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Requirement for Core 2 O-Glycans for Optimal Resistance to Helminth Infection
Author(s) -
Sarah C. Mullaly,
Menno J. Oudhoff,
HoonKi Min,
Kyle Burrows,
Frann Antignano,
David Rattray,
Alistair Chenery,
Kelly M. McNagny,
Hermann J. Ziltener,
Colby Zaph
Publication year - 2013
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0060124
Subject(s) - chemokine receptor , immunology , biology , immune system , trichuris , c c chemokine receptor type 6 , chemokine , immunity , cxc chemokine receptors , intestinal epithelium , receptor , helminths , epithelium , biochemistry , genetics
The migration of lymphocytes to the small intestine is controlled by expression of the integrin α4β7 and the chemokine receptor CCR9. However, the molecules that specifically regulate migration to the large intestine remain unclear. Immunity to infection with the large intestinal helminth parasite Trichuris muris is dependent upon CD4 + T cells that migrate to the large intestine. We examine the role of specific chemokine receptors, adhesion molecules and glycosyltransferases in the development of protective immunity to Trichuris . Mice deficient in expression of the chemokine receptors CCR2 or CCR6 were resistant to infection with Trichuris . Similarly, loss of CD34, CD43, CD44 or PSGL-1 had no effect on resistance to infection. In contrast, simultaneous deletion of the Core2 β1,6- N -acetylglucosaminyltransferase (C2GnT) enzymes C2GnT1 and C2Gnt2 resulted in delayed expulsion of worms. These results suggest that C2GnT-dependent modifications may play a role in migration of protective immune cells to the large intestine.

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