Complement Receptor 1: Disease associations and therapeutic implications

Khera, Rohan; Das, Nibhriti

doi:10.1016/j.molimm.2008.09.026

Cited by 168 publications

(121 citation statements)

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“…A large part of these effects are translated into cellular effector functions via a set of complement receptors (CR) specific for proteolytically cleaved complement fragments. CR1 (CD35) is both a complement receptor for C3b, iC3b and C4b and a complement inhibitor, by competing with factor B (FB) for C3b binding and by functioning as a co-factor for factor I (FI) [6]. CR2 (CD21) binds iC3b, and especially C3d/C3dg, CR3 (MAC-1, CD11b/CD18) binds iC3b and C3d/C3dg, whereas CR4 (gp150/95, CD11c/CD18) binds only iC3b [7][8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Production of complement components by cells of the immune system

Lubbers

Essen

Kooten

et al. 2017

Clinical and Experimental Immunology

335

250

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SummaryThe complement system is an important part of the innate immune defence. It contributes not only to local inflammation, removal and killing of pathogens, but it also assists in shaping of the adaptive immune response. Besides a role in inflammation, complement is also involved in physiological processes such as waste disposal and developmental programmes. The complement system comprises several soluble and membrane-bound proteins. The bulk of the soluble proteins is produced mainly by the liver. While several complement proteins are produced by a wide variety of cell types, other complement proteins are produced by only a few related cell types. As these data suggest that local production by specific cell types may have specific functions, more detailed studies have been employed recently analysing the local and even intracellular role of these complement proteins.Here we review the current knowledge about extrahepatic production and/ or secretion of complement components. More specifically, we address what is known about complement synthesis by cells of the human immune system.

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Section: Introductionmentioning

confidence: 99%

Production of complement components by cells of the immune system

Lubbers

Essen

Kooten

et al. 2017

Clinical and Experimental Immunology

335

250

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“…When B-cell surface CR1 is bound by ligands, it appears to prevent Bcell proliferation (Jozsi et al 2002). This is suggested as a mechanism by which CR1 is involved in autoimmune disorders (Khera and Das 2009). …”

Section: Cr1 -Protein Structure and Functionmentioning

confidence: 99%

“…by cytokines), CR1 mediates phagocytosis (Wright and Silverstein 1982), and can stimulate the release of interleukins, indicating another mechanism by which CR1 may help mediate the immune response (Bacle et al 1990). The role of CR1 expressed on T cells remains unclear (Khera and Das 2009). …”

Section: Cr1 -Protein Structure and Functionmentioning

confidence: 99%

P2‐030: Investigating the Role of Clu, Picalm, and Cr1 in Alzheimer's Disease

Lord

Turton

Braae

et al. 2014

Alzheimer's & Dementia

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In 2009, two large genome wide association studies (GWAS) found associations between common single nucleotide polymorphisms (SNPs) at three loci (CLU, PICALM and CR1) and Alzheimer's disease (AD) risk. The causal variants underlying these associations and how these impact on AD susceptibility remain unclear. Target enrichment and next generation sequencing (NGS) were used to completely resequence the three associated loci in 96 AD patients in an attempt to uncover potentially causative and rare variants that may explain the observed association signals. A pipeline was developed for the handling of pooled NGS data following a comparison of several different combinations of programs. 33 exonic SNPs were found within the three genes, along with over 1000 non-coding variants. To identify the variants most likely to be affecting AD risk, a two pronged approach was adopted. The variants were imputed in a large case-control cohort (2067 cases, 7376 controls) to test for association with AD, and the likely functional consequences of the variants were assessed using in silico resources. Several of the analysed variants showed suggestive or significant association with AD in the imputed data, and/or were predicted to have consequences on the function or regulation of the genes, suggesting avenues for future research in AD genetics. The whole method of pooled, targeted NGS and prioritisation using imputed data for association testing and in silico resources for functional analysis represents a new strategy for tracking down the illusive causation of GWAS signals. PublicationsNext generation sequencing of CLU, PICALM and CR1: pitfalls and potential solutions. Lord J,

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“…Complement activation with subsequent deposition of complement components on tumor tissues has been demonstrated (Jurianz et al, 1999). Potential of CR1 as a diagnostic and prognostic marker is being increasingly realized (Khera et al, 2009).…”

Section: Introductionmentioning

confidence: 99%