International Immunology, Vol. 11, No. 9, 1431-1439,
September 1999
© 1999 Japanese Society for Immunology
Mice lacking the transcription factor subunit Rel can clear an influenza infection and have functional anti-viral cytotoxic T cells but do not develop an optimal antibody response
Cooperative Research Centre for Vaccine Technology, Department of Microbiology and Immunology, University of Melbourne, Royal Parade, Parkville, Victoria 3052, Australia
1 Walter and Eliza Hall Institute of Medical Research, Post Office, Royal Melbourne Hospital, Parkville, Victoria 3052, Australia
Correspondence to: L. E. Brown
Rel, a haemopoietic cell-restricted member of the NF-
B/Rel family of transcription factors, has recently been shown to be important in the function of B and T lymphocytes. In an attempt to understand the role of this protein in the immune response, we examined the ability of Rel–/– mice to counter an influenza virus infection. Normal levels of virus-specific cytotoxic T cells induced in Rel–/– mice were able to clear virus from the lungs, albeit with somewhat delayed kinetics compared to normal mice. Rel–/– mice did, however, display a markedly reduced T cell proliferative response to the virus, and exhibited impaired local and systemic influenza virus-specific antibody responses. This defect was sufficient to result in an inability of vaccinated mice, but not of previously infected mice, to acquire antibody-dependent protective immunity to reinfection with the same virus. These findings establish that during the response to influenza virus, Rel function allows optimal development of humoral immunity, a role that apparently cannot be fulfilled by other NF-B/Rel proteins.
Keywords: NF-B, Rel, transcription factors
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