Decay-accelerating factor regulates T-cell immunity in the context of inflammation by influencing co-stimulatory molecule expression on antigen-presenting cells

Chongyun Fang, Takashi Miwa and Wen-Chao Song


Recent studies have indicated a role of complement in regulating T cell immunity but the mechanism of action of complement in this process remains to be clarified. Here we studied mice deficient in decay-accelerating factor (DAF), a key membrane complement regulator whose deficiency led to increased complement-dependent T cell immune responses in vivo. By crossing OT-II and OT-I T cell receptor transgenic mice with DAF-knockout mice, we found that lack of DAF on T cells did not affect their responses to antigen stimulation. Similarly, lack of DAF on antigen-presenting cells (APCs) of naïve mice did not alter their T cell-stimulating activity. In contrast, APCs from DAF-knockout mice treated with inflammatory stimuli were found to be more potent T cell stimulators than cells from similarly treated wild-type mice. Acquisition of higher T cell-stimulating activity by APCs in challenged DAF-knockout mice required C3 and C5aR and was correlated with decreased surface PD-L1 and/or increased CD40 expression. These findings implied that DAF suppressed T cell immunity as a complement regulator in the context of inflammation but did not play an intrinsic role on T cells or APCs. Collectively, our data suggest a systemic and indirect role of complement in T cell immunity.

  • Submitted April 12, 2011.
  • Accepted May 18, 2011.