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In this disease, lesions of the central nervous system (CNS) are associated with perivascular infiltration by lymphocytes. We and others have hypothesized that these T lymphocytes infiltrating the CNS may play a prominent role in TSP\/HAM. Here, we show that transient contact of human or rat astrocytes with T lymphocytes chronically infected by HTLV-1 impairs some of the major functions of brain astrocytes. Uptake of extracellular glutamate by astrocytes was significantly decreased after transient contact with infected T cells, while the expression of the glial transporters GLAST and GLT-1 was decreased. In two-compartment cultures avoiding direct cell-to-cell contact, similar results were obtained, suggesting possible involvement of soluble factors, such as cytokines and the viral protein Tax-1. Recombinant Tax-1 and tumor necrosis factor alpha (TNF-\u03b1) decreased glutamate uptake by astrocytes. Tax-1 probably acts by inducing TNF-\u03b1, as the effect of Tax-1 was abolished by anti-TNF-\u03b1 antibody. The expression of glutamate-catabolizing enzymes in astrocytes was increased for glutamine synthetase and decreased for glutamate dehydrogenase, the magnitudes of these effects being correlated with the level of Tax-1 transcripts. In conclusion, Tax-1 and cytokines produced by HTLV-1-infected T cells impair the ability of astrocytes to manage the steady-state level of glutamate, which in turn may affect neuronal and oligodendrocytic functions and survival.<\/jats:p>","DOI":"10.1128\/jvi.74.14.6433-6441.2000","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T10:06:23Z","timestamp":1027764383000},"page":"6433-6441","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":68,"title":["Human T-Cell Lymphotropic Virus Type 1-Infected T Lymphocytes Impair Catabolism and Uptake of Glutamate by Astrocytes via Tax-1 and Tumor Necrosis Factor Alpha"],"prefix":"10.1128","volume":"74","author":[{"given":"Raphae\u0308l","family":"Szymocha","sequence":"first","affiliation":[{"name":"<!--label omitted: 1-->Experimental Neurobiology and Physiopathology Unit, INSERM U433,1 and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hideo","family":"Akaoka","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Experimental Neurobiology and Physiopathology Unit, INSERM U433,1 and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Magali","family":"Dutuit","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Experimental Neurobiology and Physiopathology Unit, INSERM U433,1 and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christophe","family":"Malcus","sequence":"additional","affiliation":[{"name":"<!--label omitted: 2-->Ho\u0302pital Neurologique,2 Lyon, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marianne","family":"Didier-Bazes","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Experimental Neurobiology and Physiopathology Unit, INSERM U433,1 and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marie-Franc\u0327oise","family":"Belin","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Experimental Neurobiology and Physiopathology Unit, INSERM U433,1 and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pascale","family":"Giraudon","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Experimental Neurobiology and Physiopathology Unit, INSERM U433,1 and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.70.12.8727-8736.1996"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1097\/00004647-199908000-00001"},{"key":"e_1_3_2_4_2","first-page":"511","article-title":"Isolation and characterization of the tax protein of HTLV-I","volume":"4","author":"Beimling P.","year":"1989","unstructured":"Beimling P. 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