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Together with increasing evidence that worm infection may protect against autoimmune conditions, this raises the possibility that <jats:styled-content style=\"fixed-case\">ES<\/jats:styled-content>\u201062 may have therapeutic potential in rheumatoid arthritis and hence, it is important to fully understand its mechanism of action. To this end, we have established to date that <jats:styled-content style=\"fixed-case\">ES<\/jats:styled-content>\u201062 protection in <jats:styled-content style=\"fixed-case\">CIA<\/jats:styled-content> is associated with suppressed T helper type 1 (<jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h1)\/<jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h17 responses, reduced collagen\u2010specific <jats:styled-content style=\"fixed-case\">I<\/jats:styled-content>g<jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>2a antibodies and increased interleukin\u201010 (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010) production by splenocytes. <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010\u2010producing regulatory <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content> cells have been proposed to suppress pathogenic <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h1\/<jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h17 responses in <jats:styled-content style=\"fixed-case\">CIA<\/jats:styled-content>: interestingly therefore, although the levels of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010\u2010producing <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content> cells were decreased in the spleens of mice with <jats:styled-content style=\"fixed-case\">CIA<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> ES<\/jats:styled-content>\u201062 was found to restore these to the levels found in naive mice. In addition, exposure to <jats:styled-content style=\"fixed-case\">ES<\/jats:styled-content>\u201062 decreased effector <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>\u2010cell, particularly plasma cell, infiltration of the joints, and such infiltrating <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content> cells showed dramatically reduced levels of <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>oll\u2010like receptor 4 and the activation markers, <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>80 and <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>86. Collectively, this induction of hyporesponsiveness of effector <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>\u2010cell responses, in the context of the resetting of the levels of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010\u2010producing <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content> cells, is suggestive of a modulation of the balance between effector and regulatory <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>\u2010cell responses that may contribute to <jats:styled-content style=\"fixed-case\">ES<\/jats:styled-content>\u201062\u2010mediated suppression of <jats:styled-content style=\"fixed-case\">CIA<\/jats:styled-content>\u2010associated inflammation and inhibition of production of pathogenic collagen\u2010specific <jats:styled-content style=\"fixed-case\">I<\/jats:styled-content>g<jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>2a antibodies.<\/jats:p>","DOI":"10.1111\/imm.12208","type":"journal-article","created":{"date-parts":[[2013,11,4]],"date-time":"2013-11-04T09:19:32Z","timestamp":1383556772000},"page":"457-466","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":45,"title":["Protection against collagen\u2010induced arthritis in mice afforded by the parasitic worm product, <scp>ES<\/scp>\u201062, is associated with restoration of the levels of interleukin\u201010\u2010producing <scp>B<\/scp> cells and reduced plasma cell infiltration of the joints"],"prefix":"10.1111","volume":"141","author":[{"given":"David T.","family":"Rodgers","sequence":"first","affiliation":[{"name":"Institute of Infection Immunity and Inflammation University of Glasgow Glasgow UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Miguel A.","family":"Pineda","sequence":"additional","affiliation":[{"name":"Institute of Infection Immunity and Inflammation 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