BACKGROUND@#
Hair follicles are among a handful of organs that exhibit
immune privilege. Dysfunction of the
hair follicle immune system underlies the development of inflammatory
diseases, such as
alopecia areata. @*
METHODS@#Quantitative
reverse transcription PCR and immunostaining was used to confirm the expression of
major histocompatibility complex class I in
human dermal papilla
cells. Through transcriptomic analyses of
human keratinocyte stem cells,
major histocompatibility complex class I was identified as differentially expressed
genes.
Organ culture and patch assay were performed to assess the
ability of WNT3a
conditioned media to rescue
immune privilege. Lastly, CD8?
T cells were detected near the
hair bulb in
alopecia areata patients through
immunohistochemistry. @*RESULTS@#Inflammatory factors such as
tumor necrosis factor alpha and interferon gamma were verified to induce the expression of
major histocompatibility complex class I
proteins in dermal papilla
cells. Additionally, loss of
immune privilege of
hair follicles was rescued following
treatment with
conditioned media from outer root sheath
cells. Transcriptomic analyses found 58 up-regulated
genes and 183 down-regulated
genes related in MHC class I?
cells. Using
newborn hair patch assay, we demonstrated that WNT3a
conditioned media with
epidermal growth factor can restore
hair growth. In
alopecia areata patients, CD8?
T cells were increased during the transition from mid-anagen to late catagen. @*CONCLUSION@#Identification of mechanisms governing epithelial and mesenchymal interactions of the
hair follicle facilitates an improved
understanding of the
regulation of
hair follicle immune privilege.