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Infection and Immunity, December 2000, p. 6650-6655, Vol. 68, No. 12
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

Arthur O. Tzianabos,1,* Anil Chandraker,2 Wiltrud Kalka-Moll,1 Francesca Stingele,1,dagger Victor M. Dong,2 Robert W. Finberg,3 Robert Peach,4 and Mohamed H. Sayegh2

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.

* 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.

dagger Present address: Nestle Research Center, 1000 Lausanne 26, Switzerland.

Infection and Immunity, December 2000, p. 6650-6655, Vol. 68, No. 12
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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