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Exacerbation of collagen type II-induced arthritis in ApoE deficient mice in association with the expansion of Th1 and Th17 cells. Exacerbation of collagen type II-induced arthritis in ApoE deficient mice in association with the expansion of Th1 and Th17 cells. J. Postigo, F. Genre, M. Iglesias, M. Fernández-Rey, L. Buelta, J.C. Rodríguez-Rey, J. Merino and R. Merino. 2011-01-09T23:00:00Z<p style="text-align:justify;">​<strong class="ms-rteFontSize-2">Abstract:</strong></p><p style="text-align:justify;"><span class="ms-rteFontSize-2"><em>Objective.</em><em> </em>To explore the bidirectional relationship between the development of rheumatoid arthritis (RA) and atherosclerosis using bovine type II collagen (CII)-immunized B10.RIII apoE<sup>-</sup><sup>/</sup><sup>-</sup>mice, a murine model of spontaneous atherosclerosis and collagen-induced arthritis (CIA).</span></p><p style="text-align:justify;"><span class="ms-rteFontSize-2"><em>Methods.</em><em> </em>Male B10.RIII apoE<sup>-</sup><sup>/</sup><sup>-</sup>mice and wildtype controls were immunized with 150 µg of CII emulsified in Freund's complete adjuvant (CFA). The clinical, radiologic, and histopathologic severity of CIA, the levels of circulating IgG1 and IgG2a anti-CII antibodies, the expression of proinflammatory and anti-inflammatory cytokines in the joints, and the percentages of Th1, Th17, and Treg lymphocytes in the draining lymph nodes were evaluated during CIA induction. In addition, the size of atherosclerotic lesions was assessed in these mice 8 weeks after CIA induction.</span></p><p style="text-align:justify;"><span class="ms-rteFontSize-2"><em>Results.</em><em> </em>B10.RIII apoE<sup>-</sup><sup>/</sup><sup>-</sup>mice that were immunized with CII and CFA developed an exacerbated CIA that was accompanied by increased joint expression of multiple proinflammatory cytokines and by the expansion in the draining lymph nodes of Th1 and Th17 cells. In contrast, the size of vascular lesions in B10.RIII apoE<sup>-</sup><sup>/</sup><sup>-</sup>mice was not affected by the development of CIA.</span></p><p style="text-align:justify;"><span class="ms-rteFontSize-2"><em>Conclusion.</em><em> </em>Our findings indicate that a deficiency in apolipoprotein E and/or its consequences in cholesterol metabolism act as accelerating factors in autoimmunity by promoting Th1 and Th17 inflammatory responses.<br></span></p><p>​<strong></strong><a href="https://onlinelibrary.wiley.com/doi/full/10.1002/art.30220">Arthritis Rheum. 2011,63: 971-980. DOI: 10.1002/art.30220.</a><br></p>158

 
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Instituto de Biomedicina y Biotecnología de Cantabria.
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