WS-2-DCD200 Attenuates Hair Follicle-specific Inflammation in MiceSpeaker: Michael RosenblumMedical College of Wisconsin, Milwaukee, WI, USAAuthors: Michael D. Rosenblum1,2, Robert L. Truitt1, Jeffrey E. Woodliff1, Edit B. Olasz2, and Kim B. Yancey3.1 Department of Pediatrics, 2Department of Dermatology, Medical College of Wisconsin, Milwaukee, WI3 Department of Dermatology, University of Texas Southwestern Medical Center, Dallas,
TXImmunosuppressive molecules expressed on tissue-resident cells have the potential to regulate tissue-specific inflammation and autoimmunity. CD200 is a cell surface glycoprotein that transmits an immunosuppressive signal by ligating its receptor, CD200R. We have elucidated the expression of CD200 and CD200R in murine skin and examined the role of CD200-CD200R signaling in maintaining cutaneous immune homeostasis. CD200 was expressed on Langerhans cells (LCs) and on a subset of keratinocytes (KCs). CD200 expressing KCs preferentially localized to the outer root sheath of hair follicles (HF). CD200R was expressed on approximately one-third of freshly isolated LCs. LCs from CD200-/-mice showed a heightened state of activation. CD200 expression had a dramatic effect on protecting HFs from inflammation and autoimmune attack. Grafts of syngeneic gender-matched skin from CD200-/-donors showed persistent perifollicular inflammation with heightened T cell-recruitment and, ultimately, complete destruction of HFs, a phenotype resembling human cicatricial alopecia. Hair follicle destruction could be induced in a CD200-/-host by adoptive transfer of T cells from a mouse previously grafted with CD200-/-skin. Our results suggest that the CD200-CD200R signaling pathway plays a role in establishing and maintaining immune homeostasis in the skin. This pathway may be especially important in attenuating HF-associated inflammation and immunity
What they are saying (in red) is that when you put hairs in a CD200 NEGATIVE hhost, and transfer T-cells from a mouse that previously had skin without CD200, the immunity would kill the follicles. Well, CD200 is lost in advanced cases of AGA. The hairs probably stay in telogen to protect themsleves from a never-ending immno attack.
BTW----Did anybody else see that bit on “why hair greys”? They have found that hairs grey because the body ends up bathing the melanocytes in hydrogen peroxide for whatever reason. It causes them to become non-active, and they dont pigment the hairs anymore. Facsinating stuff.
I dont have time to google hairloss and AIDS, but I think that I remember some of those strong AIDS drugs have hairloss side effects.