{"database":"biostudies-other","file_versions":[],"scores":null,"additional":{"submitter":["Odegard JM"],"funding":["Howard Hughes Medical Institute","NIAMS NIH HHS"],"pagination":["2873-86"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2585848"],"abstract":["The role of specialized follicular helper T (T(FH)) cells in the germinal center has become well recognized, but it is less clear how effector T cells govern the extrafollicular response, the dominant pathway of high-affinity, isotype-switched autoantibody production in the MRL/MpJ-Fas(lpr) (MRL(lpr)) mouse model of lupus. MRL(lpr) mice lacking the Icos gene have impaired extrafollicular differentiation of immunoglobulin (Ig) G(+) plasma cells accompanied by defects in CXC chemokine receptor (CXCR) 4 expression, interleukin (IL) 21 secretion, and B cell helper function in CD4 T cells. These phenotypes reflect the selective loss of a population of T cells marked by down-regulation of P-selectin glycoprotein ligand 1 (PSGL-1; also known as CD162). PSGL-1(lo) T cells from MRL(lpr) mice express CXCR4, localize to extrafollicular sites, and uniquely mediate IgG production through IL-21 and CD40L. In other autoimmune strains, PSGL-1(lo) T cells are also abundant but may exhibit either a follicular or extrafollicular phenotype. Our findings define an anatomically distinct extrafollicular population of cells that regulates plasma cell differentiation in chronic autoimmunity, indicating that specialized humoral effector T cells akin to T(FH) cells can occur outside the follicle."],"repository":["biostudies-other"],"data_source":["Europe PMC"],"omics_type":["Unknown"],"volume":["205(12)"],"journal":["The Journal of experimental medicine"],"pmcid":["PMC2585848"],"funding_grant_id":["R01 AR040072","R01 AR044076","AR44076","R37 AR040072","AR40072"],"pubmed_authors":["Kono DH","Marks BR","Flavell RA","Craft J","DiPlacido LD","Dong C","Odegard JM","Poholek AC"],"additional_accession":[]},"is_claimable":false,"name":"ICOS-dependent extrafollicular helper T cells elicit IgG production via IL-21 in systemic autoimmunity.","description":"The role of specialized follicular helper T (T(FH)) cells in the germinal center has become well recognized, but it is less clear how effector T cells govern the extrafollicular response, the dominant pathway of high-affinity, isotype-switched autoantibody production in the MRL/MpJ-Fas(lpr) (MRL(lpr)) mouse model of lupus. MRL(lpr) mice lacking the Icos gene have impaired extrafollicular differentiation of immunoglobulin (Ig) G(+) plasma cells accompanied by defects in CXC chemokine receptor (CXCR) 4 expression, interleukin (IL) 21 secretion, and B cell helper function in CD4 T cells. These phenotypes reflect the selective loss of a population of T cells marked by down-regulation of P-selectin glycoprotein ligand 1 (PSGL-1; also known as CD162). PSGL-1(lo) T cells from MRL(lpr) mice express CXCR4, localize to extrafollicular sites, and uniquely mediate IgG production through IL-21 and CD40L. In other autoimmune strains, PSGL-1(lo) T cells are also abundant but may exhibit either a follicular or extrafollicular phenotype. Our findings define an anatomically distinct extrafollicular population of cells that regulates plasma cell differentiation in chronic autoimmunity, indicating that specialized humoral effector T cells akin to T(FH) cells can occur outside the follicle.","dates":{"release":"2008-01-01T00:00:00Z","publication":"2008 Nov","modification":"2019-03-27T00:19:27Z","creation":"2019-03-27T00:19:27Z"},"accession":"S-EPMC2585848","cross_references":{"pubmed":["18981236"],"doi":["10.1084/jem.20080840 "]}}