointed to additional therapeutically targetable components of other pathways and cytokines including IL-15, IL-13 and IL-23.

The aim of this Research Topic is to gather a collection of manuscripts to advance our understanding of the underlying mechanisms that drive Alopecia Areata (AA). We welcome manuscripts that focus on (i) the pathobiology of AA and (ii) how our improved understanding of this disease may lead to the development of more effective therapies for AA in the future. We welcome the submission of Review, Mini-Review and Perspective articles that discuss the following topics:

1. The pathobiology of AA: An introductory synthesis.
2. Novel pointers to AA pathobiology from preclinical and clinical studies.
3. Animal models for studying AA and for exploring novel therapeutic strategies.
4. The clinical perspective of AA: Key features of AA clinical presentation and response to current therapy that need to be kept in focus by translational immunology research.
5. Immunobiology of the hair follicle as an immune-privileged (mini)-organ.
6. Anagen–associated hair follicle autoantigens and their potential role in AA pathobiology.
7. The role of JAK-STAT signaling in the pathogenesis of AA.
8. The roles of Th1, Th2 and IL-23 signaling in the pathogenesis of AA.
9. Innate immunity in the pathogenesis of AA including studies on NK cells, γδ-T cells and mast cells.
10. Regulatory immunocytes in AA pathobiology.
11. Biomarkers of AA disease activity and for predicting response to therapy.
12. Psychoemotional stress and AA: Neuroimmunological and neuroendocrine considerations.
13. Learning from other cutaneous autoimmune diseases: Vitiligo, Systemic Lupus Erythematosus, and beyond.
14. Future research frontiers in the translational immunopathobiology of AA.


Keywords: Alopecia Areata


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.

Alopecia Areata (AA) is a CD8+ T cell-mediated autoimmune disease that is directed against anagen-associated autoantigens which become exposed to the immune system following the collapse of the hair follicle’s physiological immune privilege, and presumably only when hair follicles undergo active growth, produce a hair shaft, and are engaged in pigment synthesis (anagen).

The mechanisms that contribute to the development of AA are currently under investigation. A major genome wide association study (GWAS) strongly supported the importance of NKG2D in AA, which had previously been suggested by immunohistological analyses. In a large cohort of AA patients, expression of the genes encoding the NKG2D agonists, MICA, and even more prominently so, the MICA family member ULBP3, was found to be strongly associated with AA. Members of the γc cytokine-receptor pathway have also been implicated in AA, suggesting a role for downstream signaling via JAK molecules, with increased JAK1 and JAK3 expression detected in lesional human and mouse skin. In fact, even though properly controlled, randomized, double-blind, and prospective clinical trials on these findings remain to be published, an impressive preventive and therapeutic effect of JAK inhibitors (e.g. Ruxolitinib or Tofacitinib) has been observed in AA patients. Most studies have demonstrated a key role of IFN-γ, which signals via the JAK pathway, as a major pathogenic cytokine in AA. However, other studies and preliminary clinical case reports have pointed to additional therapeutically targetable components of other pathways and cytokines including IL-15, IL-13 and IL-23.

The aim of this Research Topic is to gather a collection of manuscripts to advance our understanding of the underlying mechanisms that drive Alopecia Areata (AA). We welcome manuscripts that focus on (i) the pathobiology of AA and (ii) how our improved understanding of this disease may lead to the development of more effective therapies for AA in the future. We welcome the submission of Review, Mini-Review and Perspective articles that discuss the following topics:

1. The pathobiology of AA: An introductory synthesis.
2. Novel pointers to AA pathobiology from preclinical and clinical studies.
3. Animal models for studying AA and for exploring novel therapeutic strategies.
4. The clinical perspective of AA: Key features of AA clinical presentation and response to current therapy that need to be kept in focus by translational immunology research.
5. Immunobiology of the hair follicle as an immune-privileged (mini)-organ.
6. Anagen–associated hair follicle autoantigens and their potential role in AA pathobiology.
7. The role of JAK-STAT signaling in the pathogenesis of AA.
8. The roles of Th1, Th2 and IL-23 signaling in the pathogenesis of AA.
9. Innate immunity in the pathogenesis of AA including studies on NK cells, γδ-T cells and mast cells.
10. Regulatory immunocytes in AA pathobiology.
11. Biomarkers of AA disease activity and for predicting response to therapy.
12. Psychoemotional stress and AA: Neuroimmunological and neuroendocrine considerations.
13. Learning from other cutaneous autoimmune diseases: Vitiligo, Systemic Lupus Erythematosus, and beyond.
14. Future research frontiers in the translational immunopathobiology of AA.


Keywords: Alopecia Areata


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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Submission Deadlines

01 February 2018 Abstract
01 June 2018 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

01 February 2018 Abstract
01 June 2018 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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