A protective role for FADD dominant negative (FADD-DN) mutant in trinitrochlorobenzene (TNCB)-induced murine contact hypersensitivity 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-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.