Surface markers of complement receptor lymphocytes.

Ross, Gordon D.; Winchester, Robert; Rabellino, Enrique M.; Hoffman, Thomas

doi:10.1172/jci109214

Cited by 29 publications

(13 citation statements)

References 33 publications

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“…Furthermore, CR1 and CR2 are probably not adjacent on the cell surface, because saturation of B cell membranes with Fab' anti-CR1 inhibited only CR1 rosettes (4,5) and saturation with F(ab')2 anti-CR2 inhibited only CR2 rosettes. Finally, even though most normal B cells express both CR1 and CR2 simultaneously, a low proportion of normal B lymphocytes also express either CR1 or CR2 individually (9,14).…”

Section: Discussionmentioning

confidence: 98%

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Isolation of lymphocyte membrane complement receptor type two (the C3d receptor) and preparation of receptor-specific antibody.

Lambris¹,

Dobson²,

Ross³

1981

Proc. Natl. Acad. Sci. U.S.A.

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A glycoprotein binding complement component C3d was isolated from media used for culture of Raji human lymphoblastoid cells. Analysis by sodium dodecyl sulfate/polyacrylamide gel electrophoresis. and gas/liquid chromatography indicated that the C3d-binding glycoprotein consisted of a single polypeptide chain with extensive intrachain. disulfide bonds, a molecular weight of 72,000, and several different bound carbohydrates. Several, lines of evidence-indicated that this mediumderived C3d-binding protein originated from membrane complement receptor type two (CR2, the C3d receptor), presumably shed during membrane turnover. The C3d-binding protein bound to sheep erythrocytes coated with C3d (EC3d) but not to sheep erythrocytes coated with C3b (EC3b). Antisera, prepared by immunization with the purified C3d-binding glycoprotein, inhibited lymphocyte rosette formation with EC3d but not with ECAb. Analysis by sodium dodecyl sulfate gel electrophoresis of the radiolabeled and. solubilized lymphocyte antigens reactive with the anti-C3d-binding protein sera revealed a single-chain cell-surface protein of molecular weight 72,000 that was apparently identical to the isolated C3d-binding protein. Parallel assay of lymphocytes for CR2 by direct immunofluorescence withlF(ab')2 anti-C3d-binding protein (anti-CR2) and rosette formation with EC3d indicated that both assays had the same specificity and nearly the same sensitivity. With both systems CR2 expression was limited to B cells, and was undetectable on T cells, monocytes, or neutrophils.Bone marrow-derived (B) lymphocytes express two distinct types of membrane receptors for the third component of complement (C3) (1), a receptor for f1lH globulin (2) and' surfacebound C5 (3). Complement (C) receptor type one (CR1, the C3b receptor) has recently been isolated and shown to be a 205,000 Mr glycoprotein (4). Isolated CR1 bound to both C4b, and Cab, and lymphocytes treated with Fab' anti-CRI did not form rosettes with the erythrocyte-complement complexes EC3b or EAC14b (5). Previous attempts to isolate lymphocyte C recteptor type two (CR2, the C3d receptor) have been unsuccessful (6). CR2 differs from CRI in that it is expressed exclusively on lymphocytes, whereas CR1 is also expressed on monocytes, neutrophils, erythrocytes, and, kidney cells (7). Although the functions of CR1 and. CR2 are unknown, B colls do respond to either 81H receptor triggering or the cleavage of surface C5 by releasing endogenous C3b inactivator (C3bINA) (2, *).In the present study, media from B-type lymphoblastoid cells were shown to contain a soluble C3d-binding protein. This C3d-binding protein was purified and found to be a glycoprotein of 72,000 Mr. Antibody prepared by immunization of rabbits with the C3d-binding protein inhibited lymphocyte rosette formation with EC3d'but not with EC3b, and reacted with a single cell-surface protein of 72,000 Mr. MATERIALS AND METHODSLymphoid Cells, Neutrophils, and Spent Culture Media. Normal human blood mononuclear cells and neutrophils were isolated o...

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Section: Discussionmentioning

confidence: 98%

“…C receptors and surface Ig were detected by rosette assay and immunofluorescence, respectively (2,12,14). Fluid-phase C3d-binding protein (CR2) was detected by two different assays with EC3d containing 1.5 X 103 C3d molecules per EC3d complex.…”

Section: Methodsmentioning

confidence: 99%

Isolation of lymphocyte membrane complement receptor type two (the C3d receptor) and preparation of receptor-specific antibody.

Lambris¹,

Dobson²,

Ross³

1981

Proc. Natl. Acad. Sci. U.S.A.

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“…EA(IgM)C3b indicator cells were prepared with purified human complement components and AKR mouse serum exactly as described by Ross and Polley (1976). Human C1 and C4 were prepared as described (Ross and Polley, 1976), and human C2 was obtained commercially (Cordis Labs, Miami, FL).…”

Section: Cellsmentioning

confidence: 99%

“…Human C1 and C4 were prepared as described (Ross and Polley, 1976), and human C2 was obtained commercially (Cordis Labs, Miami, FL). Briefly, 50 p1 of C1 was added to 1.0 ml of a 2.5% suspension of EA(IgM), and the mixture was incubated for 15 minutes at 37°C.…”

Section: Cellsmentioning

confidence: 99%

“…Briefly, 50 p1 of C1 was added to 1.0 ml of a 2.5% suspension of EA(IgM), and the mixture was incubated for 15 minutes at 37°C. After washing, the cells were resuspended and incubated in a predetermined optimal concentration of C4 (Ross and Polley, 1976) followed by incubation in freshly oxidized C2. Mouse C3b was coupled to the complex by resuspending cells in 2.5 ml of GVB containing 1.5 mglml Suramin (Mobay Chemical Corporation, New York, NY) and freshly thawed AKR mouse serum diluted 1:5.…”

Section: Cellsmentioning

confidence: 99%

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Complement receptor phenotypes of culture‐derived murine macrophages

Walker

Yen

1982

Journal Cellular Physiology

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The distribution of complement receptors CR1 and CR3 among macrophages derived from cultures of bone marrow, blood, and elicited or normal peritoneal cell populations was studied. Cells and colonies from the first three sources had a common phenotype, CR1+3-, whereas those from the normal peritoneal populations had either CR1+3- or CR1+3+. The former phenotype characterized spindle-shaped as well as epithelial-like macrophages; the latter was essentially restricted to colonies made up of the epithelioid cells. Both morphologic features and the CR phenotypes remained stable throughout the culture period. These phenotypic differences might be explained by the presence of at least two clonally derived types of macrophages.

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Coexistence of a primary immunodeficiency disorder and hodgkin's disease: Evidence against a B-Lymphocyte origin for the reed-sternberg cell

Bobrove

Onder

Myers

et al. 1981

Cancer

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A 44-year-old woman with a lifelong history of recurrent sinopulmonary infections developed Hodgkin's disease with characteristic Reed-Sternberg cells in a biopsy specimen of a mediastinal lymph node. Hypogammaglohulinemia was documented on several serum determinations and plasma cells were absent from biopsy specimens of the lymph node and bone marrow. lmmunochemical studies failed to demonstrate any B lymphocytes bearing surface immunoglobulin or Fc-receptors for IgC in the peripheral blood. Pokeweed mitogen stimulation of the patient's peripheral blood lymphocytes in vitro resulted in the development of virtually no plasma cells. Peripheral blood T-lymphocyte number and function were defective initially. Following chemotherapy and radiotherapy, peripheral blood E-rosette-forming cells returned to normal, hut T-cell function remained defective and B lymphocytes remained undetectable. These findings are compatible with the presence of two separate immune disorders: a primary hypo-gammaglobulinemia and Hodgkin's disease. The absence of lymphocytes bearing surface Ig or Fc-receptors for IgC in this patient adds further support against a B-lymphocyte origin for the Reed-Sternherg cell.

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Surface markers of complement receptor lymphocytes.

Cited by 29 publications

References 33 publications

Isolation of lymphocyte membrane complement receptor type two (the C3d receptor) and preparation of receptor-specific antibody.

Isolation of lymphocyte membrane complement receptor type two (the C3d receptor) and preparation of receptor-specific antibody.

Complement receptor phenotypes of culture‐derived murine macrophages

Coexistence of a primary immunodeficiency disorder and hodgkin's disease: Evidence against a B-Lymphocyte origin for the reed-sternberg cell

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