TY - JOUR
T1 - The Role of Hair Follicle Immune Privilege Collapse in Alopecia Areata
T2 - Status and Perspectives
AU - Paus, Ralf
AU - Bertolini, Marta
N1 - Funding Information:
Funding for the Summit and publication of this article was provided by the National Alopecia Areata Foundation.
PY - 2013/12
Y1 - 2013/12
N2 - Alopecia areata (AA) may represent a CD8+T cell–mediated, organ-specific autoimmune disease in which as yet elusive autoantigens are recognized, once they become exposed by ectopic major histocompatibility complex class I expression by anagen hair follicles (HFs) that have lost their relative immune privilege (IP). On this basis, AA research is chiefly challenged with identifying the autoreactive CD8+T cells and their cognate autoantigens as well as key inducers of HF-IP collapse and “HF-IP guardians” that prevent and/or can restore IP collapse. However, natural killer group 2D–positive (NKG2D+) cells (incl. NK, NKT, and CD8+T cells) and NKG2D–activating ligands from the MICA (MHC I–related chain A) family may also have a key role in AA pathogenesis, as a massive infiltrate of IFN-γ-secreting NKG2D+ cells alone suffices to induce the AA phenotype. Therefore, we speculate that AA may represent a stereotypic, but distinct HF response pattern to inflammatory insults associated with HF-IP collapse.
AB - Alopecia areata (AA) may represent a CD8+T cell–mediated, organ-specific autoimmune disease in which as yet elusive autoantigens are recognized, once they become exposed by ectopic major histocompatibility complex class I expression by anagen hair follicles (HFs) that have lost their relative immune privilege (IP). On this basis, AA research is chiefly challenged with identifying the autoreactive CD8+T cells and their cognate autoantigens as well as key inducers of HF-IP collapse and “HF-IP guardians” that prevent and/or can restore IP collapse. However, natural killer group 2D–positive (NKG2D+) cells (incl. NK, NKT, and CD8+T cells) and NKG2D–activating ligands from the MICA (MHC I–related chain A) family may also have a key role in AA pathogenesis, as a massive infiltrate of IFN-γ-secreting NKG2D+ cells alone suffices to induce the AA phenotype. Therefore, we speculate that AA may represent a stereotypic, but distinct HF response pattern to inflammatory insults associated with HF-IP collapse.
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U2 - 10.1038/jidsymp.2013.7
DO - 10.1038/jidsymp.2013.7
M3 - Review article
C2 - 24326544
AN - SCOPUS:84907227615
VL - 16
SP - S25-S27
JO - Journal of Investigative Dermatology Symposium Proceedings
JF - Journal of Investigative Dermatology Symposium Proceedings
SN - 1087-0024
IS - 1
ER -