Format

Send to

Choose Destination
Mediators Inflamm. 2014;2014:728939. doi: 10.1155/2014/728939. Epub 2014 Jul 15.

Circumsporozoite protein-specific K(d)-restricted CD8+ T cells mediate protective antimalaria immunity in sporozoite-immunized MHC-I-K(d) transgenic mice.

Author information

1
HIV and Malaria Vaccine Program, Aaron Diamond AIDS Research Center, Affiliate of The Rockefeller University, 455 First Avenue, New York, NY 10016, USA.
2
Department of Pathology, New York University School of Medicine, 545 First Avenue, New York, NY 10016, USA.

Abstract

Although the roles of CD8+ T cells and a major preerythrocytic antigen, the circumsporozoite (CS) protein, in contributing protective antimalaria immunity induced by radiation-attenuated sporozoites, have been shown by a number of studies, the extent to which these players contribute to antimalaria immunity is still unknown. To address this question, we have generated C57BL/6 (B6) transgenic (Tg) mice, expressing K(d) molecules under the MHC-I promoter, called MHC-I-K(d)-Tg mice. In this study, we first determined that a single immunizing dose of IrPySpz induced a significant level of antimalaria protective immunity in MHC-I-K(d)-Tg mice but not in B6 mice. Then, by depleting various T-cell subsets in vivo, we determined that CD8+ T cells are the main mediator of the protective immunity induced by IrPySpz. Furthermore, when we immunized (MHC-I-K(d)-Tg × CS-Tg) F1 mice with IrPySpz after crossing MHC-I-K(d)-Tg mice with PyCS-transgenic mice (CS-Tg), which are unable to mount PyCS-specific immunity, we found that IrPySpz immunization failed to induce protective antimalaria immunity in (MHC-I-K(d)-Tg × CS-Tg) F1 mice, thus indicating the absence of PyCS antigen-dependent immunity in these mice. These results indicate that protective antimalaria immunity induced by IrPySpz in MHC-I-K(d)-Tg mice is mediated by CS protein-specific, K(d)-restricted CD8+ T cells.

PMID:
25132735
PMCID:
PMC4124204
DOI:
10.1155/2014/728939
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Hindawi Limited Icon for PubMed Central
Loading ...
Support Center