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 Blood, 15 December 2008, Vol. 112, No. 13, pp. 5084-5094.
Prepublished online as a Blood First Edition Paper on September 23, 2008; DOI 10.1182/blood-2008-05-156646.

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IMMUNOBIOLOGY

Cyclic AMP plays a critical role in C3a-receptor–mediated regulation of dendritic cells in antigen uptake and T-cell stimulation

Ke Li1, Katie J. Anderson1, Qi Peng1, Alistair Noble2, Bao Lu3, Adrian P. Kelly4, Naiyin Wang1, Steven H. Sacks1, and Wuding Zhou1

1 Complement Laboratory, Medical Research Centre (MRC) Centre for Transplantation, and 2 Department of Asthma, Allergy & Respiratory Science, King's College London School of Medicine at Guy's Hospital, London, United Kingdom; 3 Division of Pulmonary Medicine and Ina Sue Perlmutter Laboratory, Children's Hospital, Harvard Medical School, Boston, MA; and 4 Department of Pathology, University of Cambridge, Cambridge, United Kingdom

The biochemical basis for complement acting directly on antigen-presenting cells to enhance their function in T-cell stimulation has been unclear. Here we present evidence that engagement of C3a receptor (C3aR) on the surface of dendritic cells (DCs) leads to alterations in the level of intracellular cyclic adenosine monophosphate (cAMP), a potent negative regulator of inflammatory cytokines. C3aR activation-induced depression of cAMP was associated with enhanced capacity of DCs for antigen uptake and T-cell stimulation. Conversely, C3aR-deficient DCs showed elevation of cAMP and impaired properties for antigen uptake and immune stimulation. Similarities in the phenotype of C3-deficient and C3aR-deficient DCs suggest that local production of C3 with extracellular metabolism to C3a is an important driver of DC alterations in cAMP. The finding of a link between complement and adaptive immune stimulation through cAMP offers new insight into how innate and adaptive immunity combine to generate efficient effector and memory responses.


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