Previous Article | Next Article ![]()
Infection and Immunity, December 2000, p. 6650-6655, Vol. 68, No. 12
Channing Laboratory, Department of
Medicine,1 and Laboratory of Immunogenetics and
Transplantation, Renal Division,
Brigham and Women's Hospital,2 and Division of Infectious
Diseases, Dana-Farber Cancer Institute,3
Harvard Medical School, Boston, Massachusetts, and
Bristol-Myers Squibb, Princeton, New Jersey4
Received 22 May 2000/Returned for modification 18 August
2000/Accepted 29 August 2000
Abscesses are a classic host response to infection by many
pathogenic bacteria. The immunopathogenesis of this tissue response to
infection has not been fully elucidated. Previous studies have suggested that T cells are involved in the pathologic process, but the
role of these cells remains unclear. To delineate the mechanism by
which T cells mediate abscess formation associated with intra-abdominal
sepsis, the role of T-cell activation and the contribution of
antigen-presenting cells via CD28-B7 costimulation were investigated. T
cells activated in vitro by zwitterionic bacterial polysaccharides
(Zps) known to induce abscess formation required CD28-B7 costimulation
and, when adoptively transferred to the peritoneal cavity of
naïve rats, promoted abscess formation. Blockade of T-cell
activation via the CD28-B7 pathway in animals with CTLA4Ig prevented
abscess formation following challenge with different bacterial
pathogens, including Staphylococcus aureus, Bacteroides fragilis, and a combination of
Enterococcus faecium and Bacteroides
distasonis. In contrast, these animals had an increased abscess
rate following in vivo T-cell activation via CD28 signaling. Abscess
formation in vivo and T-cell activation in vitro required costimulation
by B7-2 but not B7-1. These results demonstrate that abscess formation
by pathogenic bacteria is under the control of a common effector
mechanism that requires T-cell activation via the CD28-B7-2 pathway.
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Bacterial Pathogens Induce Abscess Formation by
CD4+ T-Cell Activation via the CD28-B7-2
Costimulatory Pathway

*
Corresponding author. Mailing address: Channing
Laboratory, 181 Longwood Ave., Boston, MA 02115. Phone: (617) 525-2610. Fax: (617) 731-1541. E-mail:
atzianabos{at}channing.harvard.edu.
Present address: Nestle Research Center, 1000 Lausanne 26, Switzerland.
This article has been cited by other articles:
| J. Bacteriol. | J. Virol. | Eukaryot. Cell |
|---|
| Microbiol. Mol. Biol. Rev. | Clin. Vaccine Immunol. | All ASM Journals |
|---|