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

Leanne Harling-McNabb, Georgia Deliyannis, David C Jackson, Steven Demetrious Gerondakis, George Grigoriadis, Lorena Elizabeth Brown

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Rel, a haemopoietic cell-restricted member of the NF-I?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-I?B/Rel proteins.
Original languageEnglish
Pages (from-to)1431 - 1439
Number of pages9
JournalInternational Immunology
Issue number9
Publication statusPublished - 1999

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