Vitiligo results from a selective loss of epidermal melanocytes and affects around 0.5% of the world population. Both sexes are affected, and there are no apparent differences in rates of occurrence according to phototype or ethnicity. Vitiligo is a disfiguring disease that remains a therapeutic challenge. A better understanding of the physio-pathology of this disease and the testing of new promising targeted therapies remains of utmost importance for patients.
Vitiligo is a complex disease, involving a combination of genetic and environmental factors, together with metabolic and immune alterations. Abnormalities leading to impaired melanocyte regeneration and/or proliferation suggest that defect(s) in melanocytes play an important role in this disease. However, it is becoming increasingly evident that inflammation and autoimmunity are also central players, in particular during the progressive phase of the disease. The critical role of the immune response during vitiligo pathogenesis has now largely been described and future emerging therapeutics are targeting the immune pathway. Indeed, most of the identified susceptibility genes (GWAS studies) are related to the immune system. Deregulation of the inflammasome and the JAK/STAT pathway has been highlighted, and Increasing evidence is pointing out the role of both innate (such as plasmacytoid dendritic cells, innate lymphoid cells, natural killer cells) and adaptive (in particular T cells) immune cells together with their related cytokines and chemokines during disease pathogenesis. In contrast, a defect in regulatory T cells number and/or function was reported. In addition, immunomodulating agents, such as JAK inhibitors, appear as promising therapeutic strategies for patients.
In this Research Topic, we aim to gather articles that will focus on the involvement of the immune response in the pathogenesis of vitiligo. We welcome basic research, translational and clinical studies that discuss (i) the genetic, molecular and cellular aspects of the role of the immune system in vitiligo, (ii) therapeutic targeting of the immune system for the treatment of vitiligo, and (iii) vitiligo-like depigmentations appearing under immune checkpoint inhibitors therapy. We welcome the submission of the following article types:
1. Original research articles
2. Review / Mini Review
3. Systematic reviews
4. Clinical trials
5. Case reports (with a particular interest in immune aspect of vitiligo)
6. Methods
Topic Editor Prof. John E. Harris is Scientific Founder of Villaris Therapeutics, Inc. Topic Editor Prof. Julien Seneschal received financial support from Sanofi Genzyme and Calypso Biotech. Topic Editor Prof. Caroline Le Poole is the CSO for Temprian Therapeutics, a company hoping to bring an HSP70iQ435A-based treatment to clinical trials for vitiligo. The approach for this treatment is different and separate from the proposed Research Topic. Please note that studies investigating HSP70iQ435A-based treatment thus fall out of the remit of this project. All other Topic Editors declare no competing interests with regards to the Research Topic subject.
Vitiligo results from a selective loss of epidermal melanocytes and affects around 0.5% of the world population. Both sexes are affected, and there are no apparent differences in rates of occurrence according to phototype or ethnicity. Vitiligo is a disfiguring disease that remains a therapeutic challenge. A better understanding of the physio-pathology of this disease and the testing of new promising targeted therapies remains of utmost importance for patients.
Vitiligo is a complex disease, involving a combination of genetic and environmental factors, together with metabolic and immune alterations. Abnormalities leading to impaired melanocyte regeneration and/or proliferation suggest that defect(s) in melanocytes play an important role in this disease. However, it is becoming increasingly evident that inflammation and autoimmunity are also central players, in particular during the progressive phase of the disease. The critical role of the immune response during vitiligo pathogenesis has now largely been described and future emerging therapeutics are targeting the immune pathway. Indeed, most of the identified susceptibility genes (GWAS studies) are related to the immune system. Deregulation of the inflammasome and the JAK/STAT pathway has been highlighted, and Increasing evidence is pointing out the role of both innate (such as plasmacytoid dendritic cells, innate lymphoid cells, natural killer cells) and adaptive (in particular T cells) immune cells together with their related cytokines and chemokines during disease pathogenesis. In contrast, a defect in regulatory T cells number and/or function was reported. In addition, immunomodulating agents, such as JAK inhibitors, appear as promising therapeutic strategies for patients.
In this Research Topic, we aim to gather articles that will focus on the involvement of the immune response in the pathogenesis of vitiligo. We welcome basic research, translational and clinical studies that discuss (i) the genetic, molecular and cellular aspects of the role of the immune system in vitiligo, (ii) therapeutic targeting of the immune system for the treatment of vitiligo, and (iii) vitiligo-like depigmentations appearing under immune checkpoint inhibitors therapy. We welcome the submission of the following article types:
1. Original research articles
2. Review / Mini Review
3. Systematic reviews
4. Clinical trials
5. Case reports (with a particular interest in immune aspect of vitiligo)
6. Methods
Topic Editor Prof. John E. Harris is Scientific Founder of Villaris Therapeutics, Inc. Topic Editor Prof. Julien Seneschal received financial support from Sanofi Genzyme and Calypso Biotech. Topic Editor Prof. Caroline Le Poole is the CSO for Temprian Therapeutics, a company hoping to bring an HSP70iQ435A-based treatment to clinical trials for vitiligo. The approach for this treatment is different and separate from the proposed Research Topic. Please note that studies investigating HSP70iQ435A-based treatment thus fall out of the remit of this project. All other Topic Editors declare no competing interests with regards to the Research Topic subject.