Immunohistochemical characterization of the inflammatory reaction in tick-borne encephalitis of dogs

Immunohistochemical characterization of the inflammatory reaction in tick-borne encephalitis of dogs The inflammatory reaction in nine cases of canine tickborne encephalitis (TBE) was characterized by immunohistochemistry. In formalin-fixed, paraffin-embedded brain sections we demonstrated inflammatory cells, microglia, astrocytes, lgG and MHC-ll-expression using specific antibodies to CD3, BLA36, lysozyme, GFAP, dog lgG, and HLA-DR and the lectin RCA-l. Immunophenotyping of the entire inflammatory reaction has not been investigated so far; thus the results of this study provide new insights into the pathogenesis of this disease: subsequent to virus-induced neuronal cell death there was proliferation and transformation of microglia, which was most prominent in the brain stem and the cerebral cortex. These cells were labelled with antibodies to lysozyme and the lectin RCA-l. Simultaneously, dramatic MHC-ll-upregulation was present in the above mentioned cells and lymphocytes. The antigen-presenting MHC-ll-positive cells were responsible for immigration of lymphocytes. The lymphocytic reaction in perivascular cuffs and meninges was T-cell dominated; in the neuropil, B-cells were more numerous, differentiated to plasma cells and gave raise to considerable intrathecal IgG production. The characteristics "reactive, MHC-ll-positive microglia, preponderance of T-cells in the perivascular cuffs, and high lgG level in the neuropil" enable us to differentiate TBE from other nonsuppurative encephalitides and serve as important milestones in the neuropathogenesis of this disease.