Takashi Kobayashi

Summary

Affiliation: Kyushu University
Country: Japan

Publications

  1. pmc TRAF6 is required for generation of the B-1a B cell compartment as well as T cell-dependent and -independent humoral immune responses
    Takashi Kobayashi
    Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
    PLoS ONE 4:e4736. 2009
  2. ncbi request reprint An RNA-binding protein alphaCP-1 is involved in the STAT3-mediated suppression of NF-kappaB transcriptional activity
    Hitomi Nishinakamura
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
    Int Immunol 19:609-19. 2007
  3. ncbi request reprint Loss of suppressor of cytokine signaling 1 in helper T cells leads to defective Th17 differentiation by enhancing antagonistic effects of IFN-gamma on STAT3 and Smads
    Kentaro Tanaka
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Higashi ku, Fukuoka 812 8582, Japan
    J Immunol 180:3746-56. 2008
  4. ncbi request reprint Prostaglandin E2 is a major soluble factor produced by stromal cells for preventing inflammatory cytokine production from dendritic cells
    Hiroshi Shiraishi
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
    Int Immunol 20:1219-29. 2008
  5. doi request reprint Suppressor of cytokine signaling 1 protects mice against concanavalin A-induced hepatitis by inhibiting apoptosis
    Takehiro Torisu
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
    Hepatology 47:1644-54. 2008
  6. pmc IFNgamma-dependent, spontaneous development of colorectal carcinomas in SOCS1-deficient mice
    Toshikatsu Hanada
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812 8582, Japan
    J Exp Med 203:1391-7. 2006
  7. pmc FLN29 deficiency reveals its negative regulatory role in the Toll-like receptor (TLR) and retinoic acid-inducible gene I (RIG-I)-like helicase signaling pathway
    Takahito Sanada
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812 8582, Japan
    J Biol Chem 283:33858-64. 2008
  8. ncbi request reprint Foxp3 inhibits RORgammat-mediated IL-17A mRNA transcription through direct interaction with RORgammat
    Kenji Ichiyama
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
    J Biol Chem 283:17003-8. 2008
  9. ncbi request reprint Selective expansion of foxp3-positive regulatory T cells and immunosuppression by suppressors of cytokine signaling 3-deficient dendritic cells
    Yumiko Matsumura
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
    J Immunol 179:2170-9. 2007
  10. pmc TRAF6 and MEKK1 play a pivotal role in the RIG-I-like helicase antiviral pathway
    Ryoko Yoshida
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812 8582, Japan
    J Biol Chem 283:36211-20. 2008

Collaborators

Detail Information

Publications36

  1. pmc TRAF6 is required for generation of the B-1a B cell compartment as well as T cell-dependent and -independent humoral immune responses
    Takashi Kobayashi
    Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
    PLoS ONE 4:e4736. 2009
    ..These results reveal critical roles for TRAF6 in TD and TI humoral immune responses and in inductive fate decisions necessary to generate the B-1 B cell compartment...
  2. ncbi request reprint An RNA-binding protein alphaCP-1 is involved in the STAT3-mediated suppression of NF-kappaB transcriptional activity
    Hitomi Nishinakamura
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
    Int Immunol 19:609-19. 2007
    ..7 cells, while small interfering RNA against alphaCP-1 reduced it. These data suggest that alphaCP-1 is involved in the STAT3-mediated suppression of NF-kappaB activity...
  3. ncbi request reprint Loss of suppressor of cytokine signaling 1 in helper T cells leads to defective Th17 differentiation by enhancing antagonistic effects of IFN-gamma on STAT3 and Smads
    Kentaro Tanaka
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Higashi ku, Fukuoka 812 8582, Japan
    J Immunol 180:3746-56. 2008
    ..SOCS1-deficient T cells will be very useful to investigate the molecular mechanism for the STAT1-mediated suppression of Th17 development...
  4. ncbi request reprint Prostaglandin E2 is a major soluble factor produced by stromal cells for preventing inflammatory cytokine production from dendritic cells
    Hiroshi Shiraishi
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
    Int Immunol 20:1219-29. 2008
    ....
  5. doi request reprint Suppressor of cytokine signaling 1 protects mice against concanavalin A-induced hepatitis by inhibiting apoptosis
    Takehiro Torisu
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
    Hepatology 47:1644-54. 2008
    ..Conclusion: These findings indicate that SOCS1 plays important negative roles in fulminant hepatitis and that forced expression of SOCS1 is therapeutic in preventing hepatitis...
  6. pmc IFNgamma-dependent, spontaneous development of colorectal carcinomas in SOCS1-deficient mice
    Toshikatsu Hanada
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812 8582, Japan
    J Exp Med 203:1391-7. 2006
    ..These data strongly suggest that SOCS1 is a unique antioncogene which prevents chronic inflammation-mediated carcinogenesis by regulation of the IFNgamma/STAT1 pathways...
  7. pmc FLN29 deficiency reveals its negative regulatory role in the Toll-like receptor (TLR) and retinoic acid-inducible gene I (RIG-I)-like helicase signaling pathway
    Takahito Sanada
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812 8582, Japan
    J Biol Chem 283:33858-64. 2008
    ....
  8. ncbi request reprint Foxp3 inhibits RORgammat-mediated IL-17A mRNA transcription through direct interaction with RORgammat
    Kenji Ichiyama
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
    J Biol Chem 283:17003-8. 2008
    ..We propose that induction of Foxp3 is the mechanism for the suppression of Th17 and polarization into inducible Treg...
  9. ncbi request reprint Selective expansion of foxp3-positive regulatory T cells and immunosuppression by suppressors of cytokine signaling 3-deficient dendritic cells
    Yumiko Matsumura
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
    J Immunol 179:2170-9. 2007
    ..These results indicate an important role of SOCS3 in determining on immunity or tolerance by DCs...
  10. pmc TRAF6 and MEKK1 play a pivotal role in the RIG-I-like helicase antiviral pathway
    Ryoko Yoshida
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812 8582, Japan
    J Biol Chem 283:36211-20. 2008
    ..These data suggest that IPS-1 requires TRAF6 and MEKK1 to activate NF-kappaB and mitogen-activated protein kinases that are critical for the optimal induction of type I interferons...
  11. pmc STAT6 Inhibits TGF-beta1-mediated Foxp3 induction through direct binding to the Foxp3 promoter, which is reverted by retinoic acid receptor
    Hiromi Takaki
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582
    J Biol Chem 283:14955-62. 2008
    ..We propose that antagonistic agents for neutralizing IL-4 could be a novel strategy to facilitate inducible Treg cell generation and the promotion of tolerance in Th2-dominated diseases such as allergy...
  12. doi request reprint Cyclic adenosine monophosphate suppresses the transcription of proinflammatory cytokines via the phosphorylated c-Fos protein
    Keiko Koga
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
    Immunity 30:372-83. 2009
    ..Multiple sites of c-Fos were phosphorylated by the IKKbeta protein. Thus, we propose that c-Fos is a substrate of IKKbeta and is responsible for the immunosuppressive effect of cAMP...
  13. doi request reprint A major lipid raft protein raftlin modulates T cell receptor signaling and enhances th17-mediated autoimmune responses
    Kazuko Saeki
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
    J Immunol 182:5929-37. 2009
    ..These data indicate that Raftlin modulates TCR signals and is necessary for the fine-tuning of T cell-mediated immune responses...
  14. ncbi request reprint Ifi202, an IFN-inducible candidate gene for lupus susceptibility in NZB/W F1 mice, is a positive regulator for NF-kappaB activation in dendritic cells
    Moriyasu Yamauchi
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
    Int Immunol 19:935-42. 2007
    ..In addition, forced expression of Ifi202 enhanced IL-12p40 mRNA induction in NZW BMDCs. Thus, Ifi202 is an important NF-kappaB activator in DCs and involved in IL-12 production, which may account for a T(h)1-prone phenotype of BWF1 mice...
  15. ncbi request reprint Silencing of SOCS1 in macrophages suppresses tumor development by enhancing antitumor inflammation
    Masayuki Hashimoto
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
    Cancer Sci 100:730-6. 2009
    ..These results suggest that inflammation induced by SOCS1-deficiency in monocytes potentiates antitumor immune responses rather than tumor-promoting inflammation...
  16. ncbi request reprint A novel Zinc finger protein, ZCCHC11, interacts with TIFA and modulates TLR signaling
    Yasumasa Minoda
    Division of Molecular and Cellular Immunology, The Medical Institute of Bioregulation, Kyushu University, Maidashi, Higashi, Fukuoka 812 8582, Japan
    Biochem Biophys Res Commun 344:1023-30. 2006
    ..We propose that ZCCHC11 is a unique TLR signal regulator, which interacts with TIFA after LPS treatment and suppresses the TRAF6-dependent activation of NF-kappaB...
  17. ncbi request reprint Adaptor protein SH2-B linking receptor-tyrosine kinase and Akt promotes adipocyte differentiation by regulating peroxisome proliferator-activated receptor gamma messenger ribonucleic acid levels
    Daigo Yoshiga
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Fukuoka 812 8582, Japan
    Mol Endocrinol 21:1120-31. 2007
    ..These data indicate that SH2-B is a key regulator of adipogenesis both in vivo and in vitro by regulating the insulin/IGF-I receptor-Akt-Foxo1-PPARgamma pathway...
  18. ncbi request reprint FLN29, a novel interferon- and LPS-inducible gene acting as a negative regulator of toll-like receptor signaling
    Ryuichi Mashima
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Maidashi, Higashi ku, Fukuoka 812 8582, Japan
    J Biol Chem 280:41289-97. 2005
    ..Taken together, FLN29 is a new negative feedback regulator of TLR signaling...
  19. ncbi request reprint Suppression of SOCS3 expression in the pancreatic beta-cell leads to resistance to type 1 diabetes
    Hiroyuki Mori
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
    Biochem Biophys Res Commun 359:952-8. 2007
    ..These results suggest that enhanced STAT3 signaling protects beta-cells from destruction induced by a genotoxic stress and that STAT3/SOCS3 can be a potential therapeutic target for the treatment of type 1 diabetes...
  20. ncbi request reprint TGF-beta1 suppresses IFN-gamma-induced NO production in macrophages by suppressing STAT1 activation and accelerating iNOS protein degradation
    Hiromi Takaki
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Fukuoka 812 8582, Japan
    Genes Cells 11:871-82. 2006
    ..e. suppression of IFN-gamma-induced STAT1 activation by an association of the IFNGR1 with the TGF-betaRI...
  21. ncbi request reprint Suppressor of cytokine signaling-1 regulates inflammatory bowel disease in which both IFNgamma and IL-4 are involved
    Takatoshi Chinen
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
    Gastroenterology 130:373-88. 2006
    ..However, the role of SOCS1 in inflammatory bowel diseases (IBDs) has not been clarified. To determine the role of SOCS1 in colitis, we generated SOCS1/T-cell receptor alpha (TCRalpha) double knockout (DKO) mice...
  22. ncbi request reprint Deletion of the SOCS3 gene in liver parenchymal cells promotes hepatitis-induced hepatocarcinogenesis
    Hisanobu Ogata
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Graduate School of Medical Science, Kyushu University, Higashiku, Fukuoka, Japan
    Gastroenterology 131:179-93. 2006
    ..We investigated the effect of deleting the SOCS3 gene on the development of hepatitis and HCC in hepatitis C virus-infected patients and mouse models...
  23. ncbi request reprint Loss of SOCS3 gene expression converts STAT3 function from anti-apoptotic to pro-apoptotic
    Yang Lu
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
    J Biol Chem 281:36683-90. 2006
    ..These data suggest that prolonged activation of STAT3 could induce apoptosis/growth arrest rather than anti-apoptosis and proliferation in certain cases, and SOCS3 is a critical regulator of this balance...
  24. ncbi request reprint The dual function of hepatic SOCS3 in insulin resistance in vivo
    Takehiro Torisu
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, University of Kyushu, Maidashi 3 1 1, Fukuoka 812 8582, Japan
    Genes Cells 12:143-54. 2007
    ..We conclude that hepatic SOCS3 is a mediator of insulin resistance in the liver; however, lack of SOCS3 in the liver promotes systemic insulin resistance by mimicking chronic inflammation...
  25. pmc Involvement of Th17 cells and the effect of anti-IL-6 therapy in autoimmune uveitis
    Takeru Yoshimura
    Department of Ophthalmology, Graduate School of Medical Science, Kyushu University, Fukuoka, Japan
    Rheumatology (Oxford) 48:347-54. 2009
    ..We initially confirmed the significant increase of several inflammatory soluble factors including IL-6 in the vitreous fluids from refractory/chronic engogenous uveitis patients...
  26. ncbi request reprint HTLV-1 Tax-mediated TAK1 activation involves TAB2 adapter protein
    Qingsheng Yu
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka, Fukuoka 812 8582, Japan
    Biochem Biophys Res Commun 365:189-94. 2008
    ..These results suggest that TAB2 may be critically involved in Tax-mediated activation of TAK1 and that NF-kappaB-activating TRAF family proteins are potential cellular E3 ubiquitin ligases toward Tax...
  27. doi request reprint Aberrant IL-4 production by SOCS3-over-expressing T cells during infection with Leishmania major exacerbates disease manifestations
    Mako Nakaya
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812 8582, Japan
    Int Immunol 23:195-202. 2011
    ..These data suggest that tight regulation of SOCS3 expression in T(h) cells is crucial for disease control during infection by L. major...
  28. doi request reprint An F-box protein, FBXW5, negatively regulates TAK1 MAP3K in the IL-1beta signaling pathway
    Yasumasa Minoda
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812 8582, Japan
    Biochem Biophys Res Commun 381:412-7. 2009
    ..Conversely, knockdown of FBXW5 resulted in the prolonged activation of TAK1 upon IL-1beta stimulation. These results suggest that FBXW5 negatively regulates TAK1 in the IL-1beta signaling pathway...
  29. ncbi request reprint Induction of hyper Th1 cell-type immune responses by dendritic cells lacking the suppressor of cytokine signaling-1 gene
    Toshikatsu Hanada
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
    J Immunol 174:4325-32. 2005
    ..We propose that reduction of the SOCS1 gene expression in DCs leads to CD8alpha(+) DC-like phenotype which promotes Th1-type hyperresponses...
  30. ncbi request reprint Keeping DCs awake by putting SOCS1 to sleep
    Takashi Kobayashi
    Molecular and Cellular Immunology Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka, 812 8582, Japan
    Trends Immunol 26:177-9. 2005
    ..This recent study demonstrates the importance of negative regulation of DC maturation and functions for DC-based immunotherapy...
  31. pmc Loss of SOCS3 in T helper cells resulted in reduced immune responses and hyperproduction of interleukin 10 and transforming growth factor-beta 1
    Ichiko Kinjyo
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Higashi ku, Fukuoka 812 8582, Japan
    J Exp Med 203:1021-31. 2006
    ..From these findings, we propose that SOCS3 regulates the production of the immunoregulatory cytokines TGF-beta1 and IL-10 through modulating STAT3 activation...
  32. ncbi request reprint Positive and negative roles of IL-6, STAT3, and SOCS3 in inflammatory arthritis
    Ichiko Kinjyo
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Maidashi, Higashi ku, Fukuoka 812 8582, Japan
    Adv Exp Med Biol 602:113-24. 2007
  33. ncbi request reprint [Intracellular negative signals and allergy]
    Akihiko Yoshimura
    Division of Molecular and Cellular Immunology Medical Institute of Bioregulation, Kyushu University, Japan
    Arerugi 56:563-9. 2007
  34. ncbi request reprint Loss of mammalian Sprouty2 leads to enteric neuronal hyperplasia and esophageal achalasia
    Takaharu Taketomi
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
    Nat Neurosci 8:855-7. 2005
    ..Anti-GDNF antibody administration corrected nerve hyperplasia in Sprouty2-deficient mice. We show Sprouty2 to be a negative regulator of GDNF for the neonatal development or survival of enteric nerve cells...
  35. ncbi request reprint Suppressors of cytokine signaling-1 and -3 regulate osteoclastogenesis in the presence of inflammatory cytokines
    Masanobu Ohishi
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Faculty of Dental Sciences, Kyushu University, Fukuoka, Japan
    J Immunol 174:3024-31. 2005
    ..Selective suppression of SOCS1 and SOCS3 in osteoclast precursors may be a possible therapeutic strategy for inflammatory bone destruction...
  36. doi request reprint Regulation of human autoimmune regulator (AIRE) gene translation by miR-220b
    Tomohito Matsuo
    Department of Medical Science and Technology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812 8582, Japan
    Gene 530:19-25. 2013
    ..Taken together, it was concluded that miR-220b inhibited the AIRE gene translation through the 3'UTR region of AIRE gene, indicating that miR-220b could serve as a regulator for human AIRE gene translation...