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Infection and Immunity, January 1999, p. 319-326, Vol. 67, No. 1
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

The Polysaccharide Portion of Lipopolysaccharide Regulates Antigen-Specific T-Cell Activation via Effects on Macrophage-Mediated Antigen Processing

Nicole M. Zirk,* Saira F. Hashmi, and H. Kirk Ziegler

Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia 30322

Received 15 June 1998/Returned for modification 5 October 1998/Accepted 16 October 1998

The lipopolysaccharide (LPS) structure of Salmonella typhimurium has been correlated with the virulence of wild-type strain LT2. Mutants of LT2 with truncated polysaccharide portions of LPS are less virulent than strains with a complete LPS structure. Polyclonal T cells and monoclonal T-cell hybridomas were more reactive to heat-killed rough mutants than to heat-killed smooth strains, as measured by interleukin-2 (IL-2) production. Using a large panel of strains with truncated LPS molecules, we found that T-cell reactivity decreased with certain lengths of polysaccharide. The decreased response was not due to differential phagocytic uptake, IL-12 production, or major histocompatibility complex class II surface expression by macrophages. Also, LT2 did not mediate any global suppression since addition of LT2 did not diminish the response of T cells specific for antigens unrelated to Salmonella. In an experiment in which processing times were varied, we found that antigens from rough strains were processed and presented more quickly than those associated with smooth strains. At longer processing times, epitopes from LT2 were presented well. We hypothesize that the slower antigen processing and presentation of wild-type Salmonella may be caused by masking of surface antigens by the longer polysaccharide portion of smooth LPS. This blocking of effective antigen presentation may contribute to the virulence of Salmonella.


* Corresponding author. Mailing address: Department of Microbiology and Immunology, Room 3170, Emory University School of Medicine, 1510 Clifton Rd., Atlanta, GA 30322. Phone: (404) 727-0294. Fax: (404) 727-3659. E-mail: nzirk{at}bimcore.emory.edu.


Infection and Immunity, January 1999, p. 319-326, Vol. 67, No. 1
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.



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