Complement receptors and regulatory proteins: immune adherence revisited and abuse by microorganisms

Atkinson, John P.; Krych, M.; Nickells, Michael; Birmingham, Daniel J.; Subramanian, Vijay; Clemenza, Liliana; Alvarez, Juan; Liszewski, Kathy

doi:10.1111/j.1365-2249.1994.tb06251.x

Cited by 7 publications

(3 citation statements)

References 30 publications

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“…Alternatively, the "peripheral sink" hypothesis of DeMattos and colleagues (2001), involving binding of circulating Ab to Ab autoantibodies, may also apply to C3-opsonized Ab in the peripheral circulation. In particular, a well-established mechanism for clearance of circulating pathogens, immune adherence (reviewed in Atkinson et al 1994;Birmingham and Hebert 2001), appears to be operative with respect to circulating Ab. Here, C3-dependent binding of Ab to human erythrocyte CR1 has been shown, and is reported to be significantly deficient in the vast majority of AD patients, as well as many mild cognitive impairment (MCI) subjects .…”

Section: Molecular Mediators the Complement Systemmentioning

confidence: 99%

Inflammation in Alzheimer Disease--A Brief Review of the Basic Science and Clinical Literature

Wyss‐Coray

Rogers

2011

Cold Spring Harbor Perspectives in Medicine

828

642

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Biochemical and neuropathological studies of brains from individuals with Alzheimer disease (AD) provide clear evidence for an activation of inflammatory pathways, and longterm use of anti-inflammatory drugs is linked with reduced risk to develop the disease. As cause and effect relationships between inflammation and AD are being worked out, there is a realization that some components of this complex molecular and cellular machinery are most likely promoting pathological processes leading to AD, whereas other components serve to do the opposite. The challenge will be to find ways of fine tuning inflammation to delay, prevent, or treat AD.

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Section: Molecular Mediators the Complement Systemmentioning

confidence: 99%

Inflammation in Alzheimer Disease--A Brief Review of the Basic Science and Clinical Literature

Wyss‐Coray

Rogers

2011

Cold Spring Harbor Perspectives in Medicine

828

642

View full text Add to dashboard Cite

show abstract

“…C4b2a cleaves C3 into the fluid phase C3a component and C3b, which is retained on the antigen-antibody complex. Both C3b and C4b are rec-ognized by the cellular receptors CD46 and CD35, which function as co-factors for factor I-mediated C3b and C4b cleavage (7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

“…Two minor isoforms consist of a7b0 and a6b1. Initially discovered as a widely expressed C3b-and C4bbinding protein, C4BP was subsequently shown to be a cofactor for the serine protease factor I, to inactivate by limited proteolysis these two components of the C3 convertase (7). C4BP also binds serum amyloid protein A (18), protein S (19) and a number of microbial agents.…”

Section: Introductionmentioning

confidence: 99%

Ligation of CD46 to CD40 inhibits CD40 signaling in B cells

Jabara

Angelini

Brodeur

et al. 2011

International Immunology

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CD40 induces B cells to switch to IgE in the presence of IL-4 and up-regulates their expression of the low-affinity receptor for IgE, CD23, which promotes the immune response to allergen complexed with IgE antibody. CD40 binds to CD40L and to the C4b-binding protein (C4BP) using distinct sites. CD46 is a receptor for the product of activated complement C4b. Some microbial antigens bind both C4BP and CD46, potentially bridging CD40 to CD46. In addition, immune complexes containing both C4b and C4BP may cross-link CD40 to CD46. We demonstrate that cross-linking CD46 to CD40 on B cells inhibits CD40-mediated up-regulation of surface CD23 expression and induction of IL-4-dependent IgE isotype switching. This was associated with inhibition of induction of Cε germ line transcripts and of activation-induced cytidine deaminase mRNA expression. Furthermore, co-ligation of CD46 to CD40 blocked CD40-mediated NF-κB activation. These observations suggest that complement components may play an important role in regulating CD40 activation of B cells and the allergic response.

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Attempts to Prepare Suitable Complement Regulatory Molecules for Clinical Xenotransplantation

Miyagawa¹,

Matsunami²,

Yoshitatsu

et al. 2001

J Cardiac Surgery

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Complement receptors and regulatory proteins: immune adherence revisited and abuse by microorganisms

Cited by 7 publications

References 30 publications

Inflammation in Alzheimer Disease--A Brief Review of the Basic Science and Clinical Literature

Inflammation in Alzheimer Disease--A Brief Review of the Basic Science and Clinical Literature

Ligation of CD46 to CD40 inhibits CD40 signaling in B cells

Attempts to Prepare Suitable Complement Regulatory Molecules for Clinical Xenotransplantation

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