Vitiligo, reactive oxygen species and T-cells

2010 ◽  
Vol 120 (3) ◽  
pp. 99-120 ◽  
Author(s):  
Steven J. Glassman

The acquired depigmenting disorder of vitiligo affects an estimated 1% of the world population and constitutes one of the commonest dermatoses. Although essentially asymptomatic, the psychosocial impact of vitiligo can be severe. The cause of vitiligo remains enigmatic, hampering efforts at successful therapy. The underlying pathogenesis of the pigment loss has, however, been clarified to some extent in recent years, offering the prospect of effective treatment, accurate prognosis and rational preventative strategies. Vitiligo occurs when functioning melanocytes disappear from the epidermis. A single dominant pathway is unlikely to account for all cases of melanocyte loss in vitiligo; rather, it is the result of complex interactions of biochemical, environmental and immunological events, in a permissive genetic milieu. ROS (reactive oxygen species) and H2O2 in excess can damage biological processes, and this situation has been documented in active vitiligo skin. Tyrosinase activity is impaired by excess H2O2 through oxidation of methionine residues in this key melanogenic enzyme. Mechanisms for repairing this oxidant damage are also damaged by H2O2, compounding the effect. Numerous proteins and peptides, in addition to tyrosinase, are similarly affected. It is possible that oxidant stress is the principal cause of vitiligo. However, there is also ample evidence of immunological phenomena in vitiligo, particularly in established chronic and progressive disease. Both innate and adaptive arms of the immune system are involved, with a dominant role for T-cells. Sensitized CD8+ T-cells are targeted to melanocyte differentiation antigens and destroy melanocytes either as the primary event in vitiligo or as a secondary promotive consequence. There is speculation on the interplay, if any, between ROS and the immune system in the pathogenesis of vitiligo. The present review focuses on the scientific evidence linking alterations in ROS and/or T-cells to vitiligo.

2010 ◽  
Vol 107 (41) ◽  
pp. 17686-17691 ◽  
Author(s):  
Marina D. Kraaij ◽  
Nigel D. L. Savage ◽  
Sandra W. van der Kooij ◽  
Karin Koekkoek ◽  
Jun Wang ◽  
...  

2012 ◽  
Vol 18 (4) ◽  
pp. 661-671 ◽  
Author(s):  
Bruno Cuzzi ◽  
Paola Cescutti ◽  
Linda Furlanis ◽  
Cristina Lagatolla ◽  
Luisa Sturiale ◽  
...  

2020 ◽  
Vol 32 (13) ◽  
pp. 943-956
Author(s):  
Desiree Anthony ◽  
Angelica Papanicolaou ◽  
Hao Wang ◽  
Huei Jiunn Seow ◽  
Eunice E. To ◽  
...  

2018 ◽  
Vol 19 (9) ◽  
pp. 2814 ◽  
Author(s):  
Svantje Tauber ◽  
Swantje Christoffel ◽  
Cora Thiel ◽  
Oliver Ullrich

Whereby several types of cultured cells are sensitive to gravity, the immune system belongs to the most affected systems during spaceflight. Since reactive oxygen species/reactive nitrogen species (ROS/RNS) are serving as signals of cellular homeostasis, particularly in the cells of the immune system, we investigated the immediate effect of altered gravity on the transcription of 86 genes involved in reactive oxygen species metabolism, antioxidative systems, and cellular response to oxidative stress, using parabolic flight and suborbital ballistic rocket experiments and microarray analysis. In human myelomonocytic U937 cells, we detected a rapid response of 19.8% of all of the investigated oxidative stress-related transcripts to 1.8 g of hypergravity and 1.1% to microgravity as early as after 20 s. Nearly all (97.2%) of the initially altered transcripts adapted after 75 s of hypergravity (max. 13.5 g), and 100% adapted after 5 min of microgravity. After the almost complete adaptation of initially altered transcripts, a significant second pool of differentially expressed transcripts appeared. In contrast, we detected nearly no response of oxidative stress-related transcripts in human Jurkat T cells to altered gravity. In conclusion, we assume a very well-regulated homeostasis and transcriptional stability of oxidative stress-related pathways in altered gravity in cells of the human immune system.


2020 ◽  
Vol 2020 ◽  
pp. 1-14 ◽  
Author(s):  
Mohammad javad Tavassolifar ◽  
Mohammad Vodjgani ◽  
Zahra Salehi ◽  
Maryam Izad

Multiple roles have been indicated for reactive oxygen species (ROS) in the immune system in recent years. ROS have been extensively studied due to their ability to damage DNA and other subcellular structures. Noticeably, they have been identified as a pivotal second messenger for T-cell receptor signaling and T-cell activation and participate in antigen cross-presentation and chemotaxis. As an agent with direct toxic effects on cells, ROS lead to the initiation of the autoimmune response. Moreover, ROS levels are regulated by antioxidant systems, which include enzymatic and nonenzymatic antioxidants. Enzymatic antioxidants include superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase. Nonenzymatic antioxidants contain vitamins C, A, and E, glutathione, and thioredoxin. Particularly, cellular antioxidant systems have important functions in maintaining the redox system homeostasis. This review will discuss the significant roles of ROS generation and antioxidant systems under normal conditions, in the immune system, and pathogenesis of multiple sclerosis.


2003 ◽  
Vol 111 (2) ◽  
pp. S169
Author(s):  
J.A. Cornejo-Garcia ◽  
M.J. Torres ◽  
C. Mayorga ◽  
C. Antunez ◽  
T. Bellon ◽  
...  

APOPTOSIS ◽  
2005 ◽  
Vol 10 (6) ◽  
pp. 1433-1443 ◽  
Author(s):  
M. Pajusto ◽  
T. H. Toivonen ◽  
J. Tarkkanen ◽  
E. Jokitalo ◽  
P. S. Mattila

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