2016
DOI: 10.1111/sji.12423
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Janus Kinase Inhibitors against Other Biological Treatments in Alopecia Areata

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Cited by 6 publications
(5 citation statements)
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“…In patients with advancing AA, changes in the activation state of peripheral blood mononuclear cells and upregulation of the co‐stimulatory molecules CD40 and CD80, the accessory molecule CD154, and interferon γ expression were identified and were independent of the extent of hair loss (Tavakolpour, ).…”
Section: Introductionmentioning
confidence: 99%
“…In patients with advancing AA, changes in the activation state of peripheral blood mononuclear cells and upregulation of the co‐stimulatory molecules CD40 and CD80, the accessory molecule CD154, and interferon γ expression were identified and were independent of the extent of hair loss (Tavakolpour, ).…”
Section: Introductionmentioning
confidence: 99%
“…For example, alopecia areata (AA) has been previously identified as a Th1/T17‐dominant disease. However, the author has hypothesized that CD8 + T cells are possibly responsible for (AA), and Th1/Th17 may not be main players .…”
Section: Autoimmune Diseases and Pregnancymentioning
confidence: 99%
“…In this disease, due to aggressive and aberrant immune responses of different subtypes of effector T cells (T effs ) and also tenuous regulatory T cells (T regs ) responses, it seems that development of AA is strongly associated with the low number and/or dysfunction of T regs alongside increase in aberrant immune responses, which have been recently discussed as the novel therapeutic options of AA Tavakolpour, 2016). In this disease, due to aggressive and aberrant immune responses of different subtypes of effector T cells (T effs ) and also tenuous regulatory T cells (T regs ) responses, it seems that development of AA is strongly associated with the low number and/or dysfunction of T regs alongside increase in aberrant immune responses, which have been recently discussed as the novel therapeutic options of AA Tavakolpour, 2016).…”
mentioning
confidence: 99%
“…The first step is to recognize the genes involved in AA, which seem to be inhibited during AA disease. In this disease, due to aggressive and aberrant immune responses of different subtypes of effector T cells (T effs ) and also tenuous regulatory T cells (T regs ) responses, it seems that development of AA is strongly associated with the low number and/or dysfunction of T regs alongside increase in aberrant immune responses, which have been recently discussed as the novel therapeutic options of AA Tavakolpour, 2016). Thus, we should seek for T regs -associated genes, like T regs transcription factor, forkhead box p3 (FOXP3) in addition to co-inhibitory molecules, including cytotoxic T-lymphocyteassociated protein 4 (CTLA-4), B-and T-lymphocyte attenuator (BTLA), programmed cell death protein 1 (PD-1), T-cell immunoglobulin, and mucin-domain containing-3 (TIM-3), CD160, lymphocyte activation gene-3 (LAG-3), and leukocyte-associated immunoglobulin-like receptor 1 (LAIR1).…”
mentioning
confidence: 99%