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* Department of Pathology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814;
Pulmonary and Critical Care Division, Department of Medicine, University of California, San Francisco, CA 94143;
Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115; and
Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110
Little is known concerning the role of T cells in regulating an
anti-polysaccharide Ig response to an intact pathogen. We
previously reported that the in vivo Ig responses to
Streptococcus pneumoniae (strain R36A), specific for
pneumococcal surface protein A (PspA) and for the phosphorylcholine
(PC) determinant of C-polysaccharide, were both dependent on
TCR-
+ T cells and B7-dependent costimulation,
although only PspA-specific memory was generated. In this report, we
show that the T cell help underlying these two Ag-specific Ig responses
is distinct. Using H-Y-specific T cell transgenic mice made
"nonleaky" by crossing with mice genetically deficient for TCR-,
we demonstrate that the T cell help for the anti-PC, in contrast to
the anti-PspA, response is TCR-nonspecific and occurs normally in
the absence of germinal center formation, although it is still
dependent on B7-dependent costimulation. Consistent with these data, we
demonstrate, using cathepsin S-/- mice, that although the
anti-PC response is largely dependent on CD4+ T cells,
there is a reduced (or lack of) dependence, relative to the
anti-PspA response, on the generation of new peptide-MHC class II
complexes. In this regard, the T cell help for an optimal anti-PC
response is delivered more rapidly than that required for an optimal
anti-PspA response. Collectively, these data demonstrate a novel
accelerated TCR-nonspecific B7-dependent form of T cell help for
augmenting a polysaccharide-specific Ig response to an intact bacterium
without the generation of memory.
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