Abstract

The principal investigator has produced a very valuable reagent, Fas-Ig, which will allow him to assess the role of the Fas/FasL interaction in central and peripheral tolerance.
The specific aims are to: 1) Determine whether Fas/FasL interactions participate in the deletion of antigen- specific CD4+8+ thymocytes in vitro. 2) Demonstrate a role for the Fas/FasL interaction in clonal deletion in vivo by injecting Fas-Ig. 3) Demonstrate a role for the Fas/FasL interaction in clonal deletion in vivo by chronically administering Fas-Ig. 4. Study the molecular pathway of Fas/FasL co-expression following TCR-dependent activation. 5. Study the molecular regulation of the FasL gene.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Project (R01)
Project #
5R01AI036938-04
Application #
2672404
Study Section
Immunological Sciences Study Section (IMS)
Project Start
1995-06-01
Project End
2000-05-31
Budget Start
1998-06-01
Budget End
1999-05-31
Support Year
4
Fiscal Year
1998
Total Cost
Indirect Cost

  Institution

Name
Boston University
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
604483045
City
Boston
State
MA
Country
United States
Zip Code
02118

  Publications

Chan, Derek V; Sharma, Rahul; Ju, Chiao-Ying A et al. (2013) A recombinant scFv-FasLext as a targeting cytotoxic agent against human Jurkat-Ras cancer. J Biomed Sci 20:16
Sharma, Rahul; Zheng, Lingjie; Deshmukh, Umesh S et al. (2007) A regulatory T cell-dependent novel function of CD25 (IL-2Ralpha) controlling memory CD8(+) T cell homeostasis. J Immunol 178:1251-5
Sharma, R; Zheng, L; Guo, X et al. (2006) Novel animal models for Sjogren's syndrome: expression and transfer of salivary gland dysfunction from regulatory T cell-deficient mice. J Autoimmun 27:289-96
Sung, Sun-Sang J; Fu, Shu Man; Rose Jr, C Edward et al. (2006) A major lung CD103 (alphaE)-beta7 integrin-positive epithelial dendritic cell population expressing Langerin and tight junction proteins. J Immunol 176:2161-72
Jodo, Satoshi; Pidiyar, Vyankatesh J; Xiao, Sheng et al. (2005) Fas ligand (CD178) cytoplasmic tail is a positive regulator of Fas ligand-mediated cytotoxicity. J Immunol 174:4470-4
Xiao, Sheng; Deshmukh, Umesh S; Jodo, Satoshi et al. (2004) Novel negative regulator of expression in Fas ligand (CD178) cytoplasmic tail: evidence for translational regulation and against Fas ligand retention in secretory lysosomes. J Immunol 173:5095-102
Xiao, Sheng; Zhang, Xingmin; Mann, Koren K et al. (2004) Changes in sensitivity of peripheral lymphocytes of autoimmune gld mice to FasL-mediated apoptosis reveal a mechanism for the preferential deletion of CD4-CD8-B220+ T cells. Int Immunol 16:759-66
Jodo, Satoshi; Kung, John T; Xiao, Sheng et al. (2003) Anti-CD95-induced lethality requires radioresistant Fcgamma RII+ cells. A novel mechanism for fulminant hepatic failure. J Biol Chem 278:7553-7
Xiao, Sheng; Sung, Sun-Sang J; Fu, Shu Man et al. (2003) Combining Fas mutation with interleukin-2 deficiency prevents Colitis and Lupus: implicating interleukin-2 for auto-reactive T cell expansion and Fas ligand for colon epithelial cell death. J Biol Chem 278:52730-8
Xiao, Sheng; Jodo, Satoshi; Sung, Sun-Sang J et al. (2002) A novel signaling mechanism for soluble CD95 ligand. Synergy with anti-CD95 monoclonal antibodies for apoptosis and NF-kappaB nuclear translocation. J Biol Chem 277:50907-13

Showing the most recent 10 out of 25 publications