Mannan-binding lectin and C1q bind to distinct structures and exert differential effects on macrophages

Bajtay, Zsuzsa; Józsi, Mihály; Bánki, Zoltán; Thiel, Steffen; Thielens, Nicole M.; Erdei, Anna

doi:10.1002/1521-4141(200006)30:6<1706::aid-immu1706>3.0.co;2-2

Cited by 26 publications

(15 citation statements)

References 24 publications

(54 reference statements)

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“…These results might be surprising since C1q, as activator of the complement system, is mainly considered as a pro-inflammatory mediator. C1q induces production of pro-inflammatory cytokines [32,33] and complement proteins [34] and regulates the deposition of immune complexes [35]. These pro-inflammatory activities of C1q contrast with the observation that C1q deficiency in humans and in animals is associated with the development of the autoimmune disease SLE [26].…”

Section: Discussionmentioning

confidence: 99%

Immune modulation of human dendritic cells by complement

et al. 2007

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Deficiency in complement proteins such as C1q is associated with the development of systemic lupus erythematosus (SLE). Here, we show that the differentiation of dendritic cells (DC) in the presence of C1q (C1qDC) gives rise to CD1a + /DC-SIGN + cells with high phagocytic capacity and low expression of CD80, CD83 and CD86. Further, when C1qDC were exposed to LPS, a significant reduction in the production of IL-6, TNF-a and IL-10 occurred with a limited up-regulation of CD80, CD83 and CD86. In addition, C1qDC were less responsive to activation by CD40L in terms of IL-12p70 secretion and CD86 expression. C1qDC showed an impaired ability to stimulate alloreactive T cells, with a reduced production of IFN-c. In conclusion, we have shown that C1q is a potent modulator of DC, resulting in cells characterized by an impaired capacity of cytokine production and an impaired up-regulation of costimulatory molecules, leading to a limited T cell response. Therefore, we hypothesize that, next to a pivotal role in the safe clearance of apoptotic cells, C1q regulates the threshold of DC activation and thereby prevents hyperactivation of the overall immune response.

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Section: Discussionmentioning

confidence: 99%

Immune modulation of human dendritic cells by complement

et al. 2007

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“…The ligand binding assay was performed as described [57]. Washed imMDCs (2 × 10 5 ) were resuspended in Tris-buffered saline (pH7.4) containing 5 mM CaCl 2 , 1% bovine serum albumin (buffer A).…”

Section: Methodsmentioning

confidence: 99%

Mannan-binding lectin regulates dendritic cell maturation and cytokine production induced by lipopolysaccharide

et al. 2011

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BackgroundMannan-binding lectin (MBL) is a pattern-recognition molecule present in serum, which is involved in the innate immune defense by activating complement and promoting opsonophagocytosis. Dendritic cells (DCs) are professional antigen presenting cells (APCs) that are crucial for the initiation of adaptive immunity. Lipopolysaccharide (LPS) has been shown to be a strong activator of the inflammatory response and immune regulation. We first examined whether MBL modulated LPS-induced cellular responses, then investigated possible mechanisms of its inhibitory effect.ResultsMBL at higher concentrations (10-20 μg/ml) significantly attenuated LPS-induced maturation of monocyte-derived DCs (MDCs) and production of proinflammatory cytokines (e.g., IL-12 and TNF-α), and inhibited their ability to activate allogeneic T lymphocytes. It bound to immature MDCs at physiological calcium concentrations, and was optimal at supraphysiological calcium concentrations. MBL also bound directly to immature MDCs and attenuated the binding of LPS to the cell surfaces, resulting in decreased LPS-induced nuclear factor-κB (NF-κB) activity in these cells.ConclusionAll these data suggest that MBL could affect the functions of DCs by modifying LPS-induced cellular responses. This study supports an important role for MBL in the regulation of adaptive immune responses and inflammatory responses.

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“…A dominant role of Fc γ RIII has been demonstrated in the induction of both TNF- α and IL-1- α production by human macrophages from patients with rheumatoid arthritis [147]. Macrophage production of C3 and C5 is increased through both the Fc [148, 149] and C1q receptors [150]. Gessner et al [148, 149] have found that production and cleavage of C5 by macrophages is regulated by Fc γ Rs.…”

Section: The Role Of Fcγrs In Cardiac Allograft Transplantation In VImentioning

confidence: 99%

Mechanisms involved in antibody- and complement-mediated allograft rejection

Wąsowska

2010

Immunol Res

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Antibody-mediated rejection has become critical clinically because this form of rejection is usually unresponsive to conventional anti-rejection therapy, and therefore, it has been recognized as a major cause of allograft loss. Our group developed experimental animal models of vascularized organ transplantation to study pathogenesis of antibody- and complement-mediated endothelial cell injury leading to graft rejection. In this review, we discuss mechanisms of antibody-mediated graft rejection resulting from activation of complement by C1q- and MBL (mannose-binding lectin)-dependent pathways and interactions with a variety of effector cells, including macrophages and monocytes through Fcγ receptors and complement receptors.

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Mannan-binding lectin and C1q bind to distinct structures and exert differential effects on macrophages

Cited by 26 publications

References 24 publications

Immune modulation of human dendritic cells by complement

Immune modulation of human dendritic cells by complement

Mannan-binding lectin regulates dendritic cell maturation and cytokine production induced by lipopolysaccharide

Mechanisms involved in antibody- and complement-mediated allograft rejection

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