title: CXCR6 identifies a putative population of retained human lung T cells characterised by co-expression of activation markers.
abstract: Expressions of activation markers have been described on the surface of T cells in the blood and the lung in both health and disease. We have studied the distribution of activation markers on human lung T cells and have found that only certain populations exist. Importantly, the presence or absence of some markers appears to predict those of others, in particular cells which express CD103 also express CD49a and CD69, whereas cells which do not express CD69 also do not express CD49a or CD103. In view of the paucity of activation marker expression in the peripheral blood, we have hypothesised that these CD69+, CD49a+, and CD103+ (triple positive) cells are retained in the lung, possess effector function (IFNgamma secretion) and express particular chemokine receptors which allow them to be maintained in this environment. We have found that the ability of the triple negative cells to secrete IFNgamma is significantly less than the triple positive cells, suggesting that the expression of activation markers can highlight a highly specialised effector cell. We have studied the expression of 14 chemokine receptors and have found that the most striking difference between the triple negative cells and the triple positive cells is the expression of CXCR6 with 12.8+/-9.8% of triple negative cells expressing CXCR6 compared to 89.5+/-5.5% of triple positive cells. We propose therefore that CXCR6 may play an important role in the retention of T cells within the lung.
authors.affiliation: Department of Infection, Immunity and Inflammation, Institute for Lung Health, Leicester University, Glenfield Hospital, Groby Road, Leicester LE3 9QP, UK.
authors.forename: Angela J
authors.initials: AJ
authors.lastname: Morgan
authors.forename: Cristina
authors.initials: C
authors.lastname: Guillen
authors.forename: Fiona A
authors.initials: FA
authors.lastname: Symon
authors.forename: Surinder S
authors.initials: SS
authors.lastname: Birring
authors.forename: James J
authors.initials: JJ
authors.lastname: Campbell
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Wardlaw
mesh_terms: D015703:Antigens, CD / Q000276:immunology / Q000378:metabolism*; D000945:Antigens, Differentiation, T-Lymphocyte / Q000276:immunology / Q000378:metabolism*; D015415:Biomarkers / Q000378:metabolism; D006801:Humans; D039001:Integrin alpha Chains / Q000276:immunology / Q000378:metabolism*; D039423:Integrin alpha1 / Q000276:immunology / Q000378:metabolism*; D007371:Interferon-gamma / Q000096:biosynthesis* / Q000276:immunology; D037181:Lectins, C-Type; D008168:Lung / Q000276:immunology* / Q000378:metabolism; D008213:Lymphocyte Activation; D000075744:Receptors, CXCR6; D019707:Receptors, Chemokine / Q000276:immunology / Q000378:metabolism*; D011991:Receptors, Virus / Q000276:immunology / Q000378:metabolism*; D013601:T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D015415:Biomarkers; D039001:Integrin alpha Chains; D039423:Integrin alpha1; D007371:Interferon-gamma; D037181:Lectins, C-Type; D000075744:Receptors, CXCR6; D019707:Receptors, Chemokine; D011991:Receptors, Virus; D000099192:CD69 Antigens; C106330:CXCR6 protein, human; C091367:alpha E integrins