A. Tipold et al., Lymphocyte subset distribution in steroid responsive meningitis-arteriitisin comparison to different canine encephalitides, J VET MED A, 46(2), 1999, pp. 75-85
Citations number
38
Categorie Soggetti
Veterinary Medicine/Animal Health
Journal title
JOURNAL OF VETERINARY MEDICINE SERIES A-PHYSIOLOGY PATHOLOGY CLINICAL MEDICINE
Steroid responsive meningitis-arteriitis (SRMA) is a well-known disease in
dogs, but the aetiology and pathogenesis are not yet understood. In the per
ipheral blood an overrepresentation of B cells was found. In the present st
udy we therefore evaluated the distribution of lymphocyte subsets in SRMA i
n paraffin-embedded tissue sections directly at the lesion sites and compar
ed the results to different canine encephalitides. An intriguing finding wa
s that the B cell/T cell distribution varied depending on the aetiology of
the disease: in viral encephalitides, T cells were the predominant cell pop
ulation in perivascular cuffs, whereas in protozoal and bacterial diseases
B cells prevailed. In SRMA an overrepresentation of B cells occurred in men
ingeal lesions, as already found in the peripheral brood. The distribution
of lymphocyte subsets was similar to bacterial and protozoal diseases and w
as not a unique phenomenon for this specific inflammatory lesion in the can
ine central nervous system (CNS). Multiple mechanisms seem to be responsibl
e for recruitment: and activation of different leukocyte subsets after alte
ration of the CNS tissue by an environmental factor. A specific finding in
SRMA was that the distribution of T and B cells depended also on the lesion
site. In contrast to meningeal lesions, in inflamed arteries T cells were
the only lymphocyte population found. In these vessels, diffuse infiltratio
n with immunoglobulins was revealed. Inactivated or resting lymphocytes and
large granular lymphocytes occurred in each of the diseases examined. Thes
e similarities between SRMA and infectious CNS diseases of the dog support
earlier suggestions that the disease is somehow triggered by a hitherto unk
nown environmental factor which leads to the dysregulation of the immune sy
stem.