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National Institute of Environmental Health Sciences

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Your Environment. Your Health.

Publication Detail

Title: Activated human B lymphocytes express cyclooxygenase-2 and cyclooxygenase inhibitors attenuate antibody production.

Authors: Ryan, Elizabeth P; Pollock, Stephen J; Pollack, Stephen J; Murant, Thomas I; Bernstein, Steven H; Felgar, Raymond E; Phipps, Richard P

Published In J Immunol, (2005 Mar 01)

Abstract: Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used for the treatment of inflammatory diseases and target cyclooxygenases 1 and 2 (Cox-1, Cox-2) that are responsible for PG production. Newer Cox-2-selective drugs have been heavily prescribed to quench inflammation. Little is known about whether or not these drugs influence human B lymphocytes and their ability to produce Ab. We report herein that activated human B cells not only highly express Cox-2 and produce PGs, but that the NSAID indomethacin and Cox-2-selective drugs profoundly inhibit the ability of human B cells to produce IgG and IgM in vitro. Human blood B cells highly express Cox-2 mRNA and protein and produce PGs after activation with CD40L, pansorbin, or CD40L plus BCR engagement. Cox-2 is also highly expressed by human tonsil B cells, as shown by immunohistochemistry. Cox-inhibiting drugs modestly affect purified B cell proliferation but profoundly reduce Ab production. The ability of whole blood to produce IgM and IgG following stimulation is also strongly inhibited. In support that Cox-2 plays a seminal role in B lymphocyte Ab production, Cox-2 knockout mice have 64% less IgM and 35% less IgG than normal littermate controls. These findings support that NSAIDs and the new Cox-2-selective drugs have an unsuspected target, the B cell, and attenuate Ab production in humans. Use of NSAIDs may therefore influence autoantibody production in autoimmune diseases and may dampen humoral immunity in response to antigenic challenge/vaccination.

PubMed ID: 15728468 Exiting the NIEHS site

MeSH Terms: Animals; Antibody Formation/drug effects*; B-Lymphocyte Subsets/drug effects; B-Lymphocyte Subsets/enzymology*; B-Lymphocyte Subsets/immunology*; Cell Proliferation/drug effects; Cells, Cultured; Cyclooxygenase 1; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors/pharmacology*; Dinoprost/biosynthesis; Dinoprostone/biosynthesis; Humans; Immunoglobulin G/blood; Immunoglobulin G/metabolism; Immunoglobulin M/blood; Immunoglobulin M/deficiency; Immunosuppressive Agents/pharmacology*; Lymphocyte Activation/drug effects; Lymphocyte Activation/immunology*; Membrane Proteins; Mice; Mice, Inbred C57BL; Mice, Knockout; Prostaglandin-Endoperoxide Synthases/biosynthesis*; Prostaglandin-Endoperoxide Synthases/deficiency; Prostaglandin-Endoperoxide Synthases/genetics; Prostaglandin-Endoperoxide Synthases/physiology; RNA, Messenger/biosynthesis; Up-Regulation/genetics; Up-Regulation/immunology

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