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From The Salk Institute for Biological Studies, P. O. Box 1809, San Diego, California 92112
Abstract
C3H/HeJ mice contain a defect in a single autosomal locus which is not linked to the H-2 histocompatibility or the heavy chain allotype loci that restricts immune, mitogenic, and polyclonal responses to bacterial lipopolysaccharides (LPS). Adult thymectomized C3H/HeJ mice that have been irradiated and reconstituted with C3HeB/FeJ bone marrow cells respond well to LPS. Cell-mixing experiments using C3H/HeJ-C3HeB/FeJ spleen cultures show that the failure of C3H/HeJ spleen cells to support responses to LPS is not due to nonspecific or LPS-induced suppressive events, or the lack of accessory cell types. C3H/HeJ and C3HeB/FeJ spleen cells bind LPS and respond to other B cell mitogens equally well. We suggest that the B lymphocytes of C3H/HeJ mice have a defect in a membrane component that is activated via interaction with LPS, and initiates the intracellular events that lead to cell proliferation.
Footnotes
1 This work was supported by Grant AI-11092 from the National Institutes of Health, a Leukemia Society of America Special Fellowship, and Grant A-105875 from the National Institutes of Health.
2 Present address: The Institute for Cancer Research, 7701 Burholme Avenue, Philadelphia, Pennsylvania 19111.
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