Top > Search of International Patents > REGULATORY-T-CELL-INCREASING AGENT, CLOSTRIDIUM CLUSTER XIVa GROWTH PROMOTER, AND COMPOSITION FOR PREVENTION, TREATMENT, OR IMPROVEMENT OF INFLAMMATORY OR ALLERGIC DISEASE OR SYMPTOM

REGULATORY-T-CELL-INCREASING AGENT, CLOSTRIDIUM CLUSTER XIVa GROWTH PROMOTER, AND COMPOSITION FOR PREVENTION, TREATMENT, OR IMPROVEMENT OF INFLAMMATORY OR ALLERGIC DISEASE OR SYMPTOM

Foreign code F200010017
File No. (S2018-0606-N0)
Posted date Jan 30, 2020
Country WIPO
International application number 2019JP018787
International publication number WO 2019216422
Date of international filing May 10, 2019
Date of international publication Nov 14, 2019
Priority data
  • 201862669680 (May 10, 2018) US
Title REGULATORY-T-CELL-INCREASING AGENT, CLOSTRIDIUM CLUSTER XIVa GROWTH PROMOTER, AND COMPOSITION FOR PREVENTION, TREATMENT, OR IMPROVEMENT OF INFLAMMATORY OR ALLERGIC DISEASE OR SYMPTOM
Abstract Provided are: a regulatory-T-cell-increasing agent that contains an IL-17F inhibitor; a Clostridium cluster XIVa growth promoter that contains an IL-17F inhibitor; and a composition for the prevention, treatment, or improvement of inflammatory or allergic disease or symptoms that contains the regulatory-T-cell-increasing agent. The IL-17F inhibitor may be a substance that inhibits the interaction between IL-17F and the IL-17F receptors, a substance that inhibits the production or expression of IL-17F, or a substance that inhibits the expression of the IL-17F receptors.
Outline of related art and contending technology BACKGROUND ART
IL-17F gene and the gene IL-17A, in both human and mouse of the present close to each other, their products is very high and the 50% amino acid homology, heterodimers are formed, the same receptor (Yao, Z. et al., 1995; Gaffen, S.L. et al., 2014; Iwakura, Y. et al., 2011). Any of these cytokines, bacterial infections and fungal infections host protection (Ishigame, H. et al., 2009; (Cai, Y. et al., 2011 the development of skin irritation Puel, A. et al., 2010), ; Hueber, W. et al., 2010; Martin, D.A. et al., 2013; Papp, K.A. et al., 2012) involved. Nevertheless, the IL-17A, and/or progression of autoimmune disease developing in the more important than IL-17F (Iwakura, Y. et al., 2011 play a role in; Ishigame, H. et al., 2009; Nakae, S. et al., 2003; Komiyama, Y. et al., 2006).
IL-17A and none of the IL-17F, TH17 cells, 3 type (ILC3) natural immune cells, a cell γ δ T, NKT cells, and CD8+ T are produced by the cells, some cells produce only one of these cytokines (Ishigame, H. et al., 2009; Yang, X.O. et al., 2008). For example, activated monocytes, mast cells, basophils, and mucosal epithelial cells, which produce only IL-17F (Ishigame, H. et al., 2009; Starnes, T. et al., 2001; Kawaguchi, M. et al., 2001). IL-17A is, cytokines and chemokines than IL-17F induce high activity. In addition, the IL-17A, lymphoid cells express high levels of IL-17 A receptor (IL-17RA) high affinity to, the IL-17F, predominantly non-hematopoietic cells express C IL-17 (IL-17RC) receptor with high affinity to (Ishigame, H. et al., 2009; Kuestner, R.E. et al., 2007). Therefore, the IL-17A and IL-17F, overlapping in the immune system has a distinct function.
Inflammatory bowel disease (IBD) is, diarrhea and weight loss and chronic inflammatory diseases of the intestines with, dextran sulfate sodium (DSS) and induced colitis is induced colitis cell CD25-CD45RBhiCD4 + T, a model of IBD. TH1 Cells, T cells in the pathogenesis of induced colitis suggesting that this model is protective (Powrie, F. et al., 1994), IL-17A (O'Connor, W., Jr. et al., 2009). IL-17A is, intestinal epithelial cells and required to maintain and tight (Lee, J.S. et al., 2015; Maxwell, J.R. et al., 2015), also, in cooperation with the epithelial repair FGF2 can be protected against induced colitis DSS (Song, X. et al., 2015) role. (Il17f - / -) Mice deficient in IL-17F DSS induced colitis (Il17a - / -) is resistant to missing (Yang, X.O. et al., 2008), IL-17A mouse is more sensitivity.
However, in the IL-17A IBD and functional differences of the mechanisms of the IL-17F has not been elucidated. In addition, other IBD inflammatory or allergic diseases or symptoms of the IL-17A for functional differences and IL-17F has not been elucidated.
Scope of claims (In Japanese)[請求項1]
 IL-17F阻害剤を含有する制御性T細胞増加剤。

[請求項2]
 クロストリジウム・クラスターXIVa菌の増殖を介して制御性T細胞を増加させる請求項1に記載の制御性T細胞増加剤。

[請求項3]
 前記IL-17F阻害剤が、IL-17FとIL-17F受容体との相互作用を阻害する物質、IL-17Fの産生又は発現を阻害する物質、及びIL-17F受容体の発現を阻害する物質から選択される少なくとも1種である請求項1又は2に記載の制御性T細胞増加剤。

[請求項4]
 前記IL-17F阻害剤が抗IL-17F抗体である請求項1~3のいずれか1項に記載の制御性T細胞増加剤。

[請求項5]
 IL-17F阻害剤を含有するクロストリジウム・クラスターXIVa菌の増殖促進剤。

[請求項6]
 前記IL-17F阻害剤が、IL-17FとIL-17F受容体との相互作用を阻害する物質、IL-17Fの産生又は発現を阻害する物質、及びIL-17F受容体の発現を阻害する物質から選択される少なくとも1種である請求項5に記載の増殖促進剤。

[請求項7]
 前記IL-17F阻害剤が抗IL-17F抗体である請求項5又は6に記載の増殖促進剤。

[請求項8]
 請求項1~4のいずれか1項に記載の制御性T細胞増加剤を含有する、炎症性又はアレルギー性の疾患又は症状の予防、治療、又は改善のための組成物。

[請求項9]
 前記疾患又は症状が炎症性腸疾患である請求項8に記載の組成物。
  • Applicant
  • ※All designated countries except for US in the data before July 2012
  • TOKYO UNIVERSITY OF SCIENCE FOUNDATION
  • Inventor
  • IWAKURA, Yoichiro
  • TANG Ce
IPC(International Patent Classification)
Specified countries National States: AE AG AL AM AO AT AU AZ BA BB BG BH BN BR BW BY BZ CA CH CL CN CO CR CU CZ DE DJ DK DM DO DZ EC EE EG ES FI GB GD GE GH GM GT HN HR HU ID IL IN IR IS JO JP KE KG KH KN KP KR KW KZ LA LC LK LR LS LU LY MA MD ME MG MK MN MW MX MY MZ NA NG NI NO NZ OM PA PE PG PH PL PT QA RO RS RU RW SA SC SD SE SG SK SL SM ST SV SY TH TJ TM TN TR TT TZ UA UG US UZ VC VN ZA ZM ZW
ARIPO: BW GH GM KE LR LS MW MZ NA RW SD SL SZ TZ UG ZM ZW
EAPO: AM AZ BY KG KZ RU TJ TM
EPO: AL AT BE BG CH CY CZ DE DK EE ES FI FR GB GR HR HU IE IS IT LT LU LV MC MK MT NL NO PL PT RO RS SE SI SK SM TR
OAPI: BF BJ CF CG CI CM GA GN GQ GW KM ML MR NE SN ST TD TG
Please contact us by E-mail or facsimile if you have any interests on this patent.

PAGE TOP

close
close
close
close
close
close