1432 IL-9/IL-9R signaling as a novel regulator of human hair follicle growth and immune privilege

In skin, IL-9 is best known as a key cytokine in contact dermatitis. Yet, we noted that its receptor (IL-9R) was also expressed the hair follicle (HF) epithelium. Therefore, asked whether IL-9R-mediated signaling modulated human HF growth and/or immune status. To address this, full-length healthy scalp HFs were organ-cultured presence/absence of recombinant (rh) for six days. Quantitative (immuno-)histomorphometry showed 5 ng/ml rhIL-9 promoted premature catagen entry, associated with tendential increase matrix keratinocyte apoptosis and TGFβ2 protein expression. While did not affect CK15 expression, it significantly decreased number CD34+ progenitor cells their CD34 Moreover, increased MHC class Ia expression immune-privileged (IP) anagen epithelium, suggesting impairs IP. Also, total perifollicular mast cells, which regulate secrete IL-9, but degranulation ex vivo. Instead, IL-9R silencing tendentially prolonged while upregulated. Our pilot study introduces IL-9/IL-9R novel regulator growth, IP, proliferation/ maturation HF-associated It suggests stimulation inhibits epithelial cell generation threatens Thus, antagonizing signaling, including IL-9Rγ chain-blocking JAK3 inhibitors, may be beneficial managing telogen effluvium androgenetic alopecia, shows shortening CD34+progenitor reduction, alopecia areata, where IP must restored.