Abstract
Protein kinase C plays a vital role in the activation of C3H/HeJ B lymphocytes by endotoxin associated protein; however, it is unlikely that G proteins are involved in the early signals stimulated by EP. On the other hand, LPS suppresses C3H/HeJ B cell DNA synthesis induced by EP which may be the result of PKC down regulation. LPS inhibits C3H/HeJ B cells from progressing through the G1 phase of the cell cycle blocking RNA synthesis within the first 12 hr after the cells are stimulated. Finally, this inhibition extends to activation of the arachidonic acid metabolism in C3H/HeJ macrophages and T cell proliferation to a limited extent.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adjuvants, Immunologic / pharmacology
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Animals
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B-Lymphocytes / immunology*
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B-Lymphocytes / metabolism
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Bacterial Proteins / immunology
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Bacterial Proteins / pharmacology*
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DNA / biosynthesis
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Dinoprostone / biosynthesis
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Endotoxins / immunology
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Endotoxins / pharmacology*
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Female
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GTP-Binding Proteins / metabolism
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In Vitro Techniques
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Lipid A / immunology
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Lipid A / pharmacology*
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Lipopolysaccharides / immunology
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Lipopolysaccharides / pharmacology*
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Lymphocyte Activation / physiology
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Male
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Mice
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Mice, Inbred C3H
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Protein Kinase C / metabolism
Substances
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Adjuvants, Immunologic
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Bacterial Proteins
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Endotoxins
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Lipid A
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Lipopolysaccharides
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lipid A-associated protein, Bacteria
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DNA
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Protein Kinase C
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GTP-Binding Proteins
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Dinoprostone