Porter BF, Ambrus A, Storts RW.. Immunohistochemical evaluation of Mx protein expression in canine encephalitides. Vet Pathol 43: 981-987

Texas A and M University, College of Veterinary Medicine and Biomedical Sciences, Department of Pathobiology, College Station, TX 77843-4467, USA.
Veterinary Pathology (Impact Factor: 1.87). 12/2006; 43(6):981-7. DOI: 10.1354/vp.43-6-981
Source: PubMed


Mx proteins are a group of interferon-induced GTPases whose expression has been demonstrated in a number of human viral infections and in some idiopathic inflammatory diseases. In this study, the expression of Mx protein was evaluated in known viral, nonviral, and idiopathic encephalitides in the dog via immunohistochemistry using an antibody against human MxA. All 12 cases of confirmed viral encephalitis, including 7 cases of canine distemper, 4 cases of canine herpesvirus, and 1 case of rabies, were Mx positive. In canine distemper cases, staining was particularly strong and a variety of cell types were positive, including astrocytes, macrophages/microglia, and neurons. Immunoreactivity for Mx protein was evident in a few cases of nonviral infectious encephalitis, including neosporosis (1/1), Chagas disease (2/3), aspergillosis (1/2), and encephalitozoonosis (1/1). Consistent staining was observed in most cases of idiopathic encephalitis, including granulomatous meningoencephalomyelitis (7/7), necrotizing meningoencephalitis of pug dogs (6/7), and necrotizing encephalitis of the Yorkshire Terrier (3/3) and Maltese (1/1) breeds. Mx staining was negative in 5 normal dog brains; 3 cases of cryptococcosis; and single cases of blastomycosis, protothecosis, and bacterial meningitis.

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    • "Immunopathological costs may also be involved in this spatial immunoheterogeneity. TNF-a and Mx2 are costly immune effectors inducing collateral damage when present at high concentration (Li and Youssoufian, 1997; Wenzel et al., 2005; Porter et al., 2006; Bradley, 2008). Lower levels of expression of the genes encoding these molecules may therefore be considered to constitute a tolerance mechanism, an adaptive process limiting pathologies at the expense of pathogen growth or reproduction (Raberg et al., 2009). "
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