
Intact Disc1-L100P mice carrying a point mutation DISC1Rgsc1390 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.
Male, B-Lymphocytes, Brain Mapping, Interleukin-6, Interleukin-17, Interleukin-1beta, Brain, Mice, Transgenic, Nerve Tissue Proteins, Interleukin-10, Mice, Inbred C57BL, Disease Models, Animal, Interferon-gamma, Mice, Gene Expression Regulation, Schizophrenia, Animals, Interleukin-2, Point Mutation, Interleukin-4
Male, B-Lymphocytes, Brain Mapping, Interleukin-6, Interleukin-17, Interleukin-1beta, Brain, Mice, Transgenic, Nerve Tissue Proteins, Interleukin-10, Mice, Inbred C57BL, Disease Models, Animal, Interferon-gamma, Mice, Gene Expression Regulation, Schizophrenia, Animals, Interleukin-2, Point Mutation, Interleukin-4
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