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Endocrinology 2002 Nov;143(11):4389-96
Vitamin D3 analogs stimulate hair growth in nude mice.
The active form of vitamin D3 can regulate epidermal keratinization by inducing terminal differentiation; and mice lacking the vitamin D receptor display defects leading to postnatal alopecia. These observations implicate the vitamin D3 pathway in regulation of hair growth. We tested the ability of 1,25 dihydroxyvitamin D3 and its synthetic analogs to stimulate hair growth in biege/nude/xid (BNX) nu/nu (nude) mice exhibiting congenital alopecia. Nude mice were treated with different vitamin D3 analogs at doses that we had previously found to be the highest dose without inducing toxicity (hypercalcemia). The mice were monitored for hair growth and were scored according to a defined scale. Skin samples were taken for histological observation of hair follicles and for extraction of RNA and protein. Vitamin D3 analogs dramatically stimulated the hair growth of nude mice, although parental 1,25 dihydroxyvitamin D3 had no effect. Hair growth occurred in a cyclical pattern, accompanied by formation of normal hair follicles and increased expression of certain keratins (Ha7, Ha8, and Hb3). Vitamin D3 analogs seem to act on keratinocytes to initiate hair follicle cycling and stimulate hair growth in mice that otherwise do not grow hair.
Eur J Dermatol 2002 Jul-Aug;12(4):327-34
Diphencyprone immunotherapy alters anti-hair follicle antibody status in patients with alopecia areata.
Alopecia areata (AA) is a relatively common reversible hair loss disorder usually manifesting as patchy areas of complete hair loss on the scalp and other body parts that can progress to complete loss of all body hair. This condition is now generally assumed to be an autoimmune disease with the hair follicle (HF) as the principal target tissue. AA may be passively transferred by T cells and there is some evidence that serum IgG may also disturb hair cycling. Here, we examine whether the status of anti-HF antibody reactivity is altered during hair regrowth associated with topical immunotherapy using the contact sensitizer diphencyprone. Eleven patients with severe AA of the scalp were treated with diphencyprone on one side of the scalp and serum was obtained from each patient before the start of therapy, after unilateral hair regrowth, during continuing hair regrowth and in some cases after complete and sustained regrowth. The presence and titer of circulating antibodies to HF was assessed by indirect immunofluorescence and immunoblotting analysis. A striking reduction was detected in both the titer and range of HF components/antigens targeted by anti-hair follicle IgG antibodies in those patients that exhibited complete and sustained hair regrowth after DCP-treatment. By contrast, unilateral hair regrowth was associated with no change, or even an increase, in anti-HF antibody titer and reactivity. Therefore we can conclude that the down-regulation of antibody reactivity is likely to be a result rather than the cause of hair regrowth induction by topical immunotherapy. As this immunotherapy is associated with a reduction in the titer/pattern of anti-HF antibodies, these may hold the key to the identity of the HF antigen targets in AA. Moreover, the presence/titer of anti-HF antibodies may be a marker of clinical disease activity or opportunity for spontaneous regrowth.
Eur J Dermatol 2002 May-Jun;12(3):236-9
HLA class II alleles in patients with alopecia areata.
Our purpose was to determine which HLA class II alleles are associated with Turkish alopecia areata patients. Also we investigated whether there was a relationship between the age of onset and severity of disease and HLA alleles or not. Sixty-five patients with alopecia areata were included in this study, and 50 healthy transplant donors were used as a control group. The total group of alopecia areata patients as well as various subgroups according to scalp hair loss were compared to the control group. HLA DNA typing was performed by polymerase chain reaction/sequence specific primer method. The frequency of DQB1*03 allele was 86.1% in all patients compared to 62.0% in controls (P = 0.005). While the frequency of DQB1*03 was significantly increased, the frequency of DRB1*03 was decreased in the all patients group (4.6% versus 22.0%, P = 0.01). In the group of scalp hair loss less than 25%; the frequency of DRB1*03 was decreased (3.2%, P = 0.02). The group of patients with 25-75% scalp hair loss was compared to control group; the frequencies of DRB1*04 (66.7% versus 28.0%, P = 0.02) was increased. When the alopecia totalis, alopecia universalis or alopecia totalis/alopecia universalis group was compared to control group; DQB1*03 was associated with an increased frequency in this group versus control group (90.9%, P = 0.03). There were no significant differences for the other DQ alleles and the DR alleles tested in the patients and in the controls. When patients with early onset were compared to patients with late onset; no significant allele differences were found. Our findings suggested that DQB1*03 allele is a marker for general susceptibility to alopecia areata and may also serve as special genetic marker for susceptibility for the severe form of alopecia areata in our population. However, this association is not related to age at onset of the disease.
Cell Struct Funct. 2003 Feb;28(1):97-104.
Autoimmune hair loss induced by alloantigen in C57BL/6 mice.
Exponentially growing Meth-A cells expressing H-2K(d).D (d) antigen were found to induce alopecia when injected intraperitoneally into normal C57BL/6 mice, which express the H-2K(b).D (b) antigen. However, the capacity to induce alopecia disappeared when Meth-A cells were treated with K252a, which inhibits protein kinases. Histologically, skin in affected areas showed dense mononuclear cell infiltration and a focal foreign-body giant-cell reaction in hair follicles. The subtyping of lymphocytes in peripheral blood demonstrated a significant difference between normal mice and Meth-A cell-injected mice. To further examine the mechanism by which the alloantigen induces alopecia, lymphocytes isolated from the peripheral blood of normal C57BL/6 mice were cultured in medium containing Meth-A cell homogenate, phytohemagglutinin (PHA) and recombinant mouse interleukin-2 (rm IL-2), and intravenously injected into normal C57BL/6 mice. The adoptive transfer of the lymphocytes induced alopecia in a similar way. These findings suggest that the protein kinase-modulated alloantigen induces alopecia by disturbing the immunological homeostasis, and that lymphokine-activated killer cells play an important role in induction of alopecia by cross-reacting with hair follicles.
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