Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 194, Issue 9, Pages 1241-1248Publisher
OXFORD UNIV PRESS INC
DOI: 10.1086/508217
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Funding
- Biotechnology and Biological Sciences Research Council [BBS/E/I/00001116, C20021] Funding Source: Medline
- NIAID NIH HHS [AI-61363] Funding Source: Medline
- Biotechnology and Biological Sciences Research Council [C20021, BBS/E/I/00001116] Funding Source: researchfish
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Burkholderia pseudomallei is the etiological agent of melioidosis, a serious human disease for which no vaccine is available. Immunization of susceptible BALB/c mice with the live attenuated mutant B. pseudomallei ilvI (referred to as 2D2) generated significant, although incomplete, immunity. Splenic B. pseudomallei-specific T cells, detected in immunized mice, proliferated and produced interferon-gamma in vitro in response to dead bacteria. Assessment of T cell antigen specificity indicated that subpopulations of B. pseudomallei-reactive T cells were responsive to BopE, a type III secretion system (TTSS) effector protein, and to a lesser extent to BipD, a TTSS translocator protein. Increased survival of severe combined immunodeficient mice adoptively transferred with T cells from immunized mice, compared with that of naive T cell recipients, demonstrated that immunization with 2D2 generated T cell-mediated immunity. CD4(+) and CD8(+) cell depletion studies demonstrated that CD4(+) cells, but not CD8(+) cells, mediated this protection in vivo. Thus, CD4(+) T cells can mediate vaccine-induced immunity to experimental melioidosis.
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