{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T09:15:59Z","timestamp":1789895759000,"version":"4.0.1"},"reference-count":66,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2002,4,1]],"date-time":"2002-04-01T00:00:00Z","timestamp":1017619200000},"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":[[2002,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Mycoplasma infection is a leading cause of pneumonia worldwide and can lead to other respiratory complications. A component of mycoplasma respiratory diseases is immunopathologic, suggesting that lymphocyte activation is a key event in the progression of these chronic inflammatory diseases. The present study delineates the changes in T cell populations and their activation after mycoplasma infection and determines their association with the pathogenesis of murine Mycoplasma respiratory disease, due to Mycoplasma pulmonis infection. Increases in T cell population numbers in lungs and lower respiratory lymph nodes were associated with the development of mycoplasma respiratory disease. Although both pulmonary Th and CD8+ T cells increased after mycoplasma infection, there was a preferential expansion of Th cells. Mycoplasma-specific Th2 responses were dominant in lower respiratory lymph nodes, while Th1 responses predominated in spleen. However, both mycoplasma-specific Th1 and Th2 cytokine (IL-4 and IFN-\u03b3) responses were present in the lungs, with Th1 cell activation as a major component of the pulmonary Th cell response. Although a smaller component of the T cell response, mycoplasma-specific CD8+ T cells were also a significant component of pulmonary lymphoid responses. In vivo depletion of CD8+ T cells resulted in dramatically more severe pulmonary disease, while depletion of CD4+ T cells reduced its severity, but there was no change in mycoplasma numbers in lungs after cell depletion. Thus, mycoplasma-specific Th1 and CD8+ T cell activation in the lung plays a critical regulatory role in development of immunopathologic reactions in Mycoplasma respiratory disease.<\/jats:p>","DOI":"10.4049\/jimmunol.168.7.3493","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T20:08:54Z","timestamp":1398024534000},"page":"3493-3501","source":"Crossref","is-referenced-by-count":69,"title":["Depletion of CD8+ T Cells Exacerbates CD4+ Th Cell-Associated Inflammatory Lesions During Murine Mycoplasma Respiratory Disease"],"prefix":"10.1093","volume":"168","author":[{"given":"Harlan P","family":"Jones","sequence":"first","affiliation":[{"name":"Department of Molecular Biology and Immunology, University of North Texas Health Science Center , Fort Worth, TX 76107"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leslie","family":"Tabor","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology and Immunology, University of North Texas Health Science Center , Fort Worth, TX 76107"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiangle","family":"Sun","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology and Immunology, University of North Texas Health Science Center , Fort Worth, TX 76107"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew D","family":"Woolard","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology and Immunology, University of North Texas Health Science Center , Fort Worth, TX 76107"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jerry W","family":"Simecka","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology and Immunology, University of North Texas Health Science Center , Fort Worth, TX 76107"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2002,4,1]]},"reference":[{"key":"2026020209044937000_R1","first-page":"681","volume-title":"J. 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