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CD4 + T‐cell localization to the large intestinal mucosa during Trichuris muris infection is mediated by Gα i ‐coupled receptors but is CCR6‐ and CXCR3‐independent
Author(s) -
Svensson Marcus,
Russell Karen,
Mack Matthias,
Else Kathryn J.
Publication year - 2010
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2009.03178.x
Subject(s) - cxcr3 , biology , c c chemokine receptor type 6 , immunology , chemokine receptor , intestinal mucosa , t cell , immune system , receptor , chemokine , medicine , biochemistry
Summary Infection of mice with the gastrointestinal nematode Trichuris muris represents a valuable tool to investigate and dissect intestinal immune responses. Resistant mouse strains respond to T. muris infection by mounting a T helper type 2 response. Previous results have shown that CD4 + T cells play a critical role in protective immunity, and that CD4 + T cells localize to the infected large intestinal mucosa to confer protection. Further, transfer of CD4 + T cells from immune mice to immunodeficient SCID mice can prevent the development of a chronic infection. In the current study, we characterize the protective CD4 + T cells, describe their chemokine receptor expression and explore the functional significance of these receptors in recruitment to the large intestinal mucosa post‐ T. muris infection. We show that the ability to mediate expulsion resides within a subpopulation of CD4 + T cells marked by down‐regulation of CD62L. These cells can be isolated from intestine‐draining mesenteric lymph nodes (MLN) from day 14 post‐infection, but are rare or absent in MLN before this and in spleen at all times post‐infection. Among CD4 + CD62L low MLN cells, the two most abundantly expressed chemokine receptors were CCR6 and CXCR3. We demonstrate for the first time that CD4 + CD62L low T‐cell migration to the large intestinal mucosa is dependent on the family of Gα i ‐coupled receptors, to which chemokine receptors belong. CCR6 and CXCR3 were however dispensable for this process because neutralization of CCR6 and CXCR3 did not prevent CD4 + CD62L low cell migration to the large intestinal mucosa during T. muris infection.