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For example, CD4 T cells are critical to the development of MAIDS. In vivo depletion of CD4 T cells before LP-BM5 infection rendered genetically susceptible B6 mice MAIDS resistant. Similarly, MAIDS did not develop in B6.nude mice. However, if reconstituted with CD4 T cells, B6.nude mice develop full-blown MAIDS. Our laboratory has shown that the interaction of B and CD4 T cells that is central to MAIDS pathogenesis requires ligation of CD154 on CD4 T cells with CD40 on B cells. However, it is not clear which additional characteristics of the phenotypically and functionally heterogeneous CD4 T-cell compartment are required. Here, in vivo adoptive transfer experiments using B6.nude recipients are employed to compare the pathogenic abilities of CD4 T-cell subsets defined on the basis of cell surface phenotypic or functional differences. Th1 and Th2 CD4 T cells equally supported MAIDS induction. The rare Thy1.2<jats:bold><jats:sup>\u2212<\/jats:sup><\/jats:bold>CD4 subset that expands upon LP-BM5 infection was not necessary for MAIDS. Interestingly, CD45RB<jats:sup>low<\/jats:sup>CD4 T cells supported significantly less disease than CD45RB<jats:sup>high<\/jats:sup>CD4 T cells. Because the decreased MAIDS pathogenesis could not be attributed to inhibition by CD45RB<jats:sup>low<\/jats:sup>CD25<jats:sup>+<\/jats:sup>natural T-regulatory cells, an intrinsic property of the CD45RB<jats:sup>low<\/jats:sup>cells appeared responsible. Similarly, there was no evidence that natural T-regulatory cells played a role in LP-BM5-induced pathogenesis in the context of the intact CD4 T-cell population.<\/jats:p>","DOI":"10.1128\/jvi.02711-05","type":"journal-article","created":{"date-parts":[[2006,5,26]],"date-time":"2006-05-26T23:09:14Z","timestamp":1148684954000},"page":"5777-5789","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":21,"title":["The Role of CD4 T Cells in the Pathogenesis of Murine AIDS"],"prefix":"10.1128","volume":"80","author":[{"given":"Wen","family":"Li","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Dartmouth Medical School"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"William R.","family":"Green","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Dartmouth Medical School"},{"name":"Norris Cotton Cancer Center, Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire 03756"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2567.2003.01678.x"},{"key":"e_1_3_2_3_2","doi-asserted-by":"crossref","first-page":"2132","DOI":"10.4049\/jimmunol.159.5.2132","volume":"159","year":"1997","unstructured":"Andrews, C., S. 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