X Zhang1,2, Y Han1, L Song1, L Huo1, X Lai1, Y Zhang1, J Zhang1, Z Hua1,2,3. 1. The State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, China. 2. Changzhou High-Tech Research Institute of Nanjing Universityand Jiangsu TargetPharma Laboratories Inc., Changzhou, China. 3. Shenzhen Research Institute of Nanjing University, Shenzhen, China.
Abstract
BACKGROUND: Fas-associated protein with death domain (FADD) is a classic adaptor protein in apoptosis. Increasing evidence has shown that FADD is also implicated in T-cell development, activation and proliferation. The role of FADD in inflammatory disorders remains largely unexplored. AIM: To assess the role of FADD in inflammatory disorders. METHODS: We established an experimental model of contact hypersensitivity (CHS) by using 2,4,6-trinitrochlorobenzene (TNCB) on transgenic mice expressing a dominant negative mutant of FADD (FADD-DN), RESULTS: CHS responses were clearly attenuated in FADD-DN mice compared with control mice. In the retroauricular lymph nodes, the ratio of CD8+ T cells was also decreased. CONCLUSION: FADD-DN appears to play a protective role in TNCB-induced CHS reactions.
BACKGROUND: Fas-associated protein with death domain (FADD) is a classic adaptor protein in apoptosis. Increasing evidence has shown that FADD is also implicated in T-cell development, activation and proliferation. The role of FADD in inflammatory disorders remains largely unexplored. AIM: To assess the role of FADD in inflammatory disorders. METHODS: We established an experimental model of contact hypersensitivity (CHS) by using 2,4,6-trinitrochlorobenzene (TNCB) on transgenic mice expressing a dominant negative mutant of FADD (FADD-DN), RESULTS:CHS responses were clearly attenuated in FADD-DNmice compared with control mice. In the retroauricular lymph nodes, the ratio of CD8+ T cells was also decreased. CONCLUSION:FADD-DN appears to play a protective role in TNCB-induced CHS reactions.