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The Journal of Immunology, 2003, 170: 1958-1963.
Copyright © 2003 by The American Association of Immunologists

CD4+ T Cells Mediate Abscess Formation in Intra-abdominal Sepsis by an IL-17-Dependent Mechanism 1

Doo Ryeon Chung*, Dennis L. Kasper*,§, Ronald J. Panzo*, Tanuja Chtinis{dagger}, Michael J. Grusby, Mohamed H. Sayegh{ddagger} and Arthur O. Tzianabos2,*

* Channing Laboratory, Department of Medicine, {dagger} Department of Neurology, and {ddagger} Laboratory of Immunogenetics and Transplantation, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115; and § Department of Microbiology and Molecular Genetics, and School of Public Health, Department of Immunology and Infectious Disease, Harvard Medical School, Boston, MA 02115

Abscess formation associated with intra-abdominal sepsis causes severe morbidity and can be fatal. Previous studies have implicated T cells in the pathogenesis of abscess formation, and we have recently shown that CD4+ T cells activated in vitro by zwitterionic capsular polysaccharides from abscess-inducing bacteria such as Staphylococcus aureus and Bacteroides fragilis initiate this host response when transferred to naive rats. In this study, we show that mice deficient in {alpha}{beta}TCR-bearing T cells or CD4+ T cells fail to develop abscesses following challenge with B. fragilis or abscess-inducing zwitterionic polysaccharides, compared with CD8-/- or wild-type animals. Transfer of CD4+ T cells from wild-type mice to {alpha}{beta}TCR-/- animals reconstituted this ability. The induction of abscesses required T cell costimulation via the CD28-B7 pathway, and T cell transfer experiments with STAT4-/- and STAT6-/- mice demonstrated that this host response is dependent on STAT4 signaling. Significantly higher levels of IL-17, a proinflammatory cytokine produced almost exclusively by activated CD4+ T cells, were associated with abscess formation in Th2-impaired (STAT6-/-) mice, while STAT4-/- mice had significantly lower levels of this cytokine than control animals. The formation of abscesses was preceded by an increase in the number of activated CD4+ T cells in the peritoneal cavity 24 h following bacterial challenge. Confocal laser-scanning microscopy analysis revealed that CD4+ T cells comprise the abscess wall in these animals and produce IL-17 at this site. Administration of a neutralizing Ab specific for IL-17 prevented abscess formation following bacterial challenge in mice. These data delineate the specific T cell response necessary for the development of intra-abdominal abscesses and underscore the role of IL-17 in this disease process.




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