Selective inhibition of tyrosine kinase 2 prevents and restores interleukin-12-induced hair follicle immune privilege collapse: a novel approach to alopecia areata therapy?

Author(s):  
J. Edelkamp
2020 ◽  
Vol 4 (6) ◽  
pp. s108
Author(s):  
Anjaneya Chimalakonda ◽  
James Burke ◽  
Lihong Cheng ◽  
Ian Catlett ◽  
Aditya Patel ◽  
...  

Abstract not available.


2014 ◽  
Vol 6 (3) ◽  
pp. 263-266
Author(s):  
Simona Corina ȘENILĂ ◽  
Ovidiu BĂLĂCESCU ◽  
Loredana BĂLĂCESCU ◽  
Elisabeta CANDREA ◽  
Loredana UNGUREANU ◽  
...  

Alopecia areata (AA) is a chronic, T-cell mediated autoimmune disease directed against the hair follicle, which partially evolves due to a loss of the immune privilege of the anagen hair follicle. The immune privilege is maintained by several factors, including a downregulation of MHC class I and II, local immunosupressants and expression of Fas ligand. The purpose of the study was to evaluate several factors involved in the collapse and restoration of the immune privilege. We investigated IDO1, IGF1 and red/IK gene expression in lesional and perilesionalscalp biopsies from alopecia areata patients. Seven paired punch-biopsies were taken from the active edge of alopecic plaque and from the perilesional scalp. Expression of IDO1, IGF1 and red/IK genes was performed by qRT-PCR. In lesional tissue, IGF1, IDO1 and red/IK genes showed an increase in the mRNA levels as compared with the perilesional scalp. By comparing the pairs of data for the investigated genes, IDO1was statistically upregulated in the lesional area. No significant differences were observed between the gene expression in mild or severe AA, from the lesional or perilesional areas. IDO1 mRNA expression was higher in patients with a relapse duration of less than 6 months as compared to patients with a relapse duration of more than 6 months; levels of IGF1 and red/IK mRNA are increased in lesionals compared to perilesional scalp area.


2018 ◽  
Vol 113 (Supplement) ◽  
pp. S355
Author(s):  
James R. Burke ◽  
Lihong Cheng ◽  
Joann Strnad ◽  
Yifan Zhang ◽  
Elizabeth M. Heimrich ◽  
...  

2020 ◽  
Vol 29 (8) ◽  
pp. 703-725 ◽  
Author(s):  
Marta Bertolini ◽  
Kevin McElwee ◽  
Amos Gilhar ◽  
Silvia Bulfone‐Paus ◽  
Ralf Paus

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Taisuke Ito

Alopecia areata is considered to be a cell-mediated autoimmune disease, in which autoreactive cytotoxic T cells recognize melanocyte-associated proteins such as tyrosinase. This review discusses recent advances in the understanding of the pathogenesis of alopecia areata, focusing on immunobiology and hormonal aspects of hair follicles (HFs). The HF is a unique “miniorgan” with its own immune and hormonal microenvironment. The immunosuppressive milieu of the anagen hair bulb modulated by immunosuppressive factors is known as “hair follicle immune privilege.” The collapse of the hair follicle immune privilege leads to autoimmune reactions against hair follicle autoantigens. Alopecia areata is sometimes triggered by viral infections such as influenza that causes excess production of interferons (IFN). IFN-γis one of the key factors that lead to the collapse of immune privilege. This paper reviews the interactions between the endocrine and immune systems and hair follicles in the pathogenesis of alopecia areata.


2017 ◽  
Vol 137 (10) ◽  
pp. S235
Author(s):  
D. Broadley ◽  
A. sharov ◽  
J. Sundberg ◽  
M. Bertolini ◽  
A.N. Mardaryev ◽  
...  

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