IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
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T. Mcclanahan | R. Kastelein | J. Mattson | D. Cua | Yi Chen | Daniel J. Cua | Robert A. Kastelein | C. Langrish | Yi Chen | W. Blumenschein | B. Basham | J. Sedgwick | Terrill McClanahan | Claire L. Langrish | Wendy M. Blumenschein | Jeanine Mattson | Beth Basham | Jonathan D. Sedgwick
[1] R. Kastelein,et al. IL-23 Provides a Limited Mechanism of Resistance to Acute Toxoplasmosis in the Absence of IL-121 , 2004, The Journal of Immunology.
[2] A. Amadori,et al. The IL-12Rβ2 gene functions as a tumor suppressor in human B cell malignancies , 2004 .
[3] A. Gurney,et al. Compromised Humoral and Delayed-Type Hypersensitivity Responses in IL-23-Deficient Mice1 , 2004, The Journal of Immunology.
[4] L. Joosten,et al. Treatment with a neutralizing anti-murine interleukin-17 antibody after the onset of collagen-induced arthritis reduces joint inflammation, cartilage destruction, and bone erosion. , 2004, Arthritis and rheumatism.
[5] A. Amadori,et al. The IL-12Rbeta2 gene functions as a tumor suppressor in human B cell malignancies. , 2004, The Journal of clinical investigation.
[6] T. Mcclanahan,et al. Divergent Pro- and Antiinflammatory Roles for IL-23 and IL-12 in Joint Autoimmune Inflammation , 2003, The Journal of experimental medicine.
[7] S. Nakae,et al. Suppression of Immune Induction of Collagen-Induced Arthritis in IL-17-Deficient Mice 1 , 2003, The Journal of Immunology.
[8] J. Shellito,et al. Cutting Edge: Roles of Toll-Like Receptor 4 and IL-23 in IL-17 Expression in Response to Klebsiella pneumoniae Infection1 , 2003, The Journal of Immunology.
[9] S. Nakae,et al. IL-17 production from activated T cells is required for the spontaneous development of destructive arthritis in mice deficient in IL-1 receptor antagonist , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[10] C. Dong. Inducible costimulator is essential for collagen-induced arthritis. , 2003, The Journal of clinical investigation.
[11] M. Kamoun,et al. Induction of Experimental Autoimmune Encephalomyelitis in IL-12 Receptor-β2-Deficient Mice: IL-12 Responsiveness Is Not Required in the Pathogenesis of Inflammatory Demyelination in the Central Nervous System1 , 2003, The Journal of Immunology.
[12] R. Kastelein,et al. Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brain , 2003, Nature.
[13] A. Gurney,et al. Interleukin-23 Promotes a Distinct CD4 T Cell Activation State Characterized by the Production of Interleukin-17* , 2003, The Journal of Biological Chemistry.
[14] Ruslan Medzhitov,et al. Toll Pathway-Dependent Blockade of CD4+CD25+ T Cell-Mediated Suppression by Dendritic Cells , 2003, Science.
[15] M. Kamoun,et al. IL-12p35-Deficient Mice Are Susceptible to Experimental Autoimmune Encephalomyelitis: Evidence for Redundancy in the IL-12 System in the Induction of Central Nervous System Autoimmune Demyelination1 , 2002, The Journal of Immunology.
[16] Daniel C. Douek,et al. Distinct lineages of TH1 cells have differential capacities for memory cell generation in vivo , 2002, Nature Immunology.
[17] B. Becher,et al. Experimental autoimmune encephalitis and inflammation in the absence of interleukin-12. , 2002, The Journal of clinical investigation.
[18] M. Feldmann,et al. Development of anti-TNF therapy for rheumatoid arthritis , 2002, Nature Reviews Immunology.
[19] A. Gurney,et al. IL‐17: prototype member of an emerging cytokine family , 2002, Journal of leukocyte biology.
[20] F. Brombacher,et al. A Protective and Agonistic Function of IL-12p40 in Mycobacterial Infection1 , 2001, The Journal of Immunology.
[21] C. Samuel,et al. The role of gamma interferon in antimicrobial immunity. , 2001, Current opinion in microbiology.
[22] A. O’Garra,et al. The molecular basis of T helper 1 and T helper 2 cell differentiation. , 2000, Trends in cell biology.
[23] M. Byrne,et al. Microbial Lipopeptides Induce the Production of IL-17 in Th Cells1 , 2000, The Journal of Immunology.
[24] J Wagner,et al. Novel p19 protein engages IL-12p40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12. , 2000, Immunity.
[25] W. Maśliński,et al. High Levels of IL-17 in Rheumatoid Arthritis Patients: IL-15 Triggers In Vitro IL-17 Production Via Cyclosporin A-Sensitive Mechanism1 , 2000, The Journal of Immunology.
[26] P. Kivisäkk,et al. Interleukin-17 mRNA expression in blood and CSF mononuclear cells is augmented in multiple sclerosis , 1999, Multiple sclerosis.
[27] P. Miossec,et al. IL-17 is produced by some proinflammatory Th1/Th0 cells but not by Th2 cells. , 1999, Journal of immunology.
[28] R. Simone,et al. Interferon-γ in Progression to Chronic Demyelination and Neurological Deficit Following Acute EAE , 1998, Molecular and Cellular Neuroscience.
[29] R. de Waal Malefyt,et al. Interleukin-17 and interferon-gamma synergize in the enhancement of proinflammatory cytokine production by human keratinocytes. , 1998, The Journal of investigative dermatology.
[30] W. Cowden,et al. IFN-gamma plays a critical down-regulatory role in the induction and effector phase of myelin oligodendrocyte glycoprotein-induced autoimmune encephalomyelitis. , 1996, Journal of immunology.
[31] E. Shevach,et al. IL-12 unmasks latent autoimmune disease in resistant mice , 1996, The Journal of experimental medicine.
[32] L. Steinman,et al. Mice with a disrupted IFN-gamma gene are susceptible to the induction of experimental autoimmune encephalomyelitis (EAE). , 1996, Journal of immunology.
[33] Meijuan Zhao,et al. Interferon-γ-Induced Oligodendrocyte Cell Death: Implications for the Pathogenesis of Multiple Sclerosis , 1995, Molecular medicine.
[34] J. Leonard,et al. Prevention of experimental autoimmune encephalomyelitis by antibodies against interleukin 12 , 1995, The Journal of experimental medicine.
[35] W. Hickey. Migration of Hematogenous Cells Through the Blood‐Brain Barrier and the Initiation of CNS Inflammation , 1991, Brain pathology.
[36] W. Carter,et al. Extracellular matrix receptors, ECMRII and ECMRI, for collagen and fibronectin correspond to VLA‐2 and VLA‐3 in the VLA family of heterodimers , 1988, Journal of cellular biochemistry.
[37] R. Hirsch,et al. EXACERBATIONS OF MULTIPLE SCLEROSIS IN PATIENTS TREATED WITH GAMMA INTERFERON , 1987, The Lancet.