The Journal of Experimental Medicine
Aegean Conferences: 2009 Conferences
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Published online 9 May 2005 doi:10.1084/jem.20041967
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 201, Number 10, 1523-1530
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BRIEF DEFINITIVE REPORT

 Decay-accelerating factor modulates induction of T cell immunity

Peter S. Heeger1,2, Peter N. Lalli1,2, Feng Lin2, Anna Valujskikh1, Jinbo Liu2, Nasima Muqim2, Yuanyuan Xu3, and M. Edward Medof2

1 Department of Immunology, Cleveland Clinic Foundation, Cleveland, OH 44195
2 Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106
3 Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, Birmingham, AL 35294

CORRESPONDENCE Peter S. Heeger: heegerp{at}ccf.org OR M. Edward Medof: mxm16{at}po.cwru.edu

Decay-accelerating factor (Daf) dissociates C3/C5 convertases that assemble on host cells and thereby prevents complement activation on their surfaces. We demonstrate that during primary T cell activation, the absence of Daf on antigen-presenting cells (APCs) and on T cells enhances T cell proliferation and augments the induced frequency of effector cells. The effect is factor D- and, at least in part, C5-dependent, indicating that local alternative pathway activation is essential. We show that cognate T cell–APC interactions are accompanied by rapid production of alternative pathway components and down-regulation of Daf expression. The findings argue that local alternative pathway activation and surface Daf protein function respectively as a costimulator and a negative modulator of T cell immunity and explain previously reported observations linking complement to T cell function. The results could have broad therapeutic implications for disorders in which T cell immunity is important.


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