SOCS-1/SSI-1-deficient NKT cells participate in severe hepatitis through dysregulated cross-talk inhibition of IFN-γ and IL-4 signaling in vivo

Immunity

Volumn 14, Issue 5, 2001, Pages 535-545

  Naka, Tetsuji ^a   Tsutsui, Hiroko ^c   Fujimoto, Minoru ^a   Kawazoe, Yoshinori ^a   Kohzaki, Hidetsugu ^a   Morita, Yoshiaki ^a   Nakagawa, Reiko ^b   Narazaki, Masashi ^a   Adachi, Keishi ^c   Yoshimoto, Tomohiro ^c   Nakanishi, Kenji ^c   Kishimoto, Tadamitsu ^d  

^a OSAKA UNIVERSITY MEDICAL SCHOOL   (Japan)

^b OSAKA UNIVERSITY GRADUATE SCHOOL OF MEDICINE   (Japan)

^c HYOGO COLLEGE OF MEDICINE   (Japan)

^d OSAKA UNIVERSITY   (Japan)

Author keywords

[No Author keywords available]

Indexed keywords

CYTOKINE; GAMMA INTERFERON; INTERLEUKIN 4; STAT1 PROTEIN; STAT6 PROTEIN;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL ACTIVATION; CONTROLLED STUDY; GENE DELETION; HEPATITIS; IN VIVO STUDY; INHIBITION KINETICS; MOUSE; NATURAL KILLER CELL; NEGATIVE FEEDBACK; NONHUMAN; PRIORITY JOURNAL; PROTEIN DEFICIENCY; SIGNAL TRANSDUCTION;

EID: 0035008978     PISSN: 10747613     EISSN: None     Source Type: Journal    
DOI: 10.1016/S1074-7613(01)00132-7     Document Type: Article

References (50)

1. Growth hormone preferentially induces the rapid, transient expression of SOCS-3, a novel inhibitor of cytokine receptor signaling
2. SOCS1 is critical inhibitor of interferon γ signaling and prevents the potentially fatal neonatal actions of this cytokine
3. + T cells produce large amounts of IL-4 and IFN-γ upon activation by anti-CD3 or CD1
4. SOCS proteins, regulators of intracellular signaling
5. Jak-STAT pathways and transcriptional activation in response to IFNs and other extracellular signaling protein
6. Interferons inhibit activation of STAT6 by interleukin 4 in human monocytes by inducing SOCS-1 gene expression
7. A new protein containing an SH2 domain that inhibits JAK kinases
8. Constitutive expression of interleukin (IL)-4 in vivo causes autoimmune-type disorders in mice
9. Defective thymocyte development and perturbed homeostasis of T cells in SOCS-1/SOCS-1 transgenic mice
10. Mechanism of inhibition of growth hormone receptor signaling by suppressor of cytokine signaling proteins
11. Cytokine-inducible SH2 protein (CIS3) and binding protein (JAB) abolish prolactin receptor-mediated STAT5 signaling
12. Cytokine receptor signaling
13. Augmentation of Vα14 NKT cell-mediated cytotoxicity by interleukin 4 in an autocrine mechanism resulting in the development of concanavalin A-induced hepatitis
14. + T cells in IL-12-induced immune responses in vivo
15. Signal transducer and activator of transcription (STAT)-induced STAT inhibitor 1 (SSI-1)/suppressor of cytokine signaling 1 (SOCS1) inhibits insulin signal transduction pathway through modulating insulin receptor substrate 1 (IRS-1) phosphorylation
16. Cytokine signal transduction
17. Socs: Physiological suppressors of cytokine signaling
18. Interleukin 4 expressed in situ selectively alters thymocyte development
19. Phenotypical analysis and cytokine release of liver infiltrating and peripheral blood T lymphocytes from patient with chronic hepatitis of different etiology
20. SOCS-1 is a potent inhibitor of IL-4 signal transduction
21. SOCS1 deficiency causes a lymphocytes-dependent perinatal lethality
22. Targeted disruption of the STAT1 gene in mice reveals unexpected physiologic specificity in the JAK-STAT signaling pathway
23. Signals transducers and activators of transcription (STAT)-induced STAT inhibitor-1 (SSI-1)/suppressor of cytokine signaling-1 (SOCS-1) suppresses tumor necrosis factor a-induced cell death in fibroblasts
24. Structure and function of a new STAT-induced STAT inhibitor
25. Accelerated apoptosis of lymphocytes by augmented induction of Bax in SSI (STAT-induced STAT inhibitor-1) deficient mice
26. Negative regulation of cytokine signaling: STAT-induced STAT inhibitor
27. Three distinct domains of SOCS-1/SOCS-1/JAB protein are required for its suppression of interleukin 6 signaling
28. Mutational analyses of the SOCS proteins suggest a dual domain requirement but distinct mechanisms for inhibition of LIF and IL-6 signal transduction
29. The suppressors of cytokine signaling (SOCS) proteins: Important feedback inhibitor of cytokine action
30. Inhibition and restoration of prolactin signal transduction by suppressors of cytokine signaling
31. SOCS/CIS protein inhibition of growth hormone-stimulated STAT5 signaling by multiple mechanism
32. A janus kinase inhibitor, JAB, is an interferon-gamma-inducible gene and confers resistance to interferons
33. The suppressor of cytokine signaling (SOCS) 1 and SOCS 3 but not SOCS 2 proteins inhibit interferon-mediated antiviral and antiproliferative activities
34. CD1-reactive natural killer T cells are required for development of systemic tolerance through an immune-privileged site
35. A family of cytokine-inducible inhibitors of signaling
36. Liver degeneration and lymphoid deficiencies in mice lacking suppressor of cytokine signaling-1
37. Inhibition of the Janus kinase-signal transducers and activators of transcription (JAK/STAT) signaling pathway
38. -/- mice
39. Essential role of STAT6 in IL-4 signaling
40. IL-4 induces allergic-like inflammatory disease and alters T cell development in transgenic mice
41. A T cell-dependent experimental liver injury in mice inducible by concanavalin A
42. SOCS-1, -2, -3: Selective targets and functions downstream of the prolactin receptor
43. + T cells for concanavalin A-induced hepatic injury in mice
44. Chronic active hepatitis in transgenic mice expressing interferon-γ in the liver
45. Importance of direct hepatocytolysis by liver macrophages in experimental fulminant hepatitis
46. Repression of IL-4-induced gene expression by IFN-γ requires Stat1 activation
47. The JAK-binding protein JAB inhibits Janus tyrosine kinase activity through binding in the activation loop
48. Negative regulation of cytokine signaling pathways
49. Bone marrow and thymus expression of interferon-γ results in severe B-cell lingeage reduction, T-cell lineage alterations, and hematopoietic progenitor deficiencies