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IL-10-deficient B10.Q mice develop more severe collagen-induced arthritis, but are protected from arthritis induced with anti-type II collagen antibodies
University of Lund, Lund, Sweden.
University of Lund, Lund, Sweden.
University of Lund, Lund, Sweden.ORCID iD: 0000-0001-7790-8197
University of Lund, Lund, Sweden.
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2001 (English)In: Journal of Immunology, ISSN 0022-1767, E-ISSN 1550-6606, Vol. 167, no 6, p. 3505-3512Article in journal (Refereed) Published
Abstract [en]

IL-10 is a pleiotropic cytokine with stimulatory and inhibitory properties, and is thought to have a protective role in rheumatoid arthritis and collagen-induced arthritis (CIA). In this study, we investigated how IL-10 deficiency affects CIA and anti-collagen type II (CII) Ab-transferred arthritis in C57BL/10.Q (B10.Q) mice. The B10.Q.IL-10(-/-) mice had an 8-cM 129/Ola fragment around the IL-10 gene. The mice were treated with antibiotics, appeared healthy, and had no colitis. T cells from IL-10(-/-) mice expressed similar levels of IFN-gamma, IL-2, and IL-4 after mitogen stimulation; however, macrophages showed a reduced TNF-alpha production compared with IL-10(+/-) littermates. IL-10(-/-) mice had an increased incidence, and a more severe CIA disease than the IL-10(+/-) littermates. To study the role of IL-10 in T cell tolerance, IL-10(-/-) were crossed into mice carrying the immunodominant epitope, CII(256-270), in cartilage (MMC) or in skin (TSC). Both IL-10(-/-) and IL-10(+/-) MMC and TSC mice were completely tolerized against CIA, indicating that lack of IL-10 in this context did not break tolerance. To investigate whether IL-10 was important in the effector phase of CIA, arthritis was induced with anti-CII Abs. Surprisingly, IL-10(-/-) were less susceptible to Ab-transferred arthritis, as only 30% showed signs of disease compared with 90% of the littermates. Therefore, IL-10 seemed to have a protective role in CIA, but seemed to exacerbate the arthritogenicity of anti-CII Abs. These data emphasize the importance of studying IL-10 in a defined genetic context in vivo, to understand its role in a complex disease like arthritis.

Place, publisher, year, edition, pages
2001. Vol. 167, no 6, p. 3505-3512
Keywords [en]
Animals, Antibodies, Monoclonal/immunology/*toxicity, Arthritis/chemically induced/*etiology/immunology, Arthritis, Experimental/genetics/*immunology, Autoimmune Diseases/genetics/*immunology, Colitis/etiology/immunology, Collagen Type II/*immunology, Cytokines/biosynthesis, Disease Models, Animal, Genotype, Immune Tolerance/immunology, Immunization, Immunization, Passive, Immunodominant Epitopes/genetics/immunology, Interleukin-10/deficiency/genetics/*physiology, Macrophages/metabolism, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Specific Pathogen-Free Organisms, Tumor Necrosis Factor-alpha/metabolism
National Category
Immunology in the medical area
Identifiers
URN: urn:nbn:se:hh:diva-48807DOI: 10.4049/jimmunol.167.6.3505PubMedID: 11544344OAI: oai:DiVA.org:hh-48807DiVA, id: diva2:1719121
Available from: 2022-12-14 Created: 2022-12-14 Last updated: 2023-02-20Bibliographically approved

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Nandakumar, Kutty Selva

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