Affiliation:
1. Section of Pulmonary and Critical Care and Gene Therapy Program, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, Louisiana
Abstract
ABSTRACT
Although a clear relationship between αβ T-cell receptor-positive (αβ-TCR
+
) CD4
+
T cells and susceptibility to
Pneumocystis carinii
infection exists, the role of other T-cell subsets is less clearly defined. Previous studies have shown that γδ-TCR
+
T cells infiltrate into the lung during
P. carinii
pneumonia. Therefore, the present study examined the role of γδ-TCR
+
T cells in host defense against
P. carinii
pneumonia. C57BL/6 (control) and B6.129P2-
Tcrd
tm1Mom
(γδ-TCR
+
T-cell-deficient) mice were inoculated intratracheally with
P. carinii
. At specific time points, mice were sacrificed and analyzed for
P. carinii
burden, T-cell subsets, and cytokine levels in lung tissue. Analysis of
P. carinii
burden showed a more rapid and complete resolution of infection in γδ-TCR
+
T-cell-deficient mice than in C57BL/6 controls. This augmented resolution was associated with elevated gamma interferon (IFN-γ) levels in bronchoalveolar lavage fluid predominantly produced by CD8
+
T cells, as well as an increased recruitment of CD8
+
T cells in general. In separate experiments, neutralization of IFN-γ or depletion of CD8
+
T cells early during infection abolished the augmented resolution previously observed in γδ-TCR
+
T-cell-deficient mice. These results show that the presence of γδ-TCR
+
T cells modulates host susceptibility to
P. carinii
pneumonia through interactions with pulmonary CD8
+
T cells and tissue production of IFN-γ.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
52 articles.
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