IMMUNOHISTOCHEMICAL CHARACTERIZATION OF INFLAMMATORY CELLS IN BRAINS OF DOGS WITH GRANULOMATOUS MENINGOENCEPHALITIS

The inflammatory cells of eleven dogs with canine granulomatous mening oencephalitis were characterized immunohistochemically. Macrophages we re identified by antibodies directed against lysozyme and the DH82 ant igen (expressed by cells of a malignant histiocytosis). T cells were d emonstrated by CD3, CD43, and CD45R antigen, and B cells by immunoglob ulin G and immunoglobulin M expression. Furthermore, staining for the major histocompatibility complex (MHC) class II antigen was evaluated. Diseased animals ranged from 1 to 9 years of age. Small and medium-si zed breeds were affected predominantly. Lesions were widespread and lo calized mainly in the brain stem, less frequently in the cerebrum or c erebellum. Alterations were represented by perivascular cuffs, parench ymal granulomas, and leptomeningeal infiltrates. Lymphocytes and macro phages comprised the dominant cell populations; their percentage varie d substantially between different animals and between sections from th e same individual. Immunohistochemically, the bulk of lymphocytes were CD3 antigen-positive T cells, while only a few cells were CD43 and CD 45R antigen-positive or were classified as B cells. The majority of ma crophages expressed both lysozyme and DH82 antigen; however, some were positive for only one antigen. MHC class II antigen-expression, obser ved only within and in close proximity to the lesions, was found on al l inflammatory cells, pericytes/endothelial cells, and microglia. Resu lts were negative for canine distemper virus antigen and nucleoprotein mRNA, rabies virus antigen, fungi, bacteria, and protozoal agents. Th is immunomorphologic study reveals that inflammatory lesions in canine granulomatous meningoencephalitis consist of a heterogeneous populati on of MHC class LI antigen-positive macrophages and predominantly CD3 antigen-positive lymphocytes. The data suggest a T cell-mediated delay ed-type hypersensitivity of an organ-specific autoimmune disease as a possible pathogenic mechanism for this unique canine brain lesion.