Role of oxidative stress and autoimmunity in onset and progression of vitiligo

Abstract

Figure S1. (a-c) Specificity of the antibody was verified in sections of paraffin-embedded HEK cells transiently transfected with human b) and , respectively. The sections were subjected to immunofluorescence; (a) HEK cells transfected with human IL-20 stained with polyclonal rabbit anti-IL-20 and detected with Alexa 488 (green); (b) HEK cells transfected with human IL-20 and stained with a preimmune serum control from the rabbit in which the polyclonal rabbit anti-IL-20 was generated and detected with Alexa 488 (green); (c) HEK cells transfected with human IL-19 were stained with polyclonal rabbit anti-IL-20, and the nuclei were marked with Hoechst (blue). Stained for IL-20 (green); (d-g) localization of IL-20 protein in lesional psoriatic skin (LS). Paraffin-embedded punch biopsies from LS were subjected to immunofluorescence. (d) Stained for IL-20 (green); (e) same tissue as (d) stained with pre-immune-rabbit serum; (f) stained for IL-20 (green) and nuclear DNA (blue); (g) same tissue as (f), the anti-IL-20 has been pre-absorbed with antigen (IL-20), also stained for nuclear DNA (blue). Figure S2. Immunofluorescence stainings for IL-20 and double immunofluorescence stainings for IL-20 and selected CD markers in untreated lesional psoriatic skin. Figure S3. Effect of treatment with calcipotriol (10 patients, mild-to-moderate psoriasis) left panel, or cyclosporin A (10 patients, moderate-severe psoriasis) right panel, before (day 0) and after treatment for 14 and 28 days and compared with non-lesional skin also at day 0.Data S1. Experimental design. Table S1. Antibodies used for staining paraffinembedded punch biopsies. Abstract: Vitiligo is an acquired depigmentation disorder characterized by the loss of functional melanocytes from the epidermis. Two major theories of vitiligo pathogenesis include autoimmunity and oxidative stress-mediated toxicity in melanocytes. The present study aimed to evaluate both the hypotheses in vitiligo patients and to investigate their role in the disease onset and progression. Antimelanocyte antibody levels and lipid peroxidation (LPO) levels were evaluated in 427 patients and 440 controls; antithyroid peroxidase (TPO) antibody levels were estimated in 102 patients and 72 controls. Patients showed a significant increase in LPO and antimelanocyte antibody levels compared to controls. Antimelanocyte antibody and LPO levels were higher in active vitiligo compared to stable. Only 9.8% of patients showed the presence of anti-TPO antibodies in their circulation. Oxidative stress may be the initial triggering event to precipitate vitiligo in Gujarat population, which is exacerbated by contributing autoimmune factors together with oxidative stress.

Association of Neuropeptide Y (NPY), Interleukin-1B (IL1B) Genetic Variants and Correlation of IL1B Transcript Levels with Vitiligo Susceptibility

“…IL1B also plays a crucial role in driving the differentiation of Th17 and Th1 cells, ultimately evoking immune response against melanocytes [71]. Our recent studies have shown decrease in regulatory T-cells, increase in CD8 + T-cells and anti-melanocyte antibody levels in GV patients which were positively correlated with disease onset and progression [72], [73].…”

The role of serum vitamin D levels in vitiligo

“…The autoimmune theory is the best-supported one, because vitiligo may be associated with other autoimmune diseases including pernicious anemia, hyperthyroidism, Hashimoto's thyroiditis, alopecia areata and adrenocortical failure. Furthermore, histological studies have demonstrated a high frequency of cytotoxic T lymphocytes specific to melanocytic antigens in vitiligo lesions, suggesting a direct, melanocyte-specific T cell attack [9, 11, 12]. …”

Oxidized tyrosinase: A possible antigenic stimulus for non-segmental vitiligo autoantibodies

“…tyrosinase related protein 1 and 2 [8][9][10][39][40][41][42][43][44], but the cellular and molecular mechanisms that are responsible for the production of autoantibodies and the ways through which these antibodies participate in skin depigmentation remain highly controversial and point of debate [11,12,[44][45][46]. Despite of these controversy, the interplay between ROS and the autoimmunity in vitiligo is understood [12,45].…”

“…Despite of these controversy, the interplay between ROS and the autoimmunity in vitiligo is understood [12,45]. As for example, the excess production of ROS cause defective apoptosis of melanocytes, resulting in release of aberrated proteins, which can serve as autoantigens leading to autoimmunity [12,46].…”