Inflammatory arthritis is associated with the release of a network of key cytokines. In T cell receptor transgenic K/BxN mice interleukin (IL)-1 plays a key role in joint swelling and destruction, as suggested by the ability of anti–IL-1receptor (IL-1R) antibody treatment to delay the onset and slow the progression of this disease. This mechanism is dependent on the signaling pathway intermediary myeloid differentiation factor 88 (MyD88), such that neither IL-1R nor MyD88-deficient mice developed visually detectable synovitis after transfer of arthritogenic sera. The Toll-like receptors (TLRs) share the same signaling pathway through MyD88 as the IL-1R. The administration of a TLR-4 ligand, lipopolysaccharide, concomitant with arthritogenic serum in IL-1 receptor–deficient mice resulted in acute paw swelling, but not in MyD88-deficient mice. Also, serum transferred arthritis was not sustained in TLR-4 mutant mice compared with controls. These results suggest that innate immune functions via TLR-4 might perpetuate inflammatory mechanisms and bypass the need for IL-1 in chronic joint inflammation.
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17 February 2003
Brief Definitive Report|
February 10 2003
Interleukin 1 Receptor Dependence of Serum Transferred Arthritis Can be Circumvented by Toll-like Receptor 4 Signaling
Jung-Yoon Choe,
Jung-Yoon Choe
Division of Rheumatology, Allergy, and Immunology, and The Sam and Rose Stein Institute for Research on Aging, University of California, San Diego, La Jolla, CA 92093
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Brian Crain,
Brian Crain
Division of Rheumatology, Allergy, and Immunology, and The Sam and Rose Stein Institute for Research on Aging, University of California, San Diego, La Jolla, CA 92093
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Sarah R. Wu,
Sarah R. Wu
Division of Rheumatology, Allergy, and Immunology, and The Sam and Rose Stein Institute for Research on Aging, University of California, San Diego, La Jolla, CA 92093
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Maripat Corr
Maripat Corr
Division of Rheumatology, Allergy, and Immunology, and The Sam and Rose Stein Institute for Research on Aging, University of California, San Diego, La Jolla, CA 92093
Search for other works by this author on:
Jung-Yoon Choe
Division of Rheumatology, Allergy, and Immunology, and The Sam and Rose Stein Institute for Research on Aging, University of California, San Diego, La Jolla, CA 92093
Brian Crain
Division of Rheumatology, Allergy, and Immunology, and The Sam and Rose Stein Institute for Research on Aging, University of California, San Diego, La Jolla, CA 92093
Sarah R. Wu
Division of Rheumatology, Allergy, and Immunology, and The Sam and Rose Stein Institute for Research on Aging, University of California, San Diego, La Jolla, CA 92093
Maripat Corr
Division of Rheumatology, Allergy, and Immunology, and The Sam and Rose Stein Institute for Research on Aging, University of California, San Diego, La Jolla, CA 92093
Address correspondence to Maripat Corr, Division of Rheumatology, Allergy, and Immunology, and The Sam and Rose Stein Institute for Research on Aging, University of California, San Diego, La Jolla, CA 92093-0663. Phone: 858-534-7817; Fax: 858-534-5399; E-mail: [email protected]
Received:
October 24 2002
Revision Received:
December 11 2002
Accepted:
December 30 2002
Online ISSN: 1540-9538
Print ISSN: 0022-1007
The Rockefeller University Press
2003
J Exp Med (2003) 197 (4): 537–542.
Article history
Received:
October 24 2002
Revision Received:
December 11 2002
Accepted:
December 30 2002
Citation
Jung-Yoon Choe, Brian Crain, Sarah R. Wu, Maripat Corr; Interleukin 1 Receptor Dependence of Serum Transferred Arthritis Can be Circumvented by Toll-like Receptor 4 Signaling . J Exp Med 17 February 2003; 197 (4): 537–542. doi: https://doi.org/10.1084/jem.20021850
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