Complement Receptor Type 1 (CR1, CD35) Is a Receptor for C1q

Klickstein, Lloyd B.; Barbashov, Sergei F.; Liu, Tun; Jack, R M; Nicholson‐Weller, Anne

doi:10.1016/s1074-7613(00)80356-8

Cited by 230 publications

(167 citation statements)

References 66 publications

(14 reference statements)

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“…CR1 (CD35) binds mainly C3b, C4b and C1q [20,21], whereas CR2 (CD21) binds the natural proteolytic fragments iC3b, C3dg and C3d [22,23]. Flow cytometry with mAb to CR1 and CR2 confirmed that B cells are positive for CR1 and CR2 (data not shown).…”

Section: Microparticles Are Transferred To Pbmc and Endothelial Cellsmentioning

confidence: 88%

Differential mechanisms of microparticle transfer toB cells and monocytes: anti‐inflammatory propertiesof microparticles

Köppler¹,

Cohen²,

Schlöndorff

et al. 2006

Eur J Immunol

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Microparticles are small vesicles released from the plasma membrane of various cell types independently of apoptosis or cell death, are transferred between cells, and carry membrane proteins from one cell to another. We have studied the mechanism of uptake of microparticles by monocytes and B cells. The transfer of microparticles to B cells was almost completely dependent on complement. Incubation of microparticles with serum resulted in opsonization of microparticles with the complement cleavage product iC3b. The subsequent transfer to B cells was mediated by the complement receptor CR2. The interaction between iC3b-opsonized microparticles and B cells reduced the activation of B cells as measured by expression of MHC class II, CD86 and CD25. In contrast, transfer of microparticles to monocytes was only partially complement dependent, but involved calcium and annexin V, and was found to change the cytokine profile of monocytes towards a reduced release of the pro-inflammatory cytokines GM-CSF and TNF-a and an increased release of the anti-inflammatory cytokine IL-10. These data show that microparticles are taken up by B cells and monocytes by different mechanisms and modulate the activation of monocytes and B cells towards an anti-inflammatory phenotype. Microparticles might be involved in counterbalancing pro-inflammatory signals arising from tissue injury or inflammation.

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Section: Microparticles Are Transferred To Pbmc and Endothelial Cellsmentioning

confidence: 88%

Differential mechanisms of microparticle transfer toB cells and monocytes: anti‐inflammatory propertiesof microparticles

Köppler¹,

Cohen²,

Schlöndorff

et al. 2006

Eur J Immunol

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“…The CR1 gene is located on chromosome 1 at the locus 1q32 in a genetic cluster of complement activation genes (de Cordoba and Rubinstein 1986). CR1 is a multifunctional protein, which is widely expressed on the extracellular membrane of, B lymphocytes, monocytes, macrophages, erythrocytes, eosinophils, some CD4-positive T cells, dendritic cells, Langerhan cells in the skin glomerular podocytes and microglia as well (Crehan et al 2013;Klickstein et al 1988Klickstein et al , 1997Korotzer et al 1995;Liu and Niu 2009). CR1 has two isoforms: CR1-F and CR1-S, where the F means the ''fast'' isoform with a smaller molecular weight while the S refers to ''slow'' isoform (Aiyaz et al 2012).…”

Section: Complement Receptormentioning

confidence: 99%

Inflammation in Alzheimer’s Disease and Molecular Genetics: Recent Update

Zhang

et al. 2015

Arch. Immunol. Ther. Exp.

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Alzheimer's disease (AD) is a complex agerelated neurodegenerative disorder of the central nervous system. Since the first description of AD in 1907, many hypotheses have been established to explain its causes. The inflammation theory is one of them. Pathological and biochemical studies of brains from AD individuals have provided solid evidence of the activation of inflammatory pathways. Furthermore, people with long-term medication of anti-inflammatory drugs have shown a reduced risk to develop the disease. After three decades of genetic study in AD, dozens of loci harboring genetic variants influencing inflammatory pathways in AD patients has been identified through genome-wide association studies (GWAS). The most well-known GWAS risk factor that is responsible for immune response and inflammation in AD development should be APOE e4 allele. However, a growing number of other GWAS risk AD candidate genes in inflammation have recently been discovered. In the present study, we try to review the inflammation in AD and immunity-associated GWAS risk genes like HLA-DRB5/DRB1, INPP5D, MEF2C, CR1, CLU and TREM2.

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“…CR1 reportedly has high affinity for C3b and lower affinity for iC3b, and also binds C4b, C1q, and MBL (12)(13)(14). Likewise, murine CR1 has binding sites for both C3b and C4b (15,16).…”

mentioning

confidence: 99%

The Virulence Function of Streptococcus pneumoniae Surface Protein A Involves Inhibition of Complement Activation and Impairment of Complement Receptor-Mediated Protection

Ren¹,

McCrory

Pass

et al. 2004

The Journal of Immunology

106

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Complement is important for elimination of invasive microbes from the host, an action achieved largely through interaction of complement-decorated pathogens with various complement receptors (CR) on phagocytes. Pneumococcal surface protein A (PspA) has been shown to interfere with complement deposition onto pneumococci, but to date the impact of PspA on CR-mediated host defense is unknown. To gauge the contribution of CRs to host defense against pneumococci and to decipher the impact of PspA on CR-dependent host defense, wild-type C57BL/6J mice and mutant mice lacking CR types 1 and 2 (CR1/2−/−), CR3 (CR3−/−), or CR4 (CR4−/−) were challenged with WU2, a PspA+ capsular serotype 3 pneumococcus, and its PspA− mutant JY1119. Pneumococci also were used to challenge factor D-deficient (FD−/−), LFA-1-deficient (LFA-1−/−), and CD18-deficient (CD18−/−) mice. We found that FD−/−, CR3−/−, and CR4−/− mice had significantly decreased longevity and survival rate upon infection with WU2. In comparison, PspA− pneumococci were virulent only in FD−/− and CR1/2−/− mice. Normal mouse serum supported more C3 deposition on pneumococci than FD−/− serum, and more iC3b was deposited onto the PspA− than the PspA+ strain. The combined results confirm earlier conclusions that the alternative pathway of complement activation is indispensable for innate immunity against pneumococcal infection and that PspA interferes with the protective role of the alternative pathway. Our new results suggest that complement receptors CR1/2, CR3, and CR4 all play important roles in host defense against pneumococcal infection.

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Complement Receptor Type 1 (CR1, CD35) Is a Receptor for C1q

Cited by 230 publications

References 66 publications

Differential mechanisms of microparticle transfer toB cells and monocytes: anti‐inflammatory propertiesof microparticles

Differential mechanisms of microparticle transfer toB cells and monocytes: anti‐inflammatory propertiesof microparticles

Inflammation in Alzheimer’s Disease and Molecular Genetics: Recent Update

The Virulence Function of Streptococcus pneumoniae Surface Protein A Involves Inhibition of Complement Activation and Impairment of Complement Receptor-Mediated Protection

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