Biomaterial Database

C3 receptors on granulocytes from patients with rheumatoid arthritis and Felty's syndrome. 1984

F C Breedveld, and G J Lafeber, and E De Vries, and M R Daha, and A Cats

The expression of receptors for the third component of complement (C3R) on polymorphonuclear cells (PMN) from patients with rheumatoid arthritis (RA) or Felty's syndrome (FS) and healthy controls (HC) was studied by means of a rosetting technique using ox erythrocytes coated with rabbit IgM and mouse complement. The percentage of rosette forming PMN (RF-PMN) was found to be increased in patients with FS (59%) and patients with RA (47%) compared to HC (18%), when measured directly after cold isolation of PMN. Incubation at 37 degrees C of cold isolated cells increased the percentage of RF-PMN in all three groups, although the values were significantly higher during the first 45 min of incubation in both patient groups. When incubated with serum from patients with FS at 37 degrees C, cold isolated donor PMN formed significantly more rosettes than after incubation with donor serum. This increase was shown to be due to the presence of circulating immune complexes in the patient sera and could be mimicked by incubating donor PMN with aggregated human IgG. As a result of these experiments it was demonstrated that the increased percentages of PMN with C3R in patients with FS or RA are most likely caused by a previous in vivo activation of PMN by immune complexes. The possible effect of such an increase in C3R expression in relation to PMN function in these patients is discussed.

UI	MeSH Term	Description	Entries
D007958	Leukocyte Count	The number of WHITE BLOOD CELLS per unit volume in venous BLOOD. A differential leukocyte count measures the relative numbers of the different types of white cells.	Blood Cell Count, White,Differential Leukocyte Count,Leukocyte Count, Differential,Leukocyte Number,White Blood Cell Count,Count, Differential Leukocyte,Count, Leukocyte,Counts, Differential Leukocyte,Counts, Leukocyte,Differential Leukocyte Counts,Leukocyte Counts,Leukocyte Counts, Differential,Leukocyte Numbers,Number, Leukocyte,Numbers, Leukocyte
D009504	Neutrophils	Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes.	LE Cells,Leukocytes, Polymorphonuclear,Polymorphonuclear Leukocytes,Polymorphonuclear Neutrophils,Neutrophil Band Cells,Band Cell, Neutrophil,Cell, LE,LE Cell,Leukocyte, Polymorphonuclear,Neutrophil,Neutrophil Band Cell,Neutrophil, Polymorphonuclear,Polymorphonuclear Leukocyte,Polymorphonuclear Neutrophil
D011947	Receptors, Antigen, B-Cell	IMMUNOGLOBULINS on the surface of B-LYMPHOCYTES. Their MESSENGER RNA contains an EXON with a membrane spanning sequence, producing immunoglobulins in the form of type I transmembrane proteins as opposed to secreted immunoglobulins (ANTIBODIES) which do not contain the membrane spanning segment.	Antigen Receptors, B-Cell,B-Cell Antigen Receptor,B-Cell Antigen Receptors,Surface Immunoglobulin,Immunoglobulins, Membrane-Bound,Immunoglobulins, Surface,Membrane Bound Immunoglobulin,Membrane-Bound Immunoglobulins,Receptors, Antigen, B Cell,Surface Immunoglobulins,Antigen Receptor, B-Cell,Antigen Receptors, B Cell,B Cell Antigen Receptor,B Cell Antigen Receptors,Bound Immunoglobulin, Membrane,Immunoglobulin, Membrane Bound,Immunoglobulin, Surface,Immunoglobulins, Membrane Bound,Membrane Bound Immunoglobulins,Receptor, B-Cell Antigen,Receptors, B-Cell Antigen
D011951	Receptors, Complement	Molecules on the surface of some B-lymphocytes and macrophages, that recognize and combine with the C3b, C3d, C1q, and C4b components of complement.	Complement Receptors,Complement Receptor,Complement Receptor Type 1,Receptor, Complement
D003165	Complement System Proteins	Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).	Complement Proteins,Complement,Complement Protein,Hemolytic Complement,Complement, Hemolytic,Protein, Complement,Proteins, Complement,Proteins, Complement System
D003176	Complement C3	A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase.	C3 Complement,C3 Precursor,Complement 3,Complement C3 Precursor,Complement Component 3,Precursor-Complement 3,Pro-C3,Pro-Complement 3,C3 Precursor, Complement,C3, Complement,Complement, C3,Component 3, Complement,Precursor Complement 3,Precursor, C3,Precursor, Complement C3,Pro C3,Pro Complement 3
D005258	Felty Syndrome	A rare complication of rheumatoid arthritis with autoimmune NEUTROPENIA; and SPLENOMEGALY.	Felty's Syndrome,Familial Felty Syndrome,Familial Felty's Syndrome,Rheumatoid Arthritis, Splenomegaly and Neutropenia,Familial Feltys Syndrome,Felty Syndrome, Familial,Felty's Syndrome, Familial,Feltys Syndrome,Syndrome, Familial Felty,Syndrome, Familial Felty's,Syndrome, Felty,Syndrome, Felty's
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000936	Antigen-Antibody Complex	The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes IMMUNE COMPLEX DISEASES.	Immune Complex,Antigen-Antibody Complexes,Immune Complexes,Antigen Antibody Complex,Antigen Antibody Complexes,Complex, Antigen-Antibody,Complex, Immune,Complexes, Antigen-Antibody,Complexes, Immune
D001172	Arthritis, Rheumatoid	A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.	Rheumatoid Arthritis