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¹ Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115
² Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115
³ Division of Infectious Diseases, University of Massachusetts Medical School, Worcester, MA 01605

CORRESPONDENCE Dennis L. Kasper: dennis_kasper{at}hms.harvard.edu

Commensalism is critical to a healthy Th1/Th2 cell balance. Polysaccharide A (PSA), which is produced by the intestinal commensal Bacteroides fragilis, activates CD4⁺ T cells, resulting in a Th1 response correcting the Th2 cell skew of germ-free mice. We identify Toll-like receptors as crucial to the convergence of innate and adaptive responses stimulated by PSA. Optimization of the Th1 cytokine interferon- in PSA-stimulated dendritic cell–CD4⁺ T cell co-cultures depends on both Toll-like receptor (TLR) 2 and antigen presentation. Synergy between the innate and adaptive responses was also shown when TLR2^–/– mice exhibited impaired intraabdominal abscess formation in response to B. fragilis. Commensal bacteria, using molecules like PSA, potentially modulate the Th1/Th2 cell balance and the response to infection by coordinating both the innate and adaptive pathways.

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