PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22933628-0 2012 Monocytes from Irf5-/- mice have an intrinsic defect in their response to pristane-induced lupus. pristane 74-82 interferon regulatory factor 5 Mus musculus 15-19 22933628-4 2012 In the present study, we examined the mechanisms by which loss of Irf5 protects mice from pristane-induced lupus at early time points of disease development. pristane 90-98 interferon regulatory factor 5 Mus musculus 66-70 22933628-6 2012 Chemotaxis assays using peritoneal lavage from pristane-injected Irf5(+/+) and Irf5(-/-) littermates support an intrinsic defect in Irf5(-/-) monocytes. pristane 47-55 interferon regulatory factor 5 Mus musculus 65-69 22678902-0 2012 Irf5-deficient mice are protected from pristane-induced lupus via increased Th2 cytokines and altered IgG class switching. pristane 39-47 interferon regulatory factor 5 Mus musculus 0-4 22678902-3 2012 Here, we demonstrate that IRF5 is required for pristane-induced SLE via its ability to control multiple facets of autoimmunity. pristane 47-55 interferon regulatory factor 5 Mus musculus 26-30 22422888-2 2012 In this study, we examined the role of IRF5 in the pathogenesis of pristane-induced lupus in mice. pristane 67-75 interferon regulatory factor 5 Mus musculus 39-43 22422888-3 2012 The pathological response to pristane in IRF5(-/-) mice shared many features with type I IFN receptor (IFNAR)(-/-) and TLR7(-/-) mice: production of anti-Sm/RNP autoantibodies, glomerulonephritis, generation of Ly6C(hi) monocytes, and IFN-I production all were greatly attenuated. pristane 29-37 interferon regulatory factor 5 Mus musculus 41-45 22422888-4 2012 Lymphocyte activation following pristane injection was greatly diminished in IRF5(-/-) mice, and Th cell differentiation was deviated from Th1 in wild-type mice toward Th2 in IRF5(-/-) mice. pristane 32-40 interferon regulatory factor 5 Mus musculus 77-81 22933628-8 2012 Bone marrow reconstitution experiments further supported an intrinsic defect in Irf5(-/-) monocytes because Irf5(+/+) monocytes were preferentially recruited to the peritoneal cavity in response to pristane. pristane 198-206 interferon regulatory factor 5 Mus musculus 108-112 22933628-9 2012 Taken together, these findings demonstrate an intrinsic role for IRF5 in the response of monocytes to pristane and their recruitment to the primary site of inflammation that is thought to trigger lupus onset in this experimental model of SLE. pristane 102-110 interferon regulatory factor 5 Mus musculus 65-69 22422888-9 2012 Collectively, these data indicate that altered production of IFN-I and other cytokines in IRF5(-/-) mice prevents pristane from inducing lupus pathology by broadly affecting T and B lymphocyte activation/differentiation. pristane 114-122 interferon regulatory factor 5 Mus musculus 90-94