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A live experimental vaccine against Burkholderia pseudomallei elicits CD4(+) T cell-mediated immunity, priming T cells specific for 2 type III secretion system proteins

Research output: Contribution to journalArticlepeer-review

  • Ashraful Haque
  • Karen Chu
  • Anna Easton
  • Mark P. Stevens
  • Edouard E. Galyov
  • Tim Atkins
  • Rick Titball
  • Gregory J. Bancroft

Related Edinburgh Organisations

Original languageEnglish
Pages (from-to)1241-1248
Number of pages8
JournalThe Journal of Infectious Diseases
Volume194
Issue number9
DOIs
Publication statusPublished - 1 Nov 2006

Abstract

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.

    Research areas

  • Animals, Bacterial Proteins/immunology, Bacterial Vaccines/immunology, Burkholderia Infections/immunology, Burkholderia Infections/prevention & control, Burkholderia pseudomallei/immunology, CD4-Positive T-Lymphocytes/immunology, CD4-Positive T-Lymphocytes/metabolism, Female, Interferon-gamma/metabolism, Mice, Mice, Inbred BALB C, Spleen/metabolism, Spleen/microbiology, Virulence

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