Alopecia areata: an autoimmune disease?

McElwee, Kevin J.; Tobin, Desmond J.; Bystryn, Jean‐Claude; King, Lloyd E.; Sundberg, John P.

doi:10.1111/j.1600-0625.1999.tb00385.x

Cited by 100 publications

(110 citation statements)

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“…By microarray analyses, several key effector CTL specific transcripts have been identified in mouse and human AA skin [16]. Depletion of CD4 + or CD8 + cells using monoclonal antibodies (mAb) enables hair regrowth in mouse and rat models [83][84][85]. Transfer of CD8 + T cells in conjunction with CD4 + T cells can induce extensive AA lesions in mouse models [16,77,[86][87][88].…”

Section: Cd8 + Cytotoxic Lymphocyte Mediated Hair Follicle Disruptionmentioning

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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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: Cd8 + Cytotoxic Lymphocyte Mediated Hair Follicle Disruptionmentioning

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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“…The most widely accepted hypothesis describes AA as a T-cell mediated autoimmune response targeting an unknown antigen in anagen-stage hair follicles. 8,9 It has also been postulated that compromise of immune privilege in normal hair follicles, mediated in part by interferon-gamma (INF-g), 10 has a role in the susceptibility and pathogenesis of AA. 11,12 Considerable evidence indicates that genetic elements have a significant role in the etiology of AA, as evidenced by the recent identification of a number of suggested susceptibility loci, 13 the high incidence of positive family history in affected individuals 14,15 and high twin concordance rates.…”

Section: Introductionmentioning

confidence: 99%

Peripheral blood gene expression in alopecia areata reveals molecular pathways distinguishing heritability, disease and severity

Coda¹,

Hysa²,

Seiffert-Sinha³

et al. 2010

Genes Immun

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Alopecia areata (AA) is an autoimmune hair loss disorder in which systemic disturbances have been described, but are poorly understood. To evaluate disease mechanisms, we examined gene expression in the blood of defined clinical subgroups (patchy AA persistent type, AAP, n ¼ 5; alopecia universalis, AU, n ¼ 4) and healthy controls (unaffected relatives, UaR, n ¼ 5; unaffected non-relatives, UaNR, n ¼ 4) using microarrays. Unsupervised hierarchical clustering separates all four patient and control groups, producing three distinct expression patterns reflective of 'inheritance', 'disease' and 'severity' signatures. Functional classification of differentially expressed genes (DEGs) comparing disease (AAP, AU) vs normal (UaR) groups reveals upregulation in immune response, cytokine signaling, signal transduction, cell cycle, proteolysis and cell adhesionrelated genes. Pathway analysis further reveals the activation of several genes related to natural killer-cell cytotoxicity, apoptosis, mitogen activated protein kinase, Wnt signaling and B-and T-cell receptor signaling in AA patients. Finally, 35 genes differentially expressed in AA blood overlap with DEGs previously identified in AA skin lesions. Our results implicate innate and adaptive immune processes while also revealing novel pathways, such as Wnt signaling and apoptosis, relevant to AA pathogenesis. Our data suggest that peripheral blood expression profiles of AA patients likely carry new biomarkers associated with disease susceptibility and expression.

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“…The presence of lymphocytes around and within the hair follicles and the ability to promote hair regrowth with the use of immunosuppressive agents is consistent with an autoimmune hypothesis. 16 Environmental factors:A variety of environmental factors, including infections, drugs, trauma, and stress, have been suggested as triggering factors of AA, although most patients with AA are unaware of any obvious precipitating factor. PATHOGENESIS:Injury is severest in the center, leading to sudden precipitation of a group of follicles into telogen.…”

mentioning

confidence: 99%