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Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Acta+Neuropathol 1990 ; 81 (1): 41-50 Nephropedia Template TP
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Determination of immune cells and expression of major histocompatibility complex class II antigen in encephalitic lesions of experimental Borna disease #MMPMID2085093
Deschl U; Stitz L; Herzog S; Frese K; Rott R
Acta Neuropathol 1990[]; 81 (1): 41-50 PMID2085093show ga
After intracerebral infection with Borna disease virus adult Lewis rats develop a virus-induced immunopathological reaction resulting in severe neurological symptoms and a non-purulent meningoencephalitis. The composition of inflammatory cells and major histocompatibility complex (MHC) class II antigen expression during the course of the infection was investigated using immunocytochemistry with a panel of monoclonal antibodies (mAb). Macrophages and lymphocytes of the T helper phenotype (CD4+) were dominant at all stages of infection, whereas T suppressor/cytotoxic lymphocytes (CD8+) were less frequent. B lymphocytes and plasma cells occurred mainly during later stages of the disease and marked parenchymal deposition of immunoglobulin developed. Beginning 10 days after infection massive expression of MHC class II antigen was noted up to the termination of experiments 70 days after infection. Besides lymphatic cells and macrophages, cells morphologically resembling microglia expressed this antigen. Furthermore, ependymal cells were found positive for MHC class II expression during infection whereas astrocytes remained negative. These findings are consistent with previous results which provide evidence for a delayed-type hypersensitivity reaction being operative in the pathogenesis of Borna disease.
|Animals[MESH]
|Antibodies, Monoclonal[MESH]
|Borna Disease/*immunology/pathology[MESH]
|Borna disease virus[MESH]
|Brain/*immunology/pathology[MESH]
|Female[MESH]
|Hippocampus/*immunology/pathology[MESH]
|Histocompatibility Antigens Class II/*analysis[MESH]