Open AccessSensitized CD8+T Cells Fail To Control Organism Burden but Accelerate the Onset of Lung Injury duringPneumocystis cariniiPneumonia
Author(s) -
Francis Gigliotti,
Elliott L. Crow,
Samir P. Bhagwat,
Terry W. Wright
Publication year - 2006
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.00668-06
Subject(s) - pneumocystis carinii , pneumonia , biology , organism , lung , immunology , cd8 , microbiology and biotechnology , virology , immune system , medicine , human immunodeficiency virus (hiv) , pneumocystis jirovecii , paleontology
While CD8+ cells have been shown to contribute to lung injury duringPneumocystis carinii pneumonia (PCP), there are conflicting reports concerning the ability of CD8+ cells to killP. carinii. To address these two issues, we studied the effect of the presence of CD8+ cells in two mouse models of PCP. In the reconstituted SCID mouse model, depletion of CD8+ cells in addition to CD4+ cells after reconstitution did not result in increased numbers ofP. carinii cysts compared to the numbers of cysts in mice with only CD4+ cells depleted. This result was observed regardless of whether the mice were reconstituted with naïve orP. carinii -sensitized lymphocytes. In contrast, reconstitution with sensitized lymphocytes resulted in more rapid onset of lung injury that was dependent on the presence of CD8+ cells. The course of organism replication over a 6-week period was also examined in the CD4+ -T-cell-depleted and CD4+ - and CD8+ -T-cell-depleted mouse model of PCP. Again, the organism burdens were identical at all times regardless of whether CD8+ cells were present. Thus, in the absence of CD4+ T cells, CD8+ T cells are a key contributor to the inflammatory lung injury associated with PCP. However, we were unable to demonstrate an in vivo effect of these cells on the course ofP. carinii infection.