Publication | Open Access
Graft-vs.-host disease elicits expression of class I and class II histocompatibility antigens and the presence of scattered T lymphocytes in rat central nervous system.
175
Citations
29
References
1987
Year
HistocompatibilityLymphocyte DevelopmentImmunologyImmune RegulationPathologyAntigen ProcessingImmune SystemImmunotherapyImmunogeneticsGraft-vs.-host DiseaseScattered TNeuroimmunologyCell TransplantationAllergyAutoimmune DiseaseMedicineAutoimmunityF1 Hybrid RatsTransplant RejectionMultiple SclerosisCentral Nervous SystemTransplant ImmunologyGraft Rejection
In the central nervous system (CNS) of healthy animals, T lymphocytes and cellular expression of major histocompatibility complex (MHC) gene products are virtually undetectable. Yet, in CNS immunological diseases, such as multiple sclerosis in humans, these constituents of the immune response must appear by some mechanism. Immunohistochemical examination of the CNS of F1 hybrid rats following induction of graft-vs.-host disease by parental lymphocytes revealed extensive parenchymal and vascular expression of host class I and II (Ia) MHC-encoded cell surface molecules. In addition, occasional scattered T lymphocytes were detected in the CNS of these animals. F1 hybrid rats reconstituted during the neonatal period with bone marrow cells from one parental strain also expressed increased levels of MHC antigens in the CNS. Thus, evidence is presented that the "immunological privilege" of the CNS seems to decrease or disappear during a strong systemic immune response such as graft-vs.-host disease. These findings may have important implications concerning the mechanism of induction of human CNS immunological diseases.
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