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*
Baylor Institute for Immunology Research, Dallas, TX 75204;
School of Dental Medicine, State University of New York, Stony Brook, NY 11794; and
Department of Periodontology and Oral Biology, Boston University School of Medicine, Boston, MA 02118
The adaptive immune system has evolved distinct responses against
different pathogens, but the mechanism(s) by which a particular
response is initiated is poorly understood. In this study, we
investigated the type of Ag-specific CD4+ Th and
CD8+ T cell responses elicited in vivo, in response to
soluble OVA, coinjected with LPS from two different pathogens. We used
Escherichia coli LPS, which signals through Toll-like
receptor 4 (TLR4) and LPS from the oral pathogen Porphyromonas
gingivalis, which does not appear to require TLR4 for
signaling. Coinjections of E. coli LPS + OVA or
P. gingivalis LPS + OVA induced similar clonal
expansions of OVA-specific CD4+ and CD8+ T
cells, but strikingly different cytokine profiles. E.
coli LPS induced a Th1-like response with abundant IFN-
, but
little or no IL-4, IL-13, and IL-5. In contrast, P.
gingivalis LPS induced Th and T cell responses characterized by
significant levels of IL-13, IL-5, and IL-10, but lower levels of
IFN-. Consistent with these results, E. coli LPS
induced IL-12(p70) in the CD8
+ dendritic cell (DC)
subset, while P. gingivalis LPS did not. Both LPS,
however, activated the two DC subsets to up-regulate costimulatory
molecules and produce IL-6 and TNF-. Interestingly, these LPS
appeared to have differences in their ability to signal through TLR4;
proliferation of splenocytes and cytokine secretion by splenocytes or
DCs from TLR4-deficient C3H/HeJ mice were greatly impaired in response
to E. coli LPS, but not P. gingivalis
LPS. Therefore, LPS from different bacteria activate DC subsets to
produce different cytokines, and induce distinct types of adaptive
immunity in vivo.
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