Studies on autoimmune alopecia in New Zealand Black/KN mouse

自身免疫性脱发是系统性红斑狼疮（SLE）的主要症状之一。虽然体内免疫复合物沉积和单核细胞浸润已被认为是其原因，但其机制仍不清楚。雄性新西兰黑（NZB）/KN小鼠是一种新的与关节炎相关的SIR易感小鼠，其是自发性脱发病变的特征。本实验采用NZB/KN（H-2 ~ d）小鼠、SLE易感NZB/N（H-2 ~ d）小鼠和对照NZ白色（NZW）/sk（H-2 ~ d）小鼠，对自身免疫性脱发的遗传学特征进行了研究。饲养（NZW/sk × NZB/KN）（H-2^z/d）的F1代小鼠和（F1 × F1）（H-2^d/d、H-2^z/d、H-2 ^z/z）的F2代小鼠92只。在F2小鼠中进行相关性研究，雄性NZB/KN小鼠在3月龄和12月龄时，25%和80%的上背部和尾部出现无红斑的脱毛病变。早期秃发病变表现为轻微的 ...更多信息 f在毛囊周围浸润。在NZB/N或NZW/sk小鼠中未发现脱发病变。雄性和雌性F1小鼠分别有13.3%和6.7%出现脱发。F2代44%的雄性小鼠和7.3%的雌性小鼠出现脱发。脱发与男性之间存在较强的正相关性，而与女性和H-2复合体之间无相关性。12月龄NZB/KN小鼠毛囊基底膜IG M和IG 0沉积率分别为75%和5%，而雄性NZB/N小鼠和NZW/sk小鼠均为0。雄性F2小鼠显示53%的IG M沉积阳性和33%的IG G沉积阳性，雌性F2显示相似的IG沉积发生率。结果表明，NZB/KN小鼠自身免疫性脱发与Y染色体相关抗原（Yalphaalpha）密切相关，而与H-2复合物及体内IG沉积无关。由于其他SLB易感小鼠如NZB/N和MRL/lpr小鼠的狼疮性皮肤病受H-2复合物或Ipr基因的调节，因此自身免疫性脱发的发病机制可能不同于红斑和相关免疫复合物沉积。少

Autoimmune alopecia is one of the major symptoms in systemic lupus erythematosus(SLE). Although the in vivo immune complexes deposits and mononuclear cell infiltrates have been proposed as the cause, the mechanisms are still obscure. A male New Zealand Black (NZB)/KN mouse is a novel SIR-prone mouse associated with arthritis, which is characteristic in spontaneous alopecia lesions. We designed the genetic studies on autoimmune alopecia in NZB/KN mice in relation to several autoimmune traits.NZB/KN(H-2^d), the standard SLE-prone NZB/N(H-2^d), the control NZ White (NZW)/sk (H-2^d) mice were purchased and bred in our laboratory. Fl hybrid mice of (NZW/sk x NZB/KN) (H-2^<z/d>) and 92 F2 mice of (F1x F1) (H-2^<d/d>, H-2^<z/d>, H-2^<z/z>) were raised. In F2 mice, the correlation studies were performed.Male NZB/KN mice showed alopecia lesions without erythema on the upper back and the tail regions in 25% and 80% at the age of 3 mo and 12 mo. The early alopecia lesions showed a slight number o … More f infiltrates around hair follicles. No alopecia lesions were found in NZB/N or NZW/sk mice. Male and female Fl mice showed alopecia in 13.3% and 6.7%. F2 developed alopecia in 44% of male mice and 7.3% of female mice. Strong positive association was found between alopecia and male, but not among alopecia, female and H-2 complex. Ig M and Ig 0 deposits at hair follicle basement membrane were found in 75% and 5% of 12- mo-old NZB/KN mice, and in zero of male NZB/N mice or NZW/sk mice. Male F2 mice showed 53% positivity of Ig M deposits and 33% of Ig G deposits, and female F2 showed similar incidences of Ig deposits. No associations were found among alopecia, Ig deposits, H-2 complex and proteinuria.These results suggest that autoimmune alopecia in NZB/KN mice are closely associated with Y chromosome associated antigens (Yalphaalpha), but not with H-2 complex or in vivo Ig deposits. Since lupus dermatoses in other SLB-prone mice such as NZB/N and MRL/lpr mice are regulated by H-2 complex or Ipr gene, it is likely that the pathogenesis of autoimmune alopecia is different from that of erythema and the related immune complex deposits. Less