Decay-accelerating factor modulates induction of T cell immunity.
Publication/Presentation Date
5-16-2005
Abstract
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.
Volume
201
Issue
10
First Page
1523
Last Page
1530
ISSN
0022-1007
Published In/Presented At
Heeger, P. S., Lalli, P. N., Lin, F., Valujskikh, A., Liu, J., Muqim, N., Xu, Y., & Medof, M. E. (2005). Decay-accelerating factor modulates induction of T cell immunity. The Journal of experimental medicine, 201(10), 1523–1530. https://doi.org/10.1084/jem.20041967
Disciplines
Medicine and Health Sciences
PubMedID
15883171
Department(s)
Department of Pathology and Laboratory Medicine
Document Type
Article