Abstract |
Prior studies indicated the ability of Abs to complement receptor 3 (CR3, CD11b/CD18) to suppress the production of IL-12 from immune cells. Therefore, we tested the ability of an anti-CR3 Ab (clone M1/70) to treat established IL-12-dependent Th1-mediated inflammation in murine models. Systemic administration of anti-CR3 significantly ameliorated established intestinal inflammation following the intrarectal administration of trinitrobenzene sulfonic acid (TNBS- colitis), as well as colitis and skin inflammation in C57BL/10 RAG-2(-/-) mice reconstituted with CD4+CD45RBhigh T cells. The hyperproliferative skin inflammation in this novel murine model demonstrated many characteristics of human psoriasis, and was prevented by the adoptive transfer of CD45RBlow T cells. In vitro and in vivo studies suggest that anti-CR3 treatment may act, at least in part, by directly inhibiting IL-12 production by APCs. Administration of anti-CR3 may be a useful therapeutic approach to consider for the treatment of inflammatory bowel disease and psoriasis in humans.
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Authors | Francisco Leon, Nikhat Contractor, Ivan Fuss, Thomas Marth, Edward Lahey, Shoko Iwaki, Andrea la Sala, Victoria Hoffmann, Warren Strober, Brian L Kelsall |
Journal | Journal of immunology (Baltimore, Md. : 1950)
(J Immunol)
Vol. 177
Issue 10
Pg. 6974-82
(Nov 15 2006)
ISSN: 0022-1767 [Print] United States |
PMID | 17082612
(Publication Type: Journal Article)
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Chemical References |
- Antibodies
- Inflammation Mediators
- Macrophage-1 Antigen
- Trinitrobenzenesulfonic Acid
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Topics |
- Adoptive Transfer
- Animals
- Antibodies
(administration & dosage, therapeutic use)
- CD4-Positive T-Lymphocytes
(transplantation)
- Cells, Cultured
- Colitis
(chemically induced, immunology, therapy)
- Dermatitis
(immunology, pathology, therapy)
- Disease Models, Animal
- Female
- Inflammation Mediators
(administration & dosage, therapeutic use)
- Injections, Intravenous
- Macrophage-1 Antigen
(immunology)
- Male
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Mice, Nude
- Psoriasis
(immunology, pathology, therapy)
- Trinitrobenzenesulfonic Acid
(toxicity)
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