{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T14:30:58Z","timestamp":1791297058548,"version":"4.1.0"},"reference-count":0,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[1994,1,1]],"date-time":"1994-01-01T00:00:00Z","timestamp":757382400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1994,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Moderately virulent strains of Cryptococcusneoformans, inoculated via the trachea, cause a pulmonary infection in BALB\/c mice that was gradually resolved by T lymphocyte-dependent mechanisms. The current studies, using monoclonal antibodies to deplete T cell subsets, demonstrated that CD4+ and CD8+ T cells combined to mediate a prominent pulmonary inflammatory infiltrate that included lymphocytes, macrophages, neutrophils, and eosinophils. The inflammatory response peaked 2 weeks after infection and coincided with the beginning of gradual pulmonary clearance of the infection. CD4\/CD8 double, deficiency (4-8-) markedly reduced the influx of all cells into the lungs. A CD4 deficiency had a more profound effect on the total number of inflammatory cells recruited to the lungs than a CD8 deficiency. Depletion of either CD8+ or CD4+ T cells significantly decreased pulmonary macrophages and neutrophils, but only a CD4 deficiency prevented the influx of eosinophils. Recruitment of CD8+ T cells occurred independently of CD4+ T cells, but CD4+ T cell recruitment to the lungs was significantly reduced in CD8-deficient mice. Mitogen-stimulated infiltrating lung lymphocytes from infected 4+8+ mice secreted both T helper cell type 1 (Th1) [interferon-\u03b3 (IFN-\u03b3) and interleukin-2 (IL-2)] and Th2 (IL-4, IL-5, and IL-10) cytokines. CD4 deficiency resulted in loss of T cells secreting IL-4, IL-5, and IL-10. However, residual CD8+ T cells still secreted IL-2 and IFN-\u03b3. Lung T cells from CD8-deficient mice secreted similar levels of IL-4, IL-5, and IL-10 on a per lung basis compared with 4+8+ mice despite decreased numbers of CD4+ T cells, but secreted reduced levels of IFN-\u03b3. These experiments indicate that (1) CD4+ T cells play a dominant role in recruiting macrophages and granulocytes to the lung and (2) CD8+ T cells also mediate cellular recruitment, increase the magnitude of CD4+ T cell numbers in the infiltrate, and contribute to the local secretion of IFN-\u03b3. Thus, these studies demonstrate that CD8+ T cells can independently mediate an inflammatory response to a large, particulate, extracellular antigen, a role heretofore attributed almost solely to CD4+ T cells. J. Leukoc. Biol. 55: 35\u201342; 1994.<\/jats:p>","DOI":"10.1002\/jlb.55.1.35","type":"journal-article","created":{"date-parts":[[2018,1,12]],"date-time":"2018-01-12T19:42:50Z","timestamp":1515786170000},"page":"35-42","source":"Crossref","is-referenced-by-count":159,"title":["The role of CD4+ and CD8+ T cells in the protective inflammatory response to a pulmonary cryptococcal infection"],"prefix":"10.1093","volume":"55","author":[{"given":"Gary B","family":"Huffnagle","sequence":"first","affiliation":[{"name":"Department of Pathology, University of Texas Southwestern Medical Center , Dallas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary F","family":"Lipscomb","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Texas Southwestern Medical Center , Dallas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie A","family":"Lovchik","sequence":"additional","affiliation":[{"name":"Immunology Graduate Program, University of Texas Southwestern Medical Center , Dallas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kathleen A","family":"Hoag","sequence":"additional","affiliation":[{"name":"Immunology Graduate Program, University of Texas Southwestern Medical Center , Dallas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nancy E","family":"Street","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Cancer Immunobiology Center, University of Texas Southwestern Medical Center , Dallas"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[1994,1,1]]},"container-title":["Journal of Leukocyte Biology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1002%2Fjlb.55.1.35","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/academic.oup.com\/jleukbio\/article-pdf\/55\/1\/35\/49770479\/jlb0035.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/academic.oup.com\/jleukbio\/article-pdf\/55\/1\/35\/49770479\/jlb0035.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,4,11]],"date-time":"2023-04-11T06:48:09Z","timestamp":1681195689000},"score":1,"resource":{"primary":{"URL":"https:\/\/academic.oup.com\/jleukbio\/article\/55\/1\/35\/6978710"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1994,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-online":{"date-parts":[[1994,1,1]]},"published-print":{"date-parts":[[1994,1,1]]}},"URL":"https:\/\/doi.org\/10.1002\/jlb.55.1.35","relation":{},"ISSN":["0741-5400","1938-3673"],"issn-type":[{"value":"0741-5400","type":"print"},{"value":"1938-3673","type":"electronic"}],"subject":[],"published-other":{"date-parts":[[1994,1]]},"published":{"date-parts":[[1994,1,1]]}}}