CD4+ T-cell localization to the large intestinal mucosa during Trichuris muris infection is mediated by G alpha i-coupled receptors but is CCR6- and CXCR3-independent.

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  • Author(s): Svensson M;Svensson M; Russell K; Mack M; Else KJ
  • Source:
    Immunology [Immunology] 2010 Feb; Vol. 129 (2), pp. 257-67. Date of Electronic Publication: 2009 Sep 09.
  • Publication Type:
    Journal Article; Research Support, Non-U.S. Gov't
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Blackwell Scientific Publications Country of Publication: England NLM ID: 0374672 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1365-2567 (Electronic) Linking ISSN: 00192805 NLM ISO Abbreviation: Immunology Subsets: MEDLINE
    • Publication Information:
      Original Publication: Oxford : Blackwell Scientific Publications
    • Subject Terms:
      Immunity, Mucosal*/drug effects; CD4-Positive T-Lymphocytes/*metabolism ; GTP-Binding Protein alpha Subunits/*metabolism ; Intestinal Mucosa/*metabolism ; Trichuriasis/*immunology ; Trichuris/*immunology; Adoptive Transfer ; Animals ; Antibodies, Blocking/immunology ; CD4-Positive T-Lymphocytes/drug effects ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/parasitology ; CD4-Positive T-Lymphocytes/pathology ; Cell Movement/drug effects ; Cell Movement/immunology ; Cells, Cultured ; GTP-Binding Protein alpha Subunits/immunology ; Intestinal Mucosa/pathology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, SCID ; Pertussis Toxin/pharmacology ; Receptors, CCR6/metabolism ; Receptors, CXCR3/metabolism ; Trichuriasis/pathology ; Trichuris/pathogenicity
    • Abstract:
      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 G alpha(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.
    • References:
      J Clin Invest. 2002 Oct;110(8):1113-21. (PMID: 12393847)
      J Exp Med. 2003 Sep 15;198(6):963-9. (PMID: 12963696)
      Endocrinology. 2008 Nov;149(11):5747-57. (PMID: 18653719)
      Parasitology. 1967 Aug;57(3):515-24. (PMID: 6048569)
      J Immunol. 1994 Apr 1;152(7):3282-93. (PMID: 7511642)
      J Immunol. 2004 Sep 15;173(6):3668-75. (PMID: 15356112)
      J Exp Med. 2002 Jan 7;195(1):135-41. (PMID: 11781372)
      J Immunol. 1991 Jul 1;147(1):306-11. (PMID: 1675654)
      Immunology. 2009 Feb;126(2):246-55. (PMID: 18624733)
      Microcirculation. 2007 Sep-Oct;14(7):753-66. (PMID: 17885999)
      J Exp Med. 2000 Sep 4;192(5):761-8. (PMID: 10974041)
      Science. 2005 Jun 3;308(5727):1463-5. (PMID: 15933199)
      Parasite Immunol. 1995 Mar;17(3):161-5. (PMID: 7792100)
      J Exp Med. 1999 May 17;189(10):1631-8. (PMID: 10330442)
      Parasitology. 1954 May;44(1-2):50-7. (PMID: 13166371)
      Blood. 2006 May 1;107(9):3447-54. (PMID: 16391017)
      Parasitology. 2000 Dec;121 Pt 6:631-7. (PMID: 11155934)
      Prog Biophys Mol Biol. 2003 Oct;83(2):101-30. (PMID: 12865075)
      Parasitology. 1990 Aug;101 Pt 1:61-7. (PMID: 2235076)
      J Immunol. 2005 Nov 15;175(10):6713-22. (PMID: 16272327)
      Adv Parasitol. 2004;57:255-307. (PMID: 15504540)
      J Immunol. 2001 Apr 1;166(7):4697-704. (PMID: 11254730)
      J Hepatol. 2009 Sep;51(3):510-9. (PMID: 19608294)
      Science. 1996 Apr 5;272(5258):60-6. (PMID: 8600538)
      Parasite Immunol. 2008 Mar;30(3):163-70. (PMID: 18251970)
    • Grant Information:
      081120 United Kingdom Wellcome Trust
    • Accession Number:
      0 (Antibodies, Blocking)
      0 (CCR6 protein, mouse)
      0 (Cxcr3 protein, mouse)
      0 (GTP-Binding Protein alpha Subunits)
      0 (Receptors, CCR6)
      0 (Receptors, CXCR3)
      EC 2.4.2.31 (Pertussis Toxin)
    • Publication Date:
      Date Created: 20091015 Date Completed: 20100818 Latest Revision: 20211020
    • Publication Date:
      20231215
    • Accession Number:
      PMC2814467
    • Accession Number:
      10.1111/j.1365-2567.2009.03178.x
    • Accession Number:
      19824922