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Decay-accelerating factor regulates T-cell immunity in the context of inflammation by influencing costimulatory molecule expression on antigen-presenting cells. | LitMetric

AI Article Synopsis

  • Recent research highlights the involvement of complement in T-cell immunity, but the specific mechanisms are still unclear.
  • The study examined mice lacking decay-accelerating factor (DAF), revealing that DAF deficiency boosted complement-dependent T-cell immune responses, but did not affect T-cell responses to antigens directly.
  • Findings indicate that DAF serves to suppress T-cell immunity by enhancing the T-cell stimulating capacity of antigen-presenting cells during inflammation, underscoring a systemic and indirect role for complement in T-cell regulation.

Article Abstract

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 naive 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3148154PMC
http://dx.doi.org/10.1182/blood-2011-04-348474DOI Listing

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