Structure and Modulation of Fc and Complement Receptors

1984 ◽  
pp. 171-187
Author(s):  
Jay C. Unkeless ◽  
Samuel D. Wright
Keyword(s):  
Complement Receptors

Complement Receptors in Neutrophils

1995 ◽  
Vol 15 (2) ◽  
pp. 107-131 ◽  
Author(s):  
Henrik Sengelov
Keyword(s):  
Complement Receptors

scholarly journals New aspects in the regulation of human B cell functions by complement receptors CR1, CR2, CR3 and CR4

2021 ◽  
Author(s):  
Anna Erdei ◽  
Kristóf G. Kovács ◽  
Zsuzsa Nagy-Baló ◽  
Szilvia Lukácsi ◽  
Bernadett Mácsik-Valent ◽  
...  
Keyword(s):  
B Cell ◽  
Complement Receptors ◽  
Cell Functions ◽  
Human B Cell

The complement receptors CD46, CD55 and CD59 are regulated by the tumour microenvironment of head and neck cancer to facilitate escape of complement attack

2014 ◽  
Vol 50 (12) ◽  
pp. 2152-2161 ◽  
Author(s):  
Rebecca Kesselring ◽  
Annette Thiel ◽  
Ralph Pries ◽  
Stefan Fichtner-Feigl ◽  
Stefan Brunner ◽  
...  
Keyword(s):  
Head And Neck Cancer ◽  
Head And Neck ◽  
Neck Cancer ◽  
Tumour Microenvironment ◽  
Complement Receptors

scholarly journals Deficiency of decay-accelerating factor and complement receptor 1–related gene/protein y on murine platelets leads to complement-dependent clearance by the macrophage phagocytic receptor CRIg

Blood ◽  
2008 ◽  
Vol 112 (4) ◽  
pp. 1109-1119 ◽  
Author(s):  
David D. Kim ◽  
Takashi Miwa ◽  
Yuko Kimura ◽  
Reto A. Schwendener ◽  
Menno van Lookeren Campagne ◽  
...  
Keyword(s):  
Human Platelets ◽  
Transfer Model ◽  
Complement Receptor ◽  
Dependent Manner ◽  
Complement Receptors ◽  
Related Gene ◽  
Decay Accelerating Factor ◽  
Gene Ablation ◽  
Complement Receptor 1

Abstract Complement activation on human platelets is known to cause platelet degranulation and activation. To evaluate how normal platelets escape complement attack in vivo, we studied the fate of murine platelets deficient in 2 membrane complement regulatory proteins using an adoptive transfer model. We show here that deficiency of either decay-accelerating factor (DAF) or complement receptor 1–related gene/protein y (Crry) on murine platelets was inconsequential, whereas DAF and Crry double deficiency led to rapid clearance of platelets from circu-lation in a complement- and macrophage-dependent manner. This finding contrasted with the observation on erythrocytes, where Crry deficiency alone resulted in complement susceptibility. Quantitative flow cytometry revealed that DAF and Crry were expressed at similar levels on platelets, whereas Crry expression was 3 times higher than DAF on erythrocytes. Antibody blocking or gene ablation of the newly identified complement receptor CRIg, but not complement receptor 3 (CR3), rescued DAF/Crry-deficient platelets from complement-dependent elimination. Surprisingly, deficiency of CRIg, CR3, and other known complement receptors failed to prevent Crry-deficient erythrocytes from complement-mediated clearance. These results show a critical but redundant role of DAF and Crry in platelet survival and suggest that complement-opsonized platelets and erythrocytes engage different complement receptors on tissue macrophages in vivo.

Modulation in the expression of type 1 (CR1/CD35) and type 3 (CR3/CD11b) complement receptors on leukocytes from patients with Visceral leishmaniasis

2020 ◽  
Vol 218 ◽  
pp. 107970
Author(s):  
Cássio Marinho Campelo ◽  
Igor Carvalho Pinheiro ◽  
Bruno de Melo Tavares ◽  
Guilherme Alves de Lima Henn ◽  
Camila Fernandes ◽  
...  
Keyword(s):  
Visceral Leishmaniasis ◽  
Complement Receptors ◽  
Type 3

scholarly journals Augmentation of macrophage complement receptor function in vitro. I. Characterization of the cellular interactions required for the generation of a T-lymphocyte product that enhances macrophage complement receptor function.

1979 ◽  
Vol 150 (3) ◽  
pp. 653-675 ◽  
Author(s):  
J A Griffin ◽  
F M Griffin
Keyword(s):  
T Lymphocytes ◽  
Complex Disease ◽  
Peritoneal Macrophages ◽  
Fc Receptor ◽  
Microbial Pathogens ◽  
Complement Receptor ◽  
Complement Receptors ◽  
Cellular Interactions ◽  
Receptor Function

The function of complement receptors of mouse peritoneal macrophages was converted in vitro from mediating only attachment of macrophage complement receptor function was achieved by treating freshly explanted macrophages with supernates from cultures containing T lymphocytes and appropriately triggered macrophages. Fc receptor-mediated phagocyctosis by macrophages was required for the production of active supernates, for neither ingestion via the cells' complement receptors nor ingestion via nonimmunologic means was a sufficient stimulus for the macrophages' participation in the generation of supernatant activity. Fc receptor-triggered macrophages interacted by a contact dependent, but histocompatibility independent, mechanism with T lymphocytes, thereby signalling the lymphocytes to elaborate the active product. The possible significance of enhanced macrophage complement receptor function in inflammation, host defense against microbial pathogens, immune complex disease, and neoplasia is discussed.

Complement Receptors

1977 ◽  
pp. 145-176 ◽  
Author(s):  
Celso Bianco ◽  
Victor Nussenzweig
Keyword(s):  
Complement Receptors
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