In:
Immunology, Wiley, Vol. 141, No. 3 ( 2014-03), p. 457-466
Kurzfassung:
We have previously reported that ES ‐62, a molecule secreted by the parasitic filarial nematode A canthocheilonema viteae , protects mice from developing collagen‐induced arthritis ( CIA ). Together with increasing evidence that worm infection may protect against autoimmune conditions, this raises the possibility that ES ‐62 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 ES ‐62 protection in CIA is associated with suppressed T helper type 1 ( T h1)/ T h17 responses, reduced collagen‐specific I g G 2a antibodies and increased interleukin‐10 ( IL ‐10) production by splenocytes. IL ‐10‐producing regulatory B cells have been proposed to suppress pathogenic T h1/ T h17 responses in CIA : interestingly therefore, although the levels of IL ‐10‐producing B cells were decreased in the spleens of mice with CIA , ES ‐62 was found to restore these to the levels found in naive mice. In addition, exposure to ES ‐62 decreased effector B ‐cell, particularly plasma cell, infiltration of the joints, and such infiltrating B cells showed dramatically reduced levels of T oll‐like receptor 4 and the activation markers, CD 80 and CD 86. Collectively, this induction of hyporesponsiveness of effector B ‐cell responses, in the context of the resetting of the levels of IL ‐10‐producing B cells, is suggestive of a modulation of the balance between effector and regulatory B ‐cell responses that may contribute to ES ‐62‐mediated suppression of CIA ‐associated inflammation and inhibition of production of pathogenic collagen‐specific I g G 2a antibodies.
Materialart:
Online-Ressource
ISSN:
0019-2805
,
1365-2567
DOI:
10.1111/imm.2014.141.issue-3
Sprache:
Englisch
Verlag:
Wiley
Publikationsdatum:
2014
ZDB Id:
2006481-0
