Trichohyalin is a Potential Major Autoantigen in Human Alopecia Areata

Leung, Man Ching; Sutton, Chris W.; Fenton, David A.; Tobin, Desmond J.

doi:10.1021/pr100422u

Cited by 64 publications

(64 citation statements)

References 47 publications

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“…The absence of co-stimulation during antigen presentation can induce deletion and anergy of cognate T cells [187]. It implies that an AA treatment may interfere with co-stimulation or APC assisted activation of effector CD8 + T cells [188]. Cytotoxic T-lymphocyte-associated antigen 4-IgG (CTLA4-Ig), known as abatacept and belatacept, prevents binding of CTLA4 on T cells to CD80 and CD86 on APCs.…”

Section: Interference With Antigen Presentation and Costimulationmentioning

confidence: 99%

“…Development of ASIT for human AA has not been launched since the primary autoantigens of AA remain undetermined [188]. Studies suggest enrichment of CD8 + T cell subsets that target hair follicle keratinocyte expressed trichohyalin and melanocyte expressed epitopes, though other antigens are also likely targeted [215].…”

Section: Anergy Promotion In Pathogeneic T Cellsmentioning

confidence: 99%

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The role of lymphocytes in the development and treatment of alopecia areata

Guo

Cheng

Shapiro

et al. 2015

Expert Review of Clinical Immunology

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SummaryAlopecia areata (AA) development is associated with both innate and adaptive immune cell activation, migration to peri-and intra-follicular regions, and hair follicle disruption. Both CD4+ and CD8+ lymphocytes are abundant in AA lesions; however, CD8+ cytotoxic T lymphocytes are more likely to enter inside hair follicles, circumstantially suggesting that they have a significant role to play in AA development. Several rodent models recapitulate important features of the human autoimmune disease and demonstrate that CD8+ cytotoxic T lymphocytes are fundamentally required for AA induction and perpetuation. However, the initiating events, the selfantigens involved, and the molecular signaling pathways, all need further exploration. Studying CD8+ cytotoxic T lymphocytes and their fate decisions in AA development may reveal new and improved treatment approaches.

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Section: Interference With Antigen Presentation and Costimulationmentioning

confidence: 99%

Section: Anergy Promotion In Pathogeneic T Cellsmentioning

confidence: 99%

The role of lymphocytes in the development and treatment of alopecia areata

Guo

Cheng

Shapiro

et al. 2015

Expert Review of Clinical Immunology

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“…[24,25] Hair follicle-specific antibodies are increased in peripheral blood of AA patients, especially to keratin 16 and trichohyalin. [26] It is believed that hair follicle is an immune-privileged site. [9] In healthy hair follicle epithelium, major histocompatibility complex (MHC) class I and II molecules are not expressed and TGF-,IGF-1, and -MSH are more expressed.…”

Section: Etiopathogenesis Etiopathogenesismentioning

confidence: 99%

Alopecia areata: An update

Seetharam¹

2013

Indian J Dermatol Venereol Leprol

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Alopecia areata (AA) is a common form of non-scarring hair loss of scalp and/or body. Genetic predisposition, autoimmunity, and environmental factors play a major role in the etiopathogenesis of AA. Patchy AA is the most common form. Atopy and autoimmune thyroiditis are most common associated conditions. Peribulbar and intrabulbar lymphocytic inflammatory infiltrate resembling "swarm of bees" is characteristic on histopathology. Treatment is mainly focused to contain the disease activity. Corticosteroids are the preferred treatments in form of topical, intralesional, or systemic therapy. Camouflage in the form of wigs may be an alternative option in refractory cases.

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“…The underlying mechanisms by which antigenic deiminated proteins arise might be relevant to the pathogenesis of various immune diseases. Although TCHH was reported to be a major autoantigen in the sera of the patients with alopecia areata (Leung et al 2010 ), it has not been determined whether deimination of TCHH is related to human diseases. The resistance of hair cuticles against mechanical insults has shown to be conferred, at least in part, by disulfi de cross-links of S100A3 (Inoue et al 2000 ;Kizawa et al 2005b ).…”

Section: Discussionmentioning

confidence: 99%