A. Kipar et al., IMMUNOHISTOCHEMICAL CHARACTERIZATION OF INFLAMMATORY CELLS IN BRAINS OF DOGS WITH GRANULOMATOUS MENINGOENCEPHALITIS, Veterinary pathology, 35(1), 1998, pp. 43-52
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.