Suscripción a Biblioteca: Guest
Portal Digitalde Biblioteca Digital eLibros Revistas Referencias y Libros de Ponencias Colecciones
Critical Reviews™ in Eukaryotic Gene Expression
Factor de Impacto: 1.841 Factor de Impacto de 5 años: 1.927 SJR: 0.649 SNIP: 0.516 CiteScore™: 1.96

ISSN Imprimir: 1045-4403
ISSN En Línea: 2162-6502

Critical Reviews™ in Eukaryotic Gene Expression

DOI: 10.1615/CritRevEukaryotGeneExpr.2017019558
pages 277-287

Involvement of Different Genes Expressions during Immunological and Inflammatory Responses in Vitiligo

Chandra Kant Sharma
Institute of Agricultural Science, SAGE University, Indore, India-452020
Monika Sharma
Department of Bioscience and Biotechnology, Banasthali Vidyapith (Women's University), Rajasthan, India
Kanika Prasad
Department of Bioscience and Biotechnology, Banasthali University, Rajasthan, India; Birla Institute of Technology and Science, Pilani, Rajasthan, India

SINOPSIS

Vitiligo is a condition of the skin distinguished by hypo-pigmentation. Etiology of this disorder is unknown, and several theories and mechanisms have been hypothesized. The inflammatory response in vitiligo is thought to be mediated by polymorphism in genes such as FOXP3, ACE, APE, GSTP1, TLR, SOD, CTLA-4, TAP/LMP gene cluster, etc. Theories including reactive oxygen species model, Nrf2–antioxidant response element (ARE) pathway, WNT pathway, tyrosinase activity, biochemical, molecular, and cellular alterations have been hypothesized to explain vitiligo pathogenesis. Melanosomal proteins are involved in antigen processing. The antigens are expressed to the T-cells in the form of peptides with HLA class II molecules. T-cells are activated in response to the discharge of co-stimulatory molecules such as LFA-3 as well as ICAM-1. An adaptive immune response is thus elicited, and the melanocytes eventually die or start malfunctioning and the skin undergoes hypo-pigmentation. IFN-γ is known to be a melanocyte inhibitor of paracrine origin; it is clearly involved in the early onset of symptoms of vitiligo disease. The surge in the IFN-γ levels mediates augmented expression of ICAM-1 molecule on the melanocytes, thereby establishing cytokine-mediated destruction of melanocytes. Mainly, mediators released by melanocytes and the functionality of keratinocytes decrease the disease activity. Such mediators include ET-1 as well as SCF, increase the pigmentation particularly when a patient is given with the UVB treatment. By scavenging ROS and screening UV radiation, melanin limits the damage caused to the cutaneous cells by UV radiation. Various immune responses play important roles in vitiligo.


Articles with similar content:

Modulation of Innate Immune Responses by Hantaviruses
Critical Reviews™ in Immunology, Vol.30, 2010, issue 6
Andreas Rang
Human Defensins and Cathelicidins in the Skin: Beyond Direct Antimicrobial Properties
Critical Reviews™ in Immunology, Vol.26, 2006, issue 6
Hideoki Ogawa, Isao Nagaoka, Francois Niyonsaba
The Role of Plasmacytoid Dendritic Cell-Derived IFNα in Antiviral Immunity
Critical Reviews™ in Immunology, Vol.28, 2008, issue 1
Angela Dolganiuc, Gyongyi Szabo
Dendritic Cells, Interleukin 12, and CD4+ Lymphocytes in the Initiation of Class l-restricted Reactivity to a Tumor/Self Peptide
Critical Reviews™ in Immunology, Vol.18, 1998, issue 1-2
Emira Ayroldi, Maria Laura Belladonna, Maria Cristina Fioretti, Daniela Surace, Silvia Silla, Paolo Puccetti, Ursula Grohmann, Roberta Bianchi
Phage Therapy against Streptococcus pneumoniae: Modern Tool to Control Pneumonia
Critical Reviews™ in Eukaryotic Gene Expression, Vol.27, 2017, issue 4
Muhammad Imran Qadir, Sahir Sajjad