Abrogation of CD30 and OX40 signals prevents autoimmune disease in FoxP3-deficient mice.

ABSTRACT: Our previous studies have implicated signaling through the tumor necrosis family receptors OX40 and CD30 as critical for maintaining CD4 memory responses. We show that signals through both molecules are also required for CD4 effector-mediated autoimmune tissue damage. Under normal circumstances, male mice deficient in the forkhead transcription factor FoxP3, which lack regulatory CD4 T cells, develop lethal autoimmune disease in the first few weeks of life. However, in the combined absence of OX40 and CD30, FoxP3-deficient mice develop normally and breed successfully. The extensive tissue infiltration and organ destruction characteristic of FoxP3 disease does not appear in these mice, and their mortality is not associated with autoimmunity. Although the absence of OX40 plays the dominant r

SUBMITTER: Gaspal F 

PROVIDER: S-EPMC3149223 | biostudies-literature | 2011 Aug

REPOSITORIES: biostudies-literature