The identification of Fc and C3 receptors on human neutrophils

Wong, L G; Wilson, J. D.

doi:10.1016/0022-1759(75)90131-3

Cited by 74 publications

(24 citation statements)

References 9 publications

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“…Furthermore, the amount of nonconvalently bound flavins was also determined in the homogenate of whole granulocytes from patient 112. This value, too, was normal; patient II2, 4.4 pmol/106 granulocytes; 8 controls, 4.6±0.55 pmol/106 granulocytes (mean±SD).…”

Section: Methodsmentioning

confidence: 81%

Cytochrome b deficiency in an autosomal form of chronic granulomatous disease. A third form of chronic granulomatous disease recognized by monocyte hybridization.

Rs¹,

Corbeel²,

Boer³

et al. 1985

J. Clin. Invest.

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Three patients (two sisters and a brother) in one family are described with chronic granulomatous disease. The granulocytes of these patients did not respond with a metabolic burst to various stimuli and failed to kill catalase-positive microorganisms. The magnitude of the cytochrome b signal in the optical spectrum of the patients' granulocytes was <4% of the normal value, whereas the amount of noncovalently bound flavin in these cells was normal. The mode of inheritance of the genetic defect in this family is autosomal because the granulocytes of both parents (first cousins) and a nonaffected sister of the patients expressed 70-80% of the normal cytochrome b signal, showed low-normal or subnormal oxidative reactions during stimulation, and did not display mosaicism in the stimulated nitroblue-tetrazolium slide test. Somatic cell hybridization was performed between the monocytes from the affected boy in this family with monocytes from either a cytochrome b-negative male patient with X-linked chronic granulomatous disease or a cytochrome b-positive male patient with the classic autosomal form of this diseae. In both combinations, monocyte hybrids were observed with nitroblue tetrazolium reductase activity after stimulation with phorbol myristate acetate. This complementation of the oxidase activity required protein synthesis. Our results prove that the defect in this family is genetically distinct from that in the other two forms of chronic granulomatous disease. Moreover, our results also indicate that the expression of cytochrome b in human phagocytes is coded by at least two loci, one on the X chromosome and one on an autosome.

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Section: Methodsmentioning

confidence: 81%

Cytochrome b deficiency in an autosomal form of chronic granulomatous disease. A third form of chronic granulomatous disease recognized by monocyte hybridization.

Rs¹,

Corbeel²,

Boer³

et al. 1985

J. Clin. Invest.

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“…Although there is evidence that the reaction can be enhanced by the presence of C3b on the target cells (2), this phenomenon can occur in the absence of complement (3). A variety of leukocytes bear receptors for the Fc portion of IgG, including B (4), K (4,5), and T (6) lymphocytes, monocytes (7), and polymorphonuclear cells (8); several of these also have membrane receptors for C3b, namely bone marrow-derived (B) lymphocytes (9), monocytes (9), and polymorphonuclear cells (8). Considerable controversy exists over the capability of these various cell types to serve as effectors in antibody-dependent cellular cytotoxicity.…”

Section: Introductionmentioning

confidence: 99%

Antibody-Dependent Cellular Cytotoxicity in Primary Immunodeficiency Diseases and with Normal Leukocyte Subpopulations

Sanal¹,

Buckley²

1978

J. Clin. Invest.

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A B S T R A C T To gain insight into a possible role for antibody-dependent cell-mediated cytotoxicity in vivo, we examined the ability of leukocytes from 28 patients with primary immunodeficiency and from 20 normal controls to lyse three different types of antibody-coated targets in vitro. Mean cytotoxic indices ± 1 SD elicited by unfractionated mononuclear cells from normal controls were 28.74±13.26 for human HLA antibody-coated lymphocyte targets, 42.79±8.27 for rabbit IgG antibody-coated chicken erythrocyte targets, and 47.58±10.34 for human anti-CD (Ripley)-coated O+ erythrocyte targets. Significantly (P = <0.05) lower than normal mean cytotoxic indices against lymphocyte targets were seen with effector cells from 10 patients with X-linked agammaglobulinemia (3.7±4.33), in 10 with common variable agammaglobulinemia (16.05±7.74), in 3 with immunodeficiency with hyper IgM (18.41±4.88), and in 2 with severe combined immunodeficiency (3.94±0.3). Antibody-dependent cytotoxicity against chicken erythrocytes was significantly (P = <0.05) lower than normal only in the common variable agammaglobulinemic group (33.33±12.3) and against human erythrocytes only in the common variable (34.36±9.59) and hyper IgM (27.54±0.66) groups. Rosette and anti-F(ab')2 depletion studies with normal leukocytes indicated that a nonadherent, nonphagocytic, non-Ig-bearing, non-C receptor-bearing, Fc receptor-bearing lymphocyte was the only effector capable of lysing HLA antibody-coated lymphocyte targets.

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“…Dissolved Antrypol was added to other samples of NHS (0.3 ml of Antrypol solution/1 ml NHS before the zymosan treatment) [23]. Aged human serum (AS) was obtained by incuba tion of NHS at 37 °C for 14 days.…”

Section: Chemicals and Seramentioning

confidence: 99%

“…NHS was treated with boiled zymosan as described by Wong and Wilson [23]. Dissolved Antrypol was added to other samples of NHS (0.3 ml of Antrypol solution/1 ml NHS before the zymosan treatment) [23].…”

Section: Chemicals and Seramentioning

confidence: 99%

Studies on the Binding of Complement Factor C3 to the Surface of Human Blood Platelets

Endresen¹,

Mellbye²

1984

Pathophysiol Haemos Thromb

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Employing immunofluorescent staining methods, platelets from several adult patients with chronic idiopathic thrombocytopenic purpura, with systemic lupus erythematosus, and with classical rheumatoid arthritis stained positively with antisera to C3(β₁C and C3dg(α₂D). In some cases, platelet-bound C3dg antigens, but no evidence of other C3 antigens were observed. Platelets that were positive for C3 and/or C3dg were always positive for IgG or for both IgG and IgM. Platelets from normal subjects stained negatively for C3, C3dg, IgG, and IgM. Furthermore, various incubation experiments were performed to investigate the uptake of C3 and its subfragments on normal platelets. Positive platelet staining for C3 was obtained after incubation with normal and C3b-containing sera, but not after incubation with native C3. Platelets incubated with C3c(β₁A)/C3dg-containing serum gave a positive staining for C3dg, but not for C3c. None of the sera stained positively for IgG or IgM. Thus, in contrast to platelets from several of the patients, no in vivo binding of C3 antigens on normal platelets could be established. However, in vitro they could take up both C3b and C3dg, apparently by specific binding to platelet surface structures.

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The identification of Fc and C3 receptors on human neutrophils

Cited by 74 publications

References 9 publications

Cytochrome b deficiency in an autosomal form of chronic granulomatous disease. A third form of chronic granulomatous disease recognized by monocyte hybridization.

Cytochrome b deficiency in an autosomal form of chronic granulomatous disease. A third form of chronic granulomatous disease recognized by monocyte hybridization.

Antibody-Dependent Cellular Cytotoxicity in Primary Immunodeficiency Diseases and with Normal Leukocyte Subpopulations

Studies on the Binding of Complement Factor C3 to the Surface of Human Blood Platelets

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