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Leucocyte recruitment during enteric nematode infection
Author(s) -
McDermott Jacqueline R.,
Grencis Richard K.,
Else Kathryn J.
Publication year - 2001
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2001.01260.x
Subject(s) - biology , nematode , enteric virus , enteric fever , microbiology and biotechnology , nematode infection , enteric bacteria , enteric nervous system , immunology , ecology , typhoid fever , genetics , neuroscience , escherichia coli , gene
Summary Resolution of infection with the intestinal nematode Trichinella spiralis depends on the host mounting a T helper 2 (Th2) response. It is known that both mast cells and T cells play a crucial role. We have previously shown that efficient migration of mast cells to the gut during infection depends on their expression of the integrin β7. β7 forms a heterodimer complex with either αE or α4 integrin chains, αEβ7 binding to E‐cadherin expressed by epithelial cells and α4β7 binding to mucosal addressin cell adhesion molecule (MAdCAM‐1) on the endothelium. We were interested to know whether dysfunctional mast cell localization to the gut in the absence of β7 was due to the failure of α4β7 to bind to MAdCAM‐1 or the failure of αEβ7 to bind to E‐cadherin. We used blocking monoclonal antibodies against αE (M290) or α4 (PS2) or β7 (HB293) during T. spiralis infection of C57BL/6 mice and found that all antibody treatments reduced mastocytosis. In contrast, none of the antibody treatments prevented the migration of CD3 + T cells into the intestine. These results indicate that during inflammation (a) there is integrin redundancy for lymphocytes but not for mast cells and (b) both αEβ7 and α4β7 are crucial either for the entry of mast cells into the gut or for their maturation once they have entered.