Which interleukins are produced by t cells
Revision Received: November 21 Online Issn: J Exp Med 3 : — Article history Received:. Revision Received:. Cite Icon Cite. Altered peptide ligands can control CD4 T lymphocyte differentiation in vivo. Differential effects of B and anti-B monoclonal antibody treatment on the development of diabetes in the nonobese diabetic mouse. Production of natural killer cell stimulatory factor interleukin 12 by peripheral blood mononuclear cells. Mouse splenic and bone marrow cell populations that express high affinity Fc epsilon receptors and produce interleukin 4 are highly enriched in basophils.
Single-step method of RNA extraction by acid guanidinium thiocyanate-phenolchloroform. Memory effectors: a potent, IL-4—secreting helper T cell population that develops in vivo after restimulation with antigen.
Interleukin-6 triggers the association of its receptor with a possible signal transducer, gp Functional inhibition of hematopoietic and neurotrophic cytokines by blocking the interleukin-6 signal transducer gp Involvement of interleukin-6 signal transducer gp in interleukin—mediated signal transduction.
High and low affinity receptors for murine interleukin 6. Distinct distribution on B and T cells. Impaired immune and acute-phase responses in interleukin-6—deficient mice. Interleukin-6 deficient mice are protected from bone loss caused by estrogen depletion.
Interleukin-6— deficient mice are highly susceptible to Listeria monocytogenesinfection: correlation with inefficient neutrophilia. Search ADS. Mencacci, E. Cenci, R. Spaccapelo, C. Toniatti, P. Puccetti, F. Bistoni, and V. Transcription of interleukin-4 gene is regulated by multiple promoter elements. Characterization of nuclear and cytoplasmic components of the lymphoid-specific nuclear factor of activated T cells NF-AT.
Here we present data that challenge the idea of a shared developmental pathway with T helper type 1 T H 1 or T H 2 lineages and instead favor the idea of a distinct effector lineage we call 'T H '. Mosmann, T. Th1 and Th2 cells: Different patterns of lymphokine secretion leads to different functional properties. Bottomly, K. Today 9 , — Murphy, K. The lineage decisions of helper T cells. Robinson, D. Further checkpoints in Th1 development.
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Nature , — Murphy, C. Divergent pro- and antiinflammatory roles for IL and IL in joint autoimmune inflammation. Aggarwal, S. Interleukin promotes a distinct CD4 T cell activation state characterized by the production of interleukin Gran, B. ILpdeficient mice are susceptible to experimental autoimmune encephalomyelitis: evidence for redundancy in the IL system in the induction of central nervous system autoimmune demyelination.
Bettelli, E. IL and ILinduced T helper cell subsets: birds of the same feather flock together. Oppmann, B. J Allergy Clin Immunol — J Exp Med — Adv Exp Med Biol —9. Selective expression of a novel surface molecule by human Th2 cells in vivo. Mediators Inflamm a TGFbeta in the context of an inflammatory cytokine milieu supports de novo differentiation of ILproducing T cells. Immunity 24 — A crucial role for interleukin IL -1 in the induction of ILproducing T cells that mediate autoimmune encephalomyelitis.
J Leukoc Biol 88 — Development of chronic inflammatory arthropathy resembling rheumatoid arthritis in interleukin 1 receptor antagonist-deficient mice. Interleukin-1 drives pathogenic Th17 cells during spontaneous arthritis in interleukin-1 receptor antagonist-deficient mice.
Arthritis Rheum 58 — Enhanced Th1 and Th17 responses and arthritis severity in mice with a deficiency of myeloid cell-specific interleukin-1 receptor antagonist. Arthritis Rheum 62 — Critical regulation of early Th17 cell differentiation by interleukin-1 signaling. Immunity 30 — Phenotypic and functional features of human Th17 cells. Interleukins 1beta and 6 but not transforming growth factor-beta are essential for the differentiation of interleukin producing human T helper cells.
Nat Immunol 8 —9. TGF-beta indirectly favors the development of human Th17 cells by inhibiting Th1 cells. Eur J Immunol 39 — Regulating human Th17 cells via differential expression of IL-1 receptor. Blood b — Imbalance between interleukin-1 agonists and antagonists: relationship to severity of inflammatory bowel disease. Clin Exp Immunol —9. Cutting edge: IL-1 controls the IL response induced by gliadin, the etiologic agent in celiac disease.
An autoinflammatory disease with deficiency of the interleukinreceptor antagonist. N Engl J Med — IL-1 acts directly on CD4 T cells to enhance their antigen-driven expansion and differentiation. Distinctive features of classic and nonclassic Th17 derived human Th1 cells. Eur J Immunol 42 —8.
Arthritis Rheum 63 — Late developmental plasticity in the T helper 17 lineage. Th17 plasticity in human autoimmune arthritis is driven by the inflammatory environment. Genetic proof for the transient nature of the Th17 phenotype. Eur J Immunol 40 — Kamanaka, R.
Flavell, and A. Anderson, C. Oukka, V. Kuchroo, and D. Gazzinelli, R. Wysocka, S. Hieny, T. Scharton-Kersten, A. Cheever, R. Kuhn, W. Muller, G. Trinchieri, and A. Hunter, C. Ellis-Neyes, T. Slifer, S. Kanaly, G. Grunig, M. Fort, D. Rennick, and F. IL is required to prevent immune hyperactivity during infection with Trypanosoma cruzi.
Brooks, D. Trifilo, K. Edelmann, L. Teyton, D. McGavern, and M. Interleukin determines viral clearance or persistence in vivo. Ejrnaes, M. Filippi, M. Martinic, E. Ling, L. Togher, S. Crotty, and M. Resolution of a chronic viral infection after interleukin receptor blockade. Vicari, A. Chiodoni, C. Vaure, S. Ait-Yahia, C.
Dercamp, F. Matsos, O. Reynard, C. Taverne, P. Merle, M. Colombo, et al. Reversal of tumor-induced dendritic cell paralysis by CpG immunostimulatory oligonucleotide and anti-interleukin 10 receptor antibody. Guiducci, C. Vicari, S. Sangaletti, G. Trinchieri, and M. Redirecting in vivo elicited tumor infiltrating macrophages and dendritic cells towards tumor rejection.
Cancer Res. Roers, A. Siewe, E. Strittmatter, M. Deckert, D. Schluter, W. Stenzel, A. Gruber, T. Krieg, K. Rajewsky, and W. T cell-specific inactivation of the interleukin 10 gene in mice results in enhanced T cell responses but normal innate responses to lipopolysaccharide or skin irritation. Siewe, L.
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