Vitiligo

IntroductionAlopecia areata (AA) and vitiligo are both skin diseases of autoimmune origin. AA is characterized by patchy hair loss primarily on the scalp but may involve other areas as well, while vitiligo is caused by the destruction of melanocytes and results in the appearance of white patches on any part of the body. Many facts indicate similar pathogenesis of these diseases. Both dermatoses are associated with frequent coexistence of other autoimmune diseases and share common genetic risk factors. Recent data support the theory of the involvement of IL-17 in the pathogenesis of both AA and vitiligo.AimTo evaluate and compare the serum levels of interleukin (IL)-17 in patients with AA and non-segmental vitiligo (NSV). To assess whether the pattern of serum cytokine concentration can be associated with clinical details and activity of the disease.Material and methodsA cross-sectional study was conducted on 33 patients with AA, 30 patients with NSV, and 30 healthy controls. Serum levels of IL-17 were determined quantitatively by ELISA method.ResultsOur analysis identified a systemic inflammatory signature associated with AA and NSV, characterized by elevated levels of IL-17. The levels of IL-17 did not differ significantly between AA patients and NSV patients.ConclusionsOur results show that AA and vitiligo may share common etiopathogenetic pathways, which suggests the potential of developing targeted therapies for both AA and vitiligo treatment. Imbalance of T cell subpopulations and complex systemic cytokine profiles may contribute to the pathogenesis of AA and vitiligo.

Background: Vitiligo is a chronic disease that is often challenging to treat. Melanocyte destruction in vitiligo is mediated by immune pathways involving IFN-γ and CD8+ T cells. Tofacitinib, a Janus kinase (JAK) 1/3 inhibitor, can be a promising treatment for vitiligo due to its potential to inhibit IFN-γ signaling. We retrospectively reviewed the records of 16 patients (6 men, 10 women; mean age 39.7 years) with nonsegmental vitiligo refractory to conventional therapies who were treated with oral tofacitinib along with topical tacrolimus and phototherapy. Aims: To evaluate the efficacy and adverse effects of the JAK1/3 inhibitor, oral tofacitinib, in the treatment of nonsegmental vitiligo. Methods: We retrospectively reviewed the records of 16 patients (6 men, 10 women; mean age: 39.7 years) with nonsegmental vitiligo refractory to conventional therapies who were treated with oral tofacitinib along with topical tacrolimus and phototherapy. Improvement was assessed using Vitiligo Area Scoring Index (VASI) at weeks 6, 12, and 24. Hemogram, lipid profile, liver, and renal function tests were monitored during the treatment period. Results: Improvement was assessed using Vitiligo Area Scoring Index (VASI) at weeks 6, 12, and 24. Mean VASI scores improved from 5.038 at baseline to 1.269 at 24 weeks, with 13 patients (81.25%) achieving at least 50% improvement. Transient leukopenia was observed in 3 patients, and one patient developed palmar warts. Conclusions: Oral tofacitinib shows significant potential in the management of nonsegmental vitiligo, in patients unresponsive to conventional therapies especially in combination with phototherapy. No significant adverse effects were observed during the follow up period other than a transient leukopenia in three patients and palmar warts in one patient.

Vitiligo is a common pigment disorder of the skin resulting in destruction of melanocytes. Non-segmental vitiligo (NSV) is an autoimmune disorder. The etiopathogenesis of segmental vitiligo (SV) remains incompletely understood. Genetic predisposition and increased vulnerability of melanocytes towards stressors lead to a melanocyte-specific CD8+ T cell-driven immune response with a γ-interferon signature. Vitiligo may lead to significant impairment of life quality. Importantly, vitiligo can be associated with somatic and psychological disorders. Early recognition, correct classification, precise assessment of disease extent and activity, burden of disease and presence of comorbidities is crucial for a holistic therapeutic management. Shared decision making with the patient should define treatment goals including halting disease progression, induction of repigmentation, prevention of relapses, and in rare cases depigmentatation of residual normal skin. Topical treatments in addition to corticosteroids and calcineurin inhibitors now include the Janus kinase inhibitor ruxolitinib cream, as a first-line therapy officially approved for children from 12years on and adults with NSV and facial involvement. Targeted phototherapies, in combination with topical corticosteroids or calcineurin inhibitors, are used for limited NSV or SV. For extensive NSV, whole-body UVB-NB phototherapy remains a cornerstone treatment and may be combined with oral corticosteroid mini-pulses in rapidly progressive cases. Among emerging therapeutic options for NSV, oral Janus kinase inhibitors are the most advanced in clinical development.

Introduction/Background Vitiligo is a chronic autoimmune disease characterized by melanocyte destruction, leading to skin depigmentation. Limited data are available regarding the efficacy of long-term topical vitiligo treatment. In 2 randomized, double-blinded, vehicle-controlled phase 3 studies in adults and adolescents (aged ≥12 y) with nonsegmental vitiligo (TRuE-V1 [NCT04052425]; TRuE-V2 [NCT04057573]), ruxolitinib cream application resulted in statistically superior improvements in repigmentation versus vehicle in the primary and all key secondary endpoints at Week 24 and was well tolerated. In the open-label period of TRuE-V1/TRuE-V2 (Weeks 24–52) and the TRuE-V long-term extension (LTE; Weeks 52–104) study (NCT04530344), further improvements in facial and body repigmentation (as assessed by Vitiligo Area Scoring Index [VASI] responses) were observed through Week 104 among patients who continued to apply ruxolitinib cream. Objectives In this pooled analysis, we evaluated shifts in facial and total body VASI (F-VASI/T-VASI) responses among patients with vitiligo who had limited or no repigmentation at Week 24 and who continued to apply ruxolitinib cream for an additional 80 weeks. Methods In TRuE-V1/TRuE-V2, patients were randomized 2:1 to apply twice-daily 1.5% ruxolitinib cream or vehicle for 24 weeks, after which all patients could apply 1.5% ruxolitinib cream through Week 52. Patients who completed TRuE-V1/TRuE-V2 were eligible to enroll in the TRuE-V LTE. Patients who did not achieve ≥90% improvement in F-VASI at Week 52 continued to apply open-label 1.5% ruxolitinib cream until Week 104. Patients initially randomized to apply ruxolitinib cream who had <25% improvement from baseline in F-VASI or T-VASI at Week 24 and had non-missing VASI assessments at the evaluated time points were included in this analysis. Shifts in F-VASI and T-VASI were assessed among patients with no facial/body repigmentation or worsening depigmentation (≤0% improvement in F-VASI/T-VASI) and patients with limited facial/body repigmentation (>0%–<25% improvement in F-VASI/T-VASI) at Week 24. Results Among patients with no facial repigmentation at Week 24, improvements in F-VASI at Weeks 52 and 104 were observed in 77.8% (49/63) and 97.1% (34/35) of patients, respectively. Among patients with limited facial repigmentation at Week 24, F-VASI improvements at Weeks 52 and 104 were observed in 64.0% (32/50) and 83.3% (30/36) of patients, respectively. Across both groups, 54.9% (39/71) of patients achieved ≥75% improvement from baseline in F-VASI (F-VASI75) at Week 104. Among those with no body repigmentation at Week 24, T-VASI improvements at Weeks 52 and 104 were observed in 79.6% (39/49) and 93.3% (28/30) of patients, respectively. For those with limited body repigmentation at Week 24, T-VASI improvements at Weeks 52 and 104 were observed in 64.5% (80/124) and 81.6% (62/76) of patients, respectively. Across both groups who had <25% improvement in total body repigmentation at Week 24, 50.0% (53/106) of patients achieved ≥50% improvement in T-VASI (T-VASI50) at Week 104. Conclusions In the TRuE-V studies, ruxolitinib cream application for an additional 80 weeks resulted in improved repigmentation among patients with nonsegmental vitiligo who had limited or no repigmentation at Week 24. These 2-year TRuE-V results highlight the importance of prolonged treatment in patients with vitiligo, even when minimal or no repigmentation is achieved after 6 months of treatment.

Vitiligo is an acquired depigmenting skin disorder characterized by autoimmune-mediated melanocyte destruction, leading to well-defined depigmented macules and patches. Localized non-segmental vitiligo poses a significant therapeutic challenge. A total of 251 patients with localized refractory non-segmental vitiligo were randomized into four groups: combination therapy group (308 nm excimer laser + Janus kinase [JAK]inhibitors, n = 63), JAK inhibitor monotherapy group (n = 63), 308 nm excimer laser group (n = 63), and positive control group (n = 62). Treatment lasted 52 weeks. Therapeutic responses were assessed using the Vitiligo Area Scoring Index (VASI) and dermoscopy before and after treatment. Mixed-effects models compared efficacy and analyzed influencing factors. Fisher's exact test compared efficacy among groups and sites; Kruskal-Wallis test assessed melanocyte island density changes; chi-square test evaluated pigmentation stability and recurrence at the 1-year follow-up. Combination therapy with 308 nm excimer laser and oral JAK inhibitor baricitinib showed significantly greater efficacy than monotherapy and conventional treatment, with a 14.20% higher repigmentation rate than the positive control group (p < 0.001), indicating synergistic effects. By Week 4, patients with melanocyte island density ≥ 5/cm2 had markedly better repigmentation, supporting dermoscopy as an early predictive and monitoring tool. Mixed-effects analysis showed higher repigmentation in facial versus non-facial lesions, females vs. males, and reduced efficacy with longer disease duration. At the 1-year follow-up, combination therapy maintained stable pigmentation with no recurrence. The combination of 308 nm excimer laser and JAK inhibitors significantly enhances repigmentation efficiency in adult localized non-segmental vitiligo, particularly in patients with shorter disease duration and early formation of pigment islands.

IntroductionVitiligo is a chronic autoimmune disease characterized by destruction of melanocytes, leading to skin depigmentation. Vitiligo can have a high quality-of-life burden and profound impact on psychosocial well-being. The objectives of this study were to describe the self-reported patient burden among patients with nonsegmental vitiligo with ≤ 10% affected body surface area, summarize the physician-reported psychosocial and psychological impact of vitiligo on patient lives, and describe disease characteristics and treatment history, goals, and satisfaction.MethodsData were drawn from the Adelphi Vitiligo Disease Specific Programme™, a real-world, cross-sectional survey with retrospective data collection of physicians and patients with vitiligo, collected in the United States between October 2021 and April 2022. Separate surveys for dermatologists and patients contained questions on clinical and demographic characteristics of patients with vitiligo and burden of vitiligo. Treatment history, goals, and satisfaction were assessed together with the impact of vitiligo on quality of life.ResultsSixty-one dermatologists provided data for 326 patients with ≤ 10% affected body surface area (adults, n = 221; adolescents, n = 105); 90 of those patients also responded to the survey. The most common treatments were topical corticosteroids, topical calcineurin inhibitors, and narrow-band ultraviolet-B phototherapy, with the main treatment goal being repigmentation. Physician-reported treatment satisfaction was 56%; 25% of patients reported frustration with treatment options. Physicians reported impact of vitiligo on everyday life in 46% of patients. Patients reported 12.7% overall work impairment; mean scores for Hospital Anxiety and Depression Scale anxiety and depression domains were 3.5 and 2.2, respectively, and mean Vitiligo-specific Quality of Life index score was 26.9. Patients with facial involvement experienced higher burden than those without.ConclusionA high patient burden was reported by dermatologists and their patients with vitiligo who had ≤ 10% affected body surface area, including psychosocial and psychological consequences. These findings highlight an unmet need in the treatment of vitiligo.Supplementary InformationThe online version contains supplementary material available at 10.1007/s13555-024-01165-5.

Vitiligo is a frequently acquired, hereditary disease, characterized by achromic macules due to the absence of melanocytes. In contrast with earlier studies, in which the main pathogenic role was attributed to anti-melanocyte antibodies, recent papers have emphasized a role for CD8(+) cytotoxic T lymphocytes in melanocyte destruction. Fifteen percent of peripheral T cell express cutaneous lymphocyte-associated antigen (CLA), responsible for skin-homing T cell. Phototherapy is used to treat patients with generalized vitiligo and it has been shown to interfere with CLA(+) T cells in other skin diseases. To describe peripheral blood T cell subpopulations' frequency and ability to express the skin-homing molecule (CLA) in patients with non-segmental vitiligo, before and after photochemotherapy (PUVA). Twenty-two patients with generalized and active spreading vitiligo were submitted to 30 PUVA-8MOP sessions. Lymphocyte immunophenotyping was performed by flow cytometry using anti-CD3, anti-CD8 and anti-CLA monoclonal antibodies. Fifteen healthy volunteers, sex- and age-matched, were included as a control group. CD8(+) -CLA(+) T cells were significantly reduced in number in untreated vitiligo patients (P=0.008) when compared with control individuals, albeit with a more intense CLA expression (P=0.028). These findings were not altered after PUVA. No significant difference was noticed in CD4/CD8 ratios nor in CD4-CLA(+) T cell numbers between vitiligo patients and controls, both before and after PUVA. CD8-CLA(+) T cells are reduced in peripheral blood of patients with non-segmental vitiligo. This finding may be related to the previously reported increase of CD8(+) cells in both lesions and perilesional skin of these patients.

Sir, There is significant uncertainty surrounding vaccines against COVID-19. Due to the critical need, these vaccines are being developed and approved at a uniquely fast pace [1]. Currently, the approved vaccines take their action by administering the host with sequences encoding the viral spike protein. This essentially means that these gene-therapy-based vaccines, whose long-term effects remain unknown, are going to be administered globally [2]. Therefore, despite their safety and efficacy demonstrated in respective clinical trials, it is reasonable to be cautious and adopt more intensive post-marketing vigilance [3]. A forty-nine-year-old diabetic male presented with asymptomatic, rapidly growing, leukodermal patches on the scalp (Fig. 1), which began to appear suddenly fourteen days following the administration of the first dose of the Oxford–AstraZeneca (AZD1222) vaccine against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The patches were clinically consistent with vitiligo and were confirmed with their well-defined, ivory-white patches by Wood’s lamp examination (Fig. 2).There were no leucodermic patches anywhere else on the body, no family history of vitiligo, and no history of COVID-19 viral infection. After one week of reevaluation, the patch increased in size. The patient also presented with cellulitis on the right groin persistent for three days and was treated with an antibiotic with a follow-up. All baseline investigations, including a full blood count and renal and liver function tests, were normal. The patient is currently on follow-up. Cytokines play a role in regulating the immune response and the depigmentation process in vitiligo. There is an imbalance in cytokine levels in patients with vitiligo. IFN-g expression plays a role in the autoimmune process in vitiligo. The expression of the cytokine IFN-g is associated with melanocyte destruction in the active phase of vitiligo lesions [4]. IFN-g interacts with the viral receptor, resulting in the consequent reduction of several virus replicating, down-regulating genes and gene products [5]. Li et al. [6] demonstrated that IFNs are potential drug choices for SARS-CoV-2 infection. Here, we hypothesize that patients with non-segmental vitiligo (NSV), an autoimmune skin (and mucosal) disorder, may clear SARS-CoV-2 infection more efficiently and have a lower risk of COVID-19 development. Conversely, in the case of COVID-19 development, vitiligo autoimmunity may influence the cytokine storm-related disease burden. In addition, immune activation during SARS-CoV-2 infection or COVID-19 disease may increase vitiligo disease activity. Our hypothesis is based on the shift of the immune system in NSV toward adaptive type 1 (IFNg and CD8 T cells) and innate immune responses [7]. It is unclear whether the vitiligo in our patient was caused by vaccination, However, the temporal relationship between the vaccine and the development of the disease is interesting. We may, therefore, conclude that our patient had his latent vitiligo activated by the vaccine. Yet, further work is needed to demonstrate a causal relationship between vitiligo and COVID-19 vaccination. To the best of our knowledge, this is the first reported case of vitiligo associated with the administration of the Oxford–AstraZeneca (AZD1222) vaccine.

Vitiligo is acommon skin disease leading to depigmentation that is associated with progressive destruction of melanocytes. The main subtype, nonsegmental vitiligo (NSV), is considered achronic autoimmune disease leading to activation of melanocyte-specific CD8+ lymphocytes and development of acutaneous immune memory. Vitiligo can result in significant impairment of quality of life and is associated with anumber of comorbidities. Despite the existence of national guidelines and international treatment recommendations, there is astrong need for improved health care for patients with vitiligo. The options in the treatment algorithm for vitiligo are similar and consisted until recently of only topical and systemic corticosteroids, topical calcineurin inhibitors, phototherapy, and surgical interventions. New insights into the pathobiological role of the interferon signature in vitiligo have most recently contributed to the approval of the first vitiligo-specific therapy with the topical Janus kinase1/2 inhibitor ruxolitinib for patients with NSV.

Focal vitiligo is characterized by depigmented patches located in a small area without a typical segmental distribution. Focal vitiligo is classified as an undetermined type of vitiligo, and a more definitive diagnosis can be made when the lesions have not evolved into non-segmental or segmental vitiligo after a period of 1-2 years. However, the chance of progression is not known and may lead to treatment-indecision. The objective was to study the characteristics of patients with focal vitiligo and possible predictors of progression. We conducted a survey study in patients with initial diagnosis of focal vitiligo between January 2005 and June 2010. Focal vitiligo was defined as either a small acquired isolated depigmented lesion without typical segmental distribution, or two to three small acquired lesions localized in a non-segmental area with a maximum of 5 cm. The survey comprised of 21 questions concerning the patient's characteristics, the onset of focal vitiligo, progression of depigmentation and treatment history. We identified 128 eligible patients and the response rate was 40.6% (n = 52 completed questionnaires). Progression to non-segmental vitiligo occurred in 23%. The median follow-up duration was 7 years. In 11.5% of the patients, progression to non-segmental vitiligo occurred within 2 years after onset. Nevertheless, even after a first stable period of more than 2 years, another 11.5% of the patients advanced to non-segmental vitiligo. No associated prognostic factors at baseline of progression to non-segmental or long-lasting focal vitiligo were found. Focal vitiligo is a rare subtype of vitiligo and most patients have long-lasting focal lesions after onset of the disease. In this study, focal vitiligo progressed to typical non-segmental vitiligo, but not towards typical segmental vitiligo. Progression 2 years after onset of focal vitiligo, occurs in 50% of the patients with eventual progression to non-segmental vitiligo. There seem to be no clinical signs that predict progression in focal vitiligo.

Vitiligo, a widespread depigmenting skin condition is characterized by loss of melanocytes in a selective manner, resulting in nonscaly, chalky-white macules. Vitiligo is a common pigment-degrading skin disease, apparently marked by white patches on the skin and broadly classified into two categories: Segmental vitiligo and Non-segmental vitiligo. An extensive survey of AI-based diagnostic systems for segmental and nonsegmental vitiligo has also been presented. The dermatologist's experience and subjectivity in visual perception of depigmented skin lesions play a big role in Vitiligo diagnosis and its classification. So, there is a dearth need to implement machine learning approaches to improve diagnosis accuracy. Motivated by the fact, the intelligent convolutional neural networks (CNNs) based Vitiligo classification model IVC has been proposed in the research work to classify the Non-segmental vitiligo into its subtypes like Acrofacial, Focal, Generalized and Mucosal vitiligo. The dataset consisting of 507 vitiligo infected images has been collected and manually labelled to accomplish the whole research work.

(1) Background: Vitiligo is characterized by white patches on the skin caused by loss of melanocyte activity or the absence of these cells. The available treatments minimize the symptoms by retarding the process of skin depigmentation or re-pigmenting the affected regions. New studies are required for a better comprehension of the mechanisms that trigger the disease and for the development of more efficient treatments. Studies have suggested an autoimmune feature for vitiligo, based on the occurrence of other autoimmune diseases in vitiligo patients and their relatives, and on the involvement of genes related to the immune response. (2) Methods: We evaluated, by massive parallel sequencing, polymorphisms of the HLA-G gene in vitiligo patients and control samples, to verify if variants of this gene could influence the susceptibility to vitiligo. (3) Results: We detected an association with non-segmental vitiligo regarding the haplotype Distal-010101a/G*01:01:01:01/UTR-1, adjusting for population stratification by using ancestry-informative markers (AIMs). (4) Conclusions: It remains unclear whether the HLA-G variants associated with vitiligo were detected because of the high linkage disequilibrium (LD) with HLA-A*02, or if the HLA-A variants previously reported as associated with vitiligo were detected because of the high LD with HLA-G*01:01:01:01/UTR-1, or if both genes jointly contribute to vitiligo susceptibility.

The role of Langerhans cells in the pathogenesis of nonsegmental type vitiligo is still unknown. In this study, biopsies were taken from 26 patients at various stages of nonsegmental type vitiligo and morphometrically observed to investigate the kinetics of Langerhans cells in patients at various stages of the disease. A marked depletion of OKT6-positive and ATPase-positive epidermal dendritic cells was noted in patients with active nonsegmental type vitiligo. A repopulation of both OKT6-positive and ATPase-positive epidermal dendritic cells was noted in patients with stable nonsegmental type vitiligo. Profound depletion of epidermal OKT6-positive and ATPase-positive dendritic cells was noted in patients with repigmenting nonsegmental type vitiligo receiving treatments involving topical use of 0.05% Fluocinonide cream or PUVA photochemotherapy. Transmission electron microscopy confirmed the absence of epidermal dendritic cells (Langerhans cells and intermediate cells) in patients with active and repigmenting nonsegmental type vitiligo. In active nonsegmental type vitiligo, two possible explanations are proposed for the depletion of OKT6-positive and ATPase-positive epidermal dendritic cells (presumptive Langerhans cells): 1) the cells are destroyed by cytotoxic factors released during the course of destruction of melanocytes in active vitiligo, and/or 2) they leave the epidermis and migrate to regional lymph nodes to present certain antigens which are released from certain destroyed epidermal cells (keratinocytes or melanocytes) during the course of active vitiligo. The repopulated epidermal Langerhans cells may result from phenotypically transformed dermal dendritic cells in the depigmented lesions of patients with stable vitiligo. Since various therapies which result in repigmentation deplete the density of epidermal Langerhans cells markedly, it is suggested that depletion of epidermal Langerhans cells in stable vitiligo may aid in repigmentation. It is also proposed that the repopulated epidermal Langerhans cells may play a role in inhibiting the proliferation of epidermal melanocytes in depigmented lesions of stable vitiligo, thus various methods of treatment which deplete the Langerhans cells may eventually aid in the repigmentation of nonsegmental type vitiligo.

I firmly believe that vitiligo is an autoimmune disease in which autoreactive, melanocyte-specific cytotoxic T lymphocytes (CTL) escape central tolerance, break peripheral tolerance and destroy epidermal melanocytes. The evidence in favour of the autoimmune genesis of vitiligo is highly convincing. Suppression of immune reactivity by various effective treatments suggests that their immunosuppressive mechanism interferes with that which leads to the destruction of melanocytes (1-6). The association of vitiligo with other autoimmune diseases is well known (7-9). The presence of circulating anti-melanocyte antibodies points to a possible involvement of humoral immunity, while the involvement of cellular immunity is indicated by lymphocyte infiltration at the margin of lesions. In particular, the presence of cellular infiltrates during the progressive loss of melanocytes from depigmenting vitiligo skin (10) and the detection of T cells juxtapositionally apposed to remaining melanocytes (11) demonstrate the early implication of cellular immunity in the pathogenesis of the disease. Other views, however, exist. Intrinsically increased sensitivity of melanocytes to oxidative stress is said to be pathogenic. This, however, can be no more than a conjecture in the total absence of any experimental demonstration that it is a primary event. Fault can also be found with the postulation of an inappropriate reaction to neuropeptides as the leading cause. Their concentration in vitiligo skin is not sufficient to kill melanocytes, while the time course of their production is such as to rank them as a consequence rather than a cause (12). These and other proposed pathogenetic mechanisms have very little to offer in the way of proof. The point is ‘what immune cells are pathogenic? Melanocyte-specific autoantibodies are certainly present (13-17), but their pathogenic role is a mystery. The patchy distribution of cutaneous depigmentation and the very frequent symmetrical distribution of lesions fit in well with the view that autoimmune melanocyte destruction is induced by lymphocyte clones with affinities for specific areas of skin (18). We and others (19-21) have demonstrated the presence of high frequencies of melanocyte-specific CTL in the peripheral blood of patients with vitiligo. These autoreactive CTL are functionally intact and kill normal melanocytes in vitro. They display high avidity of antigen recognition and express the skin-homing receptor CLA (22). Overall, these findings strongly support an association between the presence of melanocyte-specific CTL and vitiligo, and directly point to their pathogenic role in this disease. Investigation of the association of vitiligo with melanoma has clarified the role of autoreactive CTL in its development. Identical clonally expanded CTL have been detected in a regressing melanoma and in the vitiligo-like halo surrounding the tumor (23). These and other findings assume that antigen-specific proliferation is involved in the destruction of normal and malignant melanocytes (24-26). Work from our group has contributed to the current opinion that vitiligo T cells demonstrate reactivity to antigens previously recognized as target antigens for T cells infiltrating melanoma tumors (20, 22, 27). Interestingly, in a comparison with melanoma-derived T cells, vitiligo T cells displayed greater reactivity towards melanoma cells (28). We believe that high avidity of antigen recognition represents a peculiar property of anti-melanocytic CTL from patients with vitiligo that contributes to their abnormal reactivity (29). In conclusion, melanocyte-specific CTL with high-affinity T-cell receptors most likely escape clonal deletion in the thymus and enter the circulation. By expressing CLA, they home to the skin where they express type 1 cytokine profiles and mediate melanocyte destruction. The immunological imbalances thus created may be supposed to herald the processes that also initiate a biochemical or neural mechanism for the destruction of melanocytes. Cellular autoimmunity can therefore be proposed as the sole cause and origin of vitiligo.

BackgroundVitiligo is a common acquired pigmentary disease caused by destruction of epidermal melanocytes in underlying autoimmune response. Few studies have been focused on the role of chemokines in non-segmental vitiligo (NSV) concomitant with autoimmune thyroid disease (AITD) and alopecia areata (AA).ObjectiveThe aim of this study was to determine the best serum biomarker for predictive role in the progression of vitiligo and to evaluate the influence of AA and/or AITD on vitiligo by using the biomarker.MethodsThis prospective cohort study recruited 45 NSV patients: 14 without either AITD or AA, 12 with AITD, 11 with AA, and 8 with both AITD and AA. Serum levels of CXCL1, CXCL8, CXCL9, CXCL10, CXCL12, CXCL13, and CXCL16 were analyzed by ELISA. CXCR3 mRNA expression was detected on PBMCs by RT-PCR. Improvement was evaluated using repigmentation scales.ResultsSerum CXCL10 levels, along with the expression of CXCR3 mRNA were higher in NSV patients with AITD or AA alone than in those without AITD or AA. Moreover, serum CXCL10 levels, along with the expression of CXCR3 mRNA were higher in NSV patients with both AITD and AA than in those with AITD or AA alone. Poorer repigmentation was observed in NSV patients with both AA and AITD than in those with AA or AITD alone.ConclusionCXCL10 could be a biomarker to predict the progression of NSV. Dermatologists should pay much attention to those NSV patients concomitant with AITD and/or AA, for comorbidity might lead to more active autoimmune reaction.