Involvement of IL-6, Apart from Its Role in Immunity, in Mediating a Chronic Response during Experimental Arthritis
Identifieur interne : 000A54 ( Main/Exploration ); précédent : 000A53; suivant : 000A55Involvement of IL-6, Apart from Its Role in Immunity, in Mediating a Chronic Response during Experimental Arthritis
Auteurs : Alfons S. K. De Hooge [Pays-Bas] ; Fons A. J. Van De Loo [Pays-Bas] ; Onno J. Arntz [Pays-Bas] ; Wim B. Van Den Berg [Pays-Bas]Source :
- The American Journal of Pathology [ 0002-9440 ] ; 2000.
Abstract
Interleukin-6 (IL-6) is highly produced during arthritis but its exact function is still unknown. In this study we examined if IL-6, apart from its role in immunity, was involved in the local inflammatory response in experimental arthritis. IL-6 deficient (IL-6/) and wild-type mice were first compared in the antigen-induced arthritis model. IL-6 deficiency resulted in a mild, transient inflammation whereas wild-type mice developed a chronic, destructive synovitis. Wild-type mice immunized with one-tenth of the normal antigen dose still developed chronic arthritis despite low antibody levels, excluding reduced humoral immunity in IL-6/ mice as a crucial phenomenon. In addition, passive immune-complex-induced arthritis did not differ between wild-type and IL-6/ mice. Another option is reduced levels of Th1 cells in IL-6/ mice. However, transfer of antigen-specific wild-type lymph node cells to IL-6/ mice enhanced acute joint inflammation and increased cartilage damage but still could not sustain chronic inflammation, suggesting involvement of nonimmune elements of IL-6 activity in chronicity. In line with this, nonimmunologically mediated zymosan-induced arthritis developed similarly in the first week, but only wild-type mice developed chronic synovitis. These results indicate an important role for IL-6 in propagation of joint inflammation, potentially independent of its role in immunity.
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DOI: 10.1016/S0002-9440(10)64846-8
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In this study we examined if IL-6, apart from its role in immunity, was involved in the local inflammatory response in experimental arthritis. IL-6 deficient (IL-6/) and wild-type mice were first compared in the antigen-induced arthritis model. IL-6 deficiency resulted in a mild, transient inflammation whereas wild-type mice developed a chronic, destructive synovitis. Wild-type mice immunized with one-tenth of the normal antigen dose still developed chronic arthritis despite low antibody levels, excluding reduced humoral immunity in IL-6/ mice as a crucial phenomenon. In addition, passive immune-complex-induced arthritis did not differ between wild-type and IL-6/ mice. Another option is reduced levels of Th1 cells in IL-6/ mice. However, transfer of antigen-specific wild-type lymph node cells to IL-6/ mice enhanced acute joint inflammation and increased cartilage damage but still could not sustain chronic inflammation, suggesting involvement of nonimmune elements of IL-6 activity in chronicity. In line with this, nonimmunologically mediated zymosan-induced arthritis developed similarly in the first week, but only wild-type mice developed chronic synovitis. These results indicate an important role for IL-6 in propagation of joint inflammation, potentially independent of its role in immunity.</div></front></TEI><affiliations><list><country><li>Pays-Bas</li></country><region><li>Gueldre</li></region><settlement><li>Nimègue</li></settlement></list><tree><country name="Pays-Bas"><region name="Gueldre"><name sortKey="De Hooge, Alfons S K" sort="De Hooge, Alfons S K" uniqKey="De Hooge A" first="Alfons S. K." last="De Hooge">Alfons S. K. 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