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Infection and Immunity, November 2006, p. 6310-6316, Vol. 74, No. 11
0019-9567/06/$08.00+0     doi:10.1128/IAI.00668-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Sensitized CD8⁺ T Cells Fail To Control Organism Burden but Accelerate the Onset of Lung Injury during Pneumocystis carinii Pneumonia

Francis Gigliotti,^1,2,* Elliott L. Crow,^1, Samir P. Bhagwat,¹ and Terry W. Wright^1,2

Departments of Pediatrics,¹ Microbiology and Immunology, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642²

Received 26 April 2006/ Returned for modification 21 June 2006/ Accepted 15 August 2006

While CD8⁺ cells have been shown to contribute to lung injury during Pneumocystis carinii pneumonia (PCP), there are conflicting reports concerning the ability of CD8⁺ cells to kill P. 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 of P. 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 or P. 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 of P. carinii infection.

Published ahead of print on 28 August 2006.

Editor: A. Casadevall

F.G. and E.L.C. contributed equally to the paper.

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