Journal
JOURNAL OF IMMUNOLOGY
Volume 184, Issue 3, Pages 1227-1234Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0902011
Keywords
-
Categories
Funding
- National Institutes of Health [AI078864]
- Russian Foundation for Basic Research [07-04-00447]
- International Science and Technology Center [3626]
Ask authors/readers for more resources
Mutations in the btk gene encoding Bruton's tyrosine kinase cause X-linked immune deficiency, with impaired B lymphocyte function as the major phenotype. Earlier, we demonstrated that CBA/N-xid mice, unlike the wild-type CBA mice, were not protected by bacillus Calmette-Guerin (BCG) vaccination against tuberculosis infection. Because IFN-gamma-producing T cells and activated macrophages are key elements of antituberculosis protection, it remained unclear how the mutation predominantly affecting B cell functions interferes with responses along the T cell-macrophage axis. In this study, we show that B cell deficiency leads to an abnormally rapid neutrophil migration toward the site of external stimulus. Using adoptive cell transfers and B cell genetic knockout, we demonstrate a previously unappreciated capacity of B cells to downregulate neutrophil motility. In our system, an advanced capture of BCG by neutrophils instead of macrophages leads to a significant decrease in numbers of IFN-gamma-producing T cells and impairs BCG performance in X-linked immune-deficient mice. The defect is readily compensated for by the in vivo neutrophil depletion. The Journal of Immunology, 2010, 184: 1227-1234.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available