Journal
BLOOD
Volume 107, Issue 6, Pages 2461-2469Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2005-08-3144
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Funding
- MRC [G0000771] Funding Source: UKRI
- Medical Research Council [G0000771] Funding Source: researchfish
- Medical Research Council [G0000771] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
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Impaired T-cell reactivity is a feature of C3-deficient mice in several disease models. The mechanism behind the reduced T-cell response is, however, poorly understood. We explored the hypothesis that antigen-presenting cells (APCs) from C3(-/-) mice have impair ad potency to stimulate antigen-specific: T cells, in an alloantigen-dependent model. Our results show that C3(-/-) macrophages have reduced ability to elicit alloreactive T-cell responses in vitro and in vivo, affecting both the primary and secondary responses. The C3 status of donor macrophages had a major impact on the CD4 T-cell response. The impaired CD4 T-cell response was associated with reduced expression of MHC class II on the surface of C3(-/-) macrophages, without loss of class II gene expression. Furthermore, inhibition of C3 gene expression in C3(+/+) macrophages reduced their ability to stimulate alloreactive T cells, suggesting that endogenous production of C3 could in part contribute to the potency of APCs. Our data provide compelling evidence that C3 deficiency modulates the potency of APCs to stimulate the T-cell response, suggesting a critical role for complement in the maintenance of APC function. This could offer a partial explanation as to why the T-cell response is impaired in C-/- mice.
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