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  • Title: CXCR3 is required for migration to dermal inflammation by normal and in vivo activated T cells: differential requirements by CD4 and CD8 memory subsets.
    Author: Mohan K, Cordeiro E, Vaci M, McMaster C, Issekutz TB.
    Journal: Eur J Immunol; 2005 Jun; 35(6):1702-11. PubMed ID: 15884054.
    Abstract:
    Lymphocytes in inflamed tissues express numerous chemokine receptors. The relative importance of these receptors for migration in inflammation is unclear. The role of CXCR3 in T cell subset migration was examined using monoclonal antibodies developed to rat CXCR3. CXCR3 was expressed on sixfold more CD8(+) ( approximately 30%) than CD4(+) ( approximately 5%) T cells in spleen, lymph nodes and blood, and on approximately 10% of CD4(+)CD45RC(-) (memory) and approximately 50% of CD8(+)CD45RC(+) spleen T cells. After immunization, CXCR3 increased tenfold on CD4(+) lymph node lymphoblasts ( approximately 55%), and >90% of inflammatory exudate T cells were CXCR3(+). CXCR3(+) T cells migrated significantly better than CXCR3(-) T cells to all dermal inflammatory stimuli tested in vivo, even though these T cells are a minority of the memory T cells. Blocking CXCR3 inhibited recruitment of 60-85% of unstimulated T cells and up to 90% of CD8(+)CD45RC(+) effector T cells, but caused <50% inhibition of CD4(+) and CD8(+) memory (CD45RC(-)) T cells. About 90% of T lymphoblast migration to IFN-gamma, IFN-gamma plus TNF-alpha, polyinosinic polycytidylic acid, lipopolysaccharide, and delayed-type hypersensitivity (DTH)-induced inflammation was inhibited. Blockade also reduced DTH-induced induration. Thus, CXCR3 has a non-redundant role in T cell migration to dermal inflammation and is critical for activated T lymphoblast recruitment, but memory T cells are less dependent on CXCR3 for their infiltration.
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