Review
Chemistry, Medicinal
Jianru Chen, Shuli Li, Chunying Li
Summary: Vitiligo is an autoimmune depigment disease caused by the destruction of melanocytes due to various factors, including genetic susceptibility, oxidative stress, and immune dysfunction. Research suggests that most melanocyte deaths are a result of abnormal immune responses, including heightened innate immunity, skewed T helper cells, and cytotoxic T lymphocytes.
MEDICINAL RESEARCH REVIEWS
(2021)
Review
Immunology
Erica L. Katz, John E. Harris
Summary: Vitiligo is a skin disease characterized by white spots, and significant progress has been made in understanding its pathogenesis over the past 30 years through perseverance, collaboration, and open-minded discussion. Researchers have explored various possible mechanisms through innervation, microvascular anomalies, oxidative stress, defects in melanocyte adhesion, autoimmunity, somatic mosaicism, and genetics, with animal models and improved patient sample collection methods playing important roles in translational studies.
FRONTIERS IN IMMUNOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Asako Yamamoto, Lingli Yang, Yasutaka Kuroda, Jiao Guo, Lanting Teng, Daisuke Tsuruta, Ichiro Katayama
Summary: The skin, as the outermost barrier of the body, is a major target of oxidative stress. Local synthesis of estrogen in the skin to protect from oxidative stress has been explored, with abnormal local estrogen synthesis potentially involved in skin disorders. The findings suggest potential new intervention targets for combination therapy for conditions such as vitiligo.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Review
Pharmacology & Pharmacy
Bo Xie, Yuqi Zhu, Yuqing Shen, Wen Xu, Xiuzu Song
Summary: The treatment of vitiligo is challenging due to its complex pathogenesis, which involves genetic factors, oxidative stress, and abnormal cell adhesion. It is important to suppress autoimmune attacks and activate melanocyte functions for successful treatment.
EXPERT OPINION ON THERAPEUTIC TARGETS
(2023)
Article
Oncology
Xiuyi Wu, Shanglin Jin, Yiwen Yang, Xiaoli Lu, Xiaoxi Dai, Zhongyi Xu, Chengfeng Zhang, Leihong Flora Xiang
Summary: The expression of ferroptosis markers is altered in the epidermis of vitiligo patients and iron deficiency is revealed in their blood. Erastin induces ferroptosis in human epidermal MCs in vitro, while NAC protects MCs from ferroptosis.
PIGMENT CELL & MELANOMA RESEARCH
(2022)
Review
Dermatology
Shintaro Inoue, Ichiro Katayama, Tamio Suzuki, Atsushi Tanemura, Shosuke Ito, Yuko Abe, Yasuyuki Sumikawa, Momoko Yoshikawa, Kayoko Suzuki, Akiko Yagami, Yukiko Masui, Akiko Ito, Kayoko Matsunaga
Summary: This review examines the major considerations for developing rhododendrol-induced leukoderma, providing a wide range of information on pathophysiology, mechanisms, risk evaluation, and potential treatments. The review discusses cytotoxicity of rhododendrol, cytoprotective functions, involvement of the immune system, and potential novel treatments, addressing individual differences and the mechanisms underlying the condition. Understanding rhododendrol-induced leukoderma not only sheds light on the mechanisms of non-segmental vitiligo, but also suggests possible prevention and treatment strategies.
JOURNAL OF DERMATOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Mala Singh, Mohmmad Shoab Mansuri, Ashlesha Kadam, Sayantani P. Palit, Mitesh Dwivedi, Naresh C. Laddha, Rasheedunnisa Begum
Summary: TNF-alpha levels were found to be increased in vitiligo patients, impacting melanocyte biology. Stimulation with TNF-alpha resulted in reduced cell viability, increased cellular and mitochondrial ROS, and compromised complex I activity in melanocytes. TNF-alpha exposure also led to cell apoptosis and autophagy, indicating a functional link between autophagy and melanocyte destruction in autoimmune vitiligo pathogenesis.
Article
Dermatology
Mona A. Atwa, Sara Mohammed Mohammed Ali, Nahed Youssef, Radwa El-Sayed Mahmoud Marie
Summary: Background Vitiligo is a common acquired disorder of depigmentation. IL-15, a cytokine in the IL-2 family, plays a crucial role in autoimmune diseases but has been poorly investigated in patients with vitiligo. The study found that serum IL-15 levels were significantly higher in patients with vitiligo compared to healthy controls, and there was a positive correlation between IL-15 levels and vitiligo severity.
JOURNAL OF COSMETIC DERMATOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Nan-Hyung Kim, Ha Jung Kim, Ai-Young Lee
Summary: AQP3 downregulation in vitiligo leads to oxidative stress and subsequent melanocyte death.
BIOMOLECULES & THERAPEUTICS
(2023)
Article
Dermatology
Radwa El-Sayed Mahmoud Marie, Al-Zahraa Mohamed Adel, Noha M. Abd El-Fadeal, Moustafa Mohamad Kamel Eyada
Summary: The study revealed that serum IL-38 levels were significantly higher in patients with vitiligo compared to healthy controls, and were associated with disease severity and activity.
JOURNAL OF COSMETIC DERMATOLOGY
(2022)
Article
Immunology
Mala Singh, Shahnawaz D. Jadeja, Jayvadan Vaishnav, Mohmmad Shoab Mansuri, Chandni Shah, Jay M. Mayatra, Atul Shah, Rasheedunnisa Begum
Summary: This study investigated the association between interleukin-6 (IL6) and vitiligo. The results showed that IL6 -572 G/C polymorphism was associated with vitiligo susceptibility, and increased IL6 expression in vitiligo patients had potential effects on normal human melanocytes (NHM).
IMMUNOLOGICAL INVESTIGATIONS
(2022)
Review
Dermatology
Helena Zenedin Marchioro, Caio Cesar Silva de Castro, Vinicius Medeiros Fava, Paula Hitomi Sakiyama, Gerson Dellatorre, Helio Amante Miot
Summary: Vitiligo is a complex disease caused by genetic components, metabolic factors, immune response, and cellular damage. Oxidative stress, decreased melanocyte adhesion, and autoimmune reactions play important roles in the development of vitiligo. Additionally, the activation of the type 1-IFN pathway and dysfunction of regulatory T-cells contribute to the progression of the disease.
ANAIS BRASILEIROS DE DERMATOLOGIA
(2022)
Review
Allergy
Yinghan Wang, Shuli Li, Chunying Li
Summary: Vitiligo is an autoimmune disease characterized by the loss of epidermal melanocytes, resulting in white patches on the skin, with challenges such as chronicity, treatment resistance, and negative psychosocial effects. Multiple mechanisms including genetics, environmental factors, and immune-mediated inflammation are involved in melanocyte disappearance. Understanding of the immune pathogenesis has led to the development of new therapeutic options targeting IFN-gamma signaling pathways, revolutionizing the treatment of vitiligo.
CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY
(2021)
Review
Immunology
Chen Lyu, Yonghu Sun
Summary: Vitiligo is a skin disorder characterized by the loss of melanocytes. The pathogenesis of vitiligo involves immunometabolism, including mitochondrial dysfunction, oxidative stress, and defects in metabolic pathways. These abnormalities are influenced by genetic and epigenetic factors and are associated with glucose and lipid metabolism. Melanocytes, keratinocytes, and tissue-resident memory T cells play important roles in the dysregulation of metabolic pathways in vitiligo.
FRONTIERS IN IMMUNOLOGY
(2022)
Review
Immunology
Firdosh Shah, Shivani Patel, Rasheedunnisa Begum, Mitesh Dwivedi
Summary: Vitiligo is an acquired depigmenting disorder affecting skin and mucous membranes, with autoimmunity strongly suggested as playing a role in melanocyte loss. Tissue Resident Memory T cells (TRMs) may persist in skin or peripheral tissues, reactivating to become autoreactive TRM cells and contributing to autoimmune diseases like vitiligo. Understanding different subsets of TRM cells, their retention in skin, and their pathomechanisms leading to melanocyte death may offer insights for developing effective vitiligo therapeutics.
AUTOIMMUNITY REVIEWS
(2021)
Article
Immunology
Mala Singh, Shahnawaz D. Jadeja, Jayvadan Vaishnav, Mohmmad Shoab Mansuri, Chandni Shah, Jay M. Mayatra, Atul Shah, Rasheedunnisa Begum
Summary: This study investigated the association between interleukin-6 (IL6) and vitiligo. The results showed that IL6 -572 G/C polymorphism was associated with vitiligo susceptibility, and increased IL6 expression in vitiligo patients had potential effects on normal human melanocytes (NHM).
IMMUNOLOGICAL INVESTIGATIONS
(2022)
Article
Biochemistry & Molecular Biology
Roma Patel, Nishant Parmar, Sayantani Pramanik Palit, Nirali Rathwa, A. V. Ramachandran, Rasheedunnisa Begum
Summary: This review summarizes the therapeutic potential of melatonin in various diabetic models and explores whether it can be considered a safe drug for managing diabetic complications and manifestations such as oxidative stress, inflammation, ER stress, mitochondrial dysfunction, metabolic dysregulation, etc.
Article
Genetics & Heredity
Prashant S. Giri, Rasheedunnisa Begum, Mitesh Dwivedi
Summary: The TNFA gene-308 G A polymorphism is associated with vitiligo susceptibility, with varied results among different populations. The study also indicates significant associations between gene genotypes and alleles in active vitiligo patients and those with localized vitiligo in different regions.
Article
Medicine, Research & Experimental
Nirali Rathwa, Nishant Parmar, Sayantani Pramanik Palit, Roma Patel, Ravi Sankar Bhaskaran, A. Ramachandran, Rasheedunnisa Begum
Summary: In this study, the effects of calorie restriction (CR) and gamma-aminobutyric acid (GABA) treatment on a high-fat diet (HFD) + streptozotocin (STZ) induced type 2 diabetes (T2D) mouse model were assessed. The combination therapy of CR + GABA showed improved metabolic parameters compared to monotherapies, with increased transcript levels and mitochondrial complex activities in liver, as well as enhanced pancreatic beta-cell regeneration and reduced apoptosis.
Article
Immunology
Jayvadan Vaishnav, Shahnawaz D. Jadeja, Mala Singh, Farheen Khan, Madhu Yadav, Rasheedunnisa Begum
Summary: This study investigated the association of VTCN1 intronic polymorphisms with vitiligo susceptibility in the Gujarat population and assessed the expression of VTCN1 and NRD1 genes in vitiligo patients. The results showed altered expression levels of VTCN1 and NRD1 in the blood and skin of vitiligo patients, suggesting their potential role in the development and progression of vitiligo.
IMMUNOLOGICAL INVESTIGATIONS
(2022)
Article
Immunology
Prashant S. Giri, Ankit H. Bharti, Rasheedunnisa Begum, Mitesh Dwivedi
Summary: NFATs and FOXP3 are associated with impaired regulatory T-cells (Tregs) in generalized vitiligo (GV). This study investigated the calcium mediated NFATc1 signaling pathway and its effect on Treg suppressive capacity in GV. The results showed altered calcium homeostasis in GV Tregs, leading to decreased calcineurin and NFATc1 activity. Elevated GSK-3 beta activity and DYRK1A transcripts were also involved in reduced NFATc1 activity in GV Tregs. Calcium treatment enhanced Treg-mediated suppression and increased Tregs associated cytokines, suggesting the potential of calcium-NFATc1 signaling pathway as a therapeutic target for improving Treg function in GV.
Review
Biochemistry & Molecular Biology
Prashant S. Giri, Mitesh Dwivedi
Summary: This study investigated the association of Interleukin 4 (IL4) variable number tandem repeats (VNTR) polymorphism with Rheumatoid Arthritis (RA) risk, severity, and protection through a meta-analysis. The results showed that the R2R2 genotype and R2 allele of IL4 VNTR were associated with increased RA risk in Asian populations and with RA protection in Turkish populations. Additionally, the R2R2 genotype and R2 allele were significantly associated with RA severity in different populations.
BIOCHEMICAL GENETICS
(2023)
Review
Immunology
Prashant S. Giri, Jahanvi Mistry, Mitesh Dwivedi
Summary: Vitiligo is a noncontagious autoimmune skin depigmenting disease. This meta-analysis study explores the role of regulatory T cells (Tregs) in vitiligo pathogenesis and finds that vitiligo patients have reduced Tregs' frequency, suppressive capacity, and key suppressive molecules such as FOXP3, IL-10, and TGF-beta. The study also suggests that Treg-based therapeutic interventions could be effective in vitiligo patients, supported by the increased Tregs' frequency and suppressive molecule expression after certain treatments.
JOURNAL OF IMMUNOLOGY RESEARCH
(2022)
Article
Immunology
Prashant S. Giri, Ankit H. Bharti, Mitesh Dwivedi
Summary: This study reveals for the first time the critical role of GZMB, NRP1, SERPINB9, and ITPR1 transcripts in decreased Treg suppressive capacity in GV pathogenesis, progression, and severity. Furthermore, it suggests a correlation between ITPR1 and decreased expression of GZMB and NRP1 in GV Tregs. Additionally, the study suggests that increased SERPINB9 transcripts may lead to endogenous granzyme B-mediated Tregs apoptosis and that calcium treatment of Tregs may improve their suppressive capacity.
JOURNAL OF IMMUNOLOGY RESEARCH
(2022)
Article
Multidisciplinary Sciences
Mitesh Dwivedi, Sanjay Tiwari, E. Helen Kemp, Rasheedunnisa Begum
Summary: Regulatory T cells (Tregs) are important in immune tolerance and suppressing inflammation, but their activity hinders anti-cancer immune responses. Suppressing Treg activity is a novel and effective approach for successful cancer immunotherapy, and there is growing interest in utilizing Tregs to enhance anti-cancer immunity. This review summarizes the crucial mechanisms of Tregs' suppression of anti-cancer immunity and discusses strategies to suppress or alter Tregs to improve immune response against tumors.
Article
Endocrinology & Metabolism
R. Patel, N. Parmar, S. P. Palit, N. Rathwa, R. Begum
Summary: The combination of melatonin and sitagliptin shows therapeutic potential in improving T2D manifestations. In vivo and in vitro studies demonstrate that this combination treatment can improve metabolic parameters, glyco-lipid metabolism, mitochondrial function, and insulin sensitivity.
JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION
(2023)
Article
Genetics & Heredity
Prashant Giri, Radhika Bhimani, Siddhika Patil, Mitesh Dwivedi
Summary: This study suggests that NFATC2 rs4811198 (T > G) 3' UTR and NFATC2 rs12479626 (T > C) structural SNPs may be associated with GV susceptibility, but NFAT 3' UTR and NFATC1 rs754093 (T > G) structural SNPs are not significantly associated with GV.
Article
Dermatology
Firdosh Shah, Ankit H. Bharti, Prashant S. Giri, Mitesh Dwivedi
Summary: This study found that there are defects in the numbers and functional of TRM-Tregs and antigen-specific Tregs in patients with generalized vitiligo(GV). These defects result in the inability to suppress the cytotoxic function and proliferation of CD4(+) and CD8(+) TRM cells, compromising the survival of melanocytes.
EXPERIMENTAL DERMATOLOGY
(2023)
Article
Immunology
Prashant S. Giri, Ankit H. Bharti, Jyoti Kode, Rasheedunnisa Begum, Mitesh Dwivedi
Summary: This study suggests that Harmine and Kaempferol treated Tregs may control the proliferation and production of CD8+ and CD4(+) T-cells in GV patients, leading to melanocytes' survival and proliferation.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2023)
Article
Dermatology
Matthew J. Davis, Gokul Srinivasan, Rachael Chacko, Sophie Chen, Anish Suvarna, Louis J. Vaickus, Veronica C. Torres, Sassan Hodge, Eunice Y. Chen, Sarah Preum, Kimberley S. Samkoe, Brock C. Christensen, Matthew R. Leboeuf, Joshua J. Levy
Summary: The development and application of AI algorithms are of great significance for the removal of cSCC, as they can improve operational efficiency and accuracy, especially for moderately and poorly differentiated tumors/ neoplasms. Further improvement is needed to maintain sensitivity to surrounding tissue and determine anatomical positioning.
EXPERIMENTAL DERMATOLOGY
(2024)
Article
Dermatology
Lingjing Chen, Qing Yu, Feiying Guo, Xuewen Wang, Zhenying Cai, Qiang Zhou
Summary: This study investigated the role and mechanisms of NTS in stress-induced hair growth inhibition. The results demonstrated that NTS effectively counteracted hair growth inhibition caused by stress and regulated the expression of multiple genes related to hair growth at the transcriptional level.
EXPERIMENTAL DERMATOLOGY
(2024)
