In the current study, the alopecia areata gene was introduced into the C57BL/6 （B6） mouse through repeated backcrossing/intercrossing, and the allelic homozygosity of congenic AAtJmice （named B6.KM-AA） was verifie...In the current study, the alopecia areata gene was introduced into the C57BL/6 （B6） mouse through repeated backcrossing/intercrossing, and the allelic homozygosity of congenic AAtJmice （named B6.KM-AA） was verified using microsatellites. The gross appearance, growth characteristics, pathological changes in skin, and major organs of B6.KM-AA mice were observed. Counts and proportions of CD4＋ and CD8＋ T lymphocytes in peripheral blood were determined by flow cytometry. Results show that congenic B6.KM-AA mice were obtained after 10 generations of backcrossing/intercrossing. B6.KM-AA mice grew slower than B6 control mice and AA skin lesions were developed by four weeks of age. The number of hair follicles was reduced, but hair structures were normal. Loss of hair during disease progression was associated with CD4＋ and CD8＋ T lymphocytes infiltration peri- and intrahair follicles. No pathological changes were found in other organs except for the skin. In the peripheral blood of B6.KM-AA mice, the percentage of CD4＋ T cells was lower and percentage of CD8＋ T cells higher than in control mice. These findings indicate that B6.KM-AA mice are characterized by a dysfunctional immune system, retarded development and T-cell infiltration mediated hair loss, making them a promising new animal model for human alopecia areata.展开更多
基金supported by the Public Program of the Science Technology Department,Zhejiang(2011C37077)the National Natural Science Foundation of China(31071092)
文摘In the current study, the alopecia areata gene was introduced into the C57BL/6 （B6） mouse through repeated backcrossing/intercrossing, and the allelic homozygosity of congenic AAtJmice （named B6.KM-AA） was verified using microsatellites. The gross appearance, growth characteristics, pathological changes in skin, and major organs of B6.KM-AA mice were observed. Counts and proportions of CD4＋ and CD8＋ T lymphocytes in peripheral blood were determined by flow cytometry. Results show that congenic B6.KM-AA mice were obtained after 10 generations of backcrossing/intercrossing. B6.KM-AA mice grew slower than B6 control mice and AA skin lesions were developed by four weeks of age. The number of hair follicles was reduced, but hair structures were normal. Loss of hair during disease progression was associated with CD4＋ and CD8＋ T lymphocytes infiltration peri- and intrahair follicles. No pathological changes were found in other organs except for the skin. In the peripheral blood of B6.KM-AA mice, the percentage of CD4＋ T cells was lower and percentage of CD8＋ T cells higher than in control mice. These findings indicate that B6.KM-AA mice are characterized by a dysfunctional immune system, retarded development and T-cell infiltration mediated hair loss, making them a promising new animal model for human alopecia areata.
