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Science 13 September 1991:
Vol. 253. no. 5025, pp. 1283 - 1285
DOI: 10.1126/science.1891717
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Articles

Science, Vol 253, Issue 5025, 1283-1285
Copyright © 1991 by American Association for the Advancement of Science

articles

Viral persistence in neurons explained by lack of major histocompatibility class I expression

E Joly, L Mucke, and MB Oldstone

Department of Neuropharmacology, Scripps Clinic and Research Foundation, La Jolla, CA 92037.

Viruses frequently persist in neurons, suggesting that these cells can evade immune surveillance. In a mouse model, 5 x 10(6) cytotoxic T lymphocytes (CTLs), specific for lymphocytic choriomeningitis virus (LCMV), did not lyse infected neurons or cause immunopathologic injury. In contrast, intracerebral injection of less than 10(3) CTL caused disease and death when viral antigens were expressed on leptomeningeal and choroid plexus cells of the nervous system. The neuronal cell line OBL21 expresses little or no major histocompatibility (MHC) class I surface glycoproteins and when infected with LCMV, resisted lysis by virus-specific CTLs. Expression of MHC heavy chain messenger RNA was limited, but beta 2-microglobulin messenger RNA and protein was made normally. OBL21 cells were made sensitive to CTL lysis by transfection with a fusion gene encoding another MHC class I molecule. Hence, neuronal cells probably evade immune surveillance by failing to express MHC class I molecules.


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