Редактирование: CD55

Complement decay-accelerating factor precursor (CD55 antigen) [CR] [DAF]

==Publications==

{{medline-entry
|title=Loss of complement regulatory proteins on uninfected erythrocytes in vivax and falciparum malaria anemia.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30429373
|abstract=Anemia is a major complication of malaria, driven largely by loss of uninfected RBCs during infection. RBC clearance through loss of complement regulatory proteins ([[CRP]]s) is a significant contributor to anemia in Plasmodium falciparum infection, but its role in Plasmodium vivax infection is unknown. [[CRP]] loss increases RBC susceptibility to macrophage clearance, a process that is also regulated by [[CD47]]. We compared [[CRP]]s and [[CD47]] expression on infected and uninfected RBCs in adult patients with vivax and falciparum malaria and different anemia severities from Papua, Indonesia. Complement activation and parasite-specific complement-fixing antibodies were measured by ELISA. Levels of [[CR1]] and [[CD55]] were reduced in severe anemia in both falciparum and vivax malaria. Loss of [[CRP]]s and [[CD47]] was restricted to uninfected RBCs, with infected RBCs having higher expression. There was no association among complement-fixing antibodies, complement activation, and [[CRP]] loss. Our findings demonstrate that [[CRP]] loss is a pan-species, age-independent mechanism of malarial anemia. Higher levels of [[CRP]] and [[CD47]] expression on infected RBCs suggest that parasites are protected from complement-mediated destruction and macrophage clearance. Lack of associations between protective antibodies and [[CRP]] loss highlight that complement pathogenic and protective pathways are distinct mechanisms during infection.
|mesh-terms=* Adolescent
* Adult
* Aging
* Anemia
* CD47 Antigen
* Complement Activation
* Complement System Proteins
* Erythrocytes
* Female
* Humans
* Malaria, Falciparum
* Malaria, Vivax
* Male
* Plasmodium falciparum
* Plasmodium vivax
* Young Adult
|keywords=* Complement
* Immunology
* Infectious disease
* Malaria
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6303009
}}
{{medline-entry
|title=Genetic variation in complement regulators and susceptibility to age-related macular degeneration.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/22024702
|abstract=Age-related macular degeneration (AMD) is the commonest cause of blindness in Western populations. Risk is influenced by age, genetic and environmental factors. Complement activation appears to be important in the pathogenesis and associations have been found between AMD and genetic variations in complement regulators such as complement factor H. We therefore investigated other complement regulators for association with AMD. We carried out a case-control study to test for association between AMD and single nucleotide polymorphisms (SNPs) spanning the genes encoding complement factor P ([[CFP]], properdin), [[CD46]] (membrane cofactor protein, MCP), [[CD55]] (decay accelerating factor, DAF) and [[CD59]] (protectin). All cases and controls were examined by an ophthalmologist and had independent grading of fundus photographs to confirm their disease status. 20 SNPs were genotyped in 446 cases and 262 controls. For two SNPs with p-values approaching significance additional subjects were genotyped to increase the numbers to 622 cases and 359 controls. There was no evidence of association between AMD and any of the SNPs typed in [[CFP]], [[CD46]], [[CD55]] or [[CD59]]. In a case-control sample that has shown the well established associations between AMD and variants in [[CFH]], [[CFB]] and [[C3]] there was absence of association with SNPs in [[CFP]], [[CD46]], [[CD55]] and [[CD59]]. This suggests that these are not important susceptibility genes for AMD.
|mesh-terms=* Aged
* Aged, 80 and over
* Aging
* CD55 Antigens
* CD59 Antigens
* Case-Control Studies
* Complement System Proteins
* Female
* Genetic Association Studies
* Genetic Predisposition to Disease
* Genetic Variation
* Genotype
* Humans
* Macular Degeneration
* Male
* Membrane Cofactor Protein
* Polymorphism, Single Nucleotide
* Properdin

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3657157
}}
{{medline-entry
|title=Distribution of complement anaphylatoxin receptors and membrane-bound regulators in normal human retina.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/16764856
|abstract=To characterize the distribution of membrane-bound components of the complement system in normal human retina, eyes from eight human donors with no history of ocular disease, ranging in age from 47 to 85 years were examined using immunohistochemistry to localize the C3a receptor (C3aR), C5a receptor (C5aR), [[CD46]], [[CD55]], and [[CD59]] in cryosections prepared from donor posterior segments. The C3aR was identified in the nerve fiber layer in a sawtooth-patterned band. Vimentin, used as a Müller cell marker, produced a similar staining pattern. The C5aR was detected on specific rounded structures in the inner plexiform layer and occasionally in the nerve fiber layer. [[CD46]] produced markedly specific staining of the basolateral surface of the retinal pigment epithelium. [[CD55]] was localized to the nerve fiber layer. Staining for these proteins was consistent across all eyes studied. [[CD59]] was expressed throughout the nerve fiber layer and labeled vessels that extended through the ganglion cell, inner plexiform, and inner nuclear layers, but this pattern was only confirmable in a single subject. Complement anaphylatoxin receptors and regulatory proteins are localized in different but internally consistent patterns in normal adult human retina, independent of the age of the donor. C3aR and C5aR localization only in the inner retina contrasts with previously reported findings in the central nervous system of wide spread diffuse staining. The complement regulators [[CD55]] and [[CD59]] were found primarily on the inner retina, while [[CD46]] was present exclusively in a polarized fashion on the [[RPE]].
|mesh-terms=* Aged
* Aged, 80 and over
* Aging
* CD55 Antigens
* CD59 Antigens
* Complement C3
* Female
* Humans
* Immunoenzyme Techniques
* Male
* Membrane Cofactor Protein
* Membrane Proteins
* Middle Aged
* Pigment Epithelium of Eye
* Receptor, Anaphylatoxin C5a
* Receptors, Complement
* Retina

|full-text-url=https://sci-hub.do/10.1016/j.exer.2006.04.002
}}
{{medline-entry
|title=Complement-regulatory proteins in severe malaria: too little or too much of a good thing?
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/15837610
|abstract=Data from several laboratories suggest that erythrocyte complement-regulatory proteins, in particular complement receptor 1 ([[CR1]]), are important in the pathogenesis of severe malaria. Additional studies suggest that the levels of expression of [[CR1]] and the complement regulator [[CD55]] on erythrocytes vary with age, being low in young children and increasing with age. It is proposed that the interplay between the rate at which immunity develops during malaria exposure and the changes in levels of erythrocyte complement-regulatory proteins that occur with age might contribute to the differences in epidemiology of severe malaria-associated anaemia and cerebral malaria.
|mesh-terms=* Aging
* Anemia
* Animals
* CD55 Antigens
* Disease Susceptibility
* Erythrocytes
* Humans
* Malaria
* Malaria, Cerebral
* Receptors, Complement
* Rosette Formation

|full-text-url=https://sci-hub.do/10.1016/j.pt.2005.03.004
}}