Intact Disc1-L100P mice carrying a point mutation DISC1^Rgsc1390 in the second exon of the DISC1 gene (genetic model of schizophrenia) differ from the parental C57BL/6NCrl strain by higher content of CD3⁺ T cells and reduced number of CD19⁺B cells in the peripheral blood and spleen. Analysis of T cell subpopulations revealed an increase in the number of CD3⁺CD4⁺ T helpers in the blood of mutant mice and a decrease in the level of CD3⁺CD8⁺ suppressor/cytotoxic T cells and CD3⁺CD4⁺CD25⁺ T-regulatory cells. The distribution pattern of inflammatory (IL-1β, IL-2, IL-6, IL-17, IFNγ, and TNFα) and anti-inflammatory (IL-4, IL-10) cytokines specific for Disc1-L100P mice was revealed in the brain structures involved in the pathogenesis of schizophrenia. A possible implication of immune mechanisms in the development of schizophrenia-like endophenotype of Disc1-L100P mice is discussed.

在DISC1基因的第二个外显子（精神分裂症的遗传模型）中携带点突变 DISC1 ^{Rgsc1390 的}完整 Disc1-L100P 小鼠与亲本 C57BL/6NCrl 品系的不同之处在于 CD3 ⁺ T 细胞含量更高，CD19 ⁺ B 细胞数量减少外周血和脾脏。T 细胞亚群分析显示突变小鼠血液中 CD3 ⁺ CD4 ⁺ T 辅助细胞的数量增加，CD3 ⁺ CD8 ⁺抑制/细胞毒性 T 细胞和 CD3 ⁺ CD4 ⁺ CD25 ^{+ 水平降低}T调节细胞。Disc1-L100P 小鼠特异性的炎症（IL-1β、IL-2、IL-6、IL-17、IFNγ 和 TNFα）和抗炎（IL-4、IL-10）细胞因子的分布模式在与精神分裂症发病机制有关的大脑结构。讨论了免疫机制在 Disc1-L100P 小鼠精神分裂症样内表型发展中的可能影响。