Welcome to ReachMD. This medical industry feature, titled “Taking a closer look at the pathophysiology of alopecia areata” is sponsored by Pfizer.
Alopecia areata is thought to be primarily driven by an immune attack at the hair follicle that leads to potentially reversible, non-scarring hair loss.
This can range from circular bald patches, to total scalp or full body hair loss. The likely cause of alopecia areata is immunologic, as well as other contributory factors, including genetic predisposition and environmental or external factors that can trigger an immune response.
Under normal circumstances, the hair follicle is an immune privileged site that is typically protected from immune attack. In alopecia areata, this immune protection is thought to be lost and the normal process of hair follicle growth is interrupted as it becomes susceptible to inflammatory assault.
Cytokines such as interferon gamma have been implicated in the collapse of this immune privilege through exposure of the hair follicle to pro-inflammatory immune cells, which in turn leads to perifollicular inflammation.
Activation of immune cells, including CD8 positive T cells, gamma/delta T-cells and NK cells, is believed to play a role in the immune response.
The tyrosine-protein kinase, TEC, is a component of the T-cell receptor signaling pathway that also contributes to the increased production of the inflammatory cytokines involved in alopecia areata.
Pro-inflammatory cytokines, including interferon gamma, play a central role in alopecia areata. Interferon gamma mediated cytotoxic activity maintains the immune response against the hair follicle.
A positive feedback loop involving abnormal expression of pro-inflammatory cytokines, such as interferon gamma, IL-15 and IL-2, may perpetuate alopecia areata through intracellular JAK-dependent signalling pathways.
This JAK/STAT signalling, has been shown to mediate several processes related to the pathogenesis of alopecia areata.
These inflammatory processes lead to a disruption of the regular hair growth cycle resulting in a premature loss of hair and inhibition of new hair growth.
In summary, JAK and TEC T-cell signaling pathways, may play an important role in the inflammatory response of alopecia areata.
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