Literature DB >> 6970220

Identification of types of cells in human peripheral blood that bind C1q.

A J Tenner, N R Cooper.   

Abstract

Earlier studies showed that approximately 26% of the cells present in human mononuclear cell preparations had the ability to bind purified monomeric C1q. The present studies were initiated to identify the cell types comprising the C1q binding population. Double marker fluorescence, rosetting, and morphologic studies on cell preparations depleted of or enriched in various cell types were simultaneously employed to identify those subpopulations that bound C1q. C1q binding was detected by fluorescent techniques (with FI-F(ab')2 anti-C1q). Monocytes in mononuclear cell preparations were detected by the ability to phagocytose carbonyl iron. B cells were identified by reactivity with rhodamine-conjugated F(ab')2 anti-human F(ab')2 and by rosetting with erythrocytes bearing C3b. These studies showed that monocytes and B lymphocytes comprised the majority of C1q-binding cells in mononuclear cell preparations, whereas T lymphocytes lacked this property. In addition, a minor population of nonphagocytic cells in such preparations that lacked B and T cell markers also bound C1q. Finally, a high but variable proportion of polymorphonuclear leukocytes bound C1q. Binding of C1q to PMN was concentration-dependent, saturable and specific and exhibited an equilibrium constant of 0.76 X 10(7) M-1. Thus, PMN also possess a specific receptor for C1q.

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Year:  1981        PMID: 6970220

Source DB:  PubMed          Journal:  J Immunol        ISSN: 0022-1767            Impact factor:   5.422


  25 in total

1.  Identification of C1q as the heat-labile serum cofactor required for immune complexes to stimulate endothelial expression of the adhesion molecules E-selectin and intercellular and vascular cell adhesion molecules 1.

Authors:  C Lozada; R I Levin; M Huie; R Hirschhorn; D Naime; M Whitlow; P A Recht; B Golden; B N Cronstein
Journal:  Proc Natl Acad Sci U S A       Date:  1995-08-29       Impact factor: 11.205

2.  C1q-mediated chemotaxis by human neutrophils: involvement of gClqR and G-protein signalling mechanisms.

Authors:  L E Leigh; B Ghebrehiwet; T P Perera; I N Bird; P Strong; U Kishore; K B Reid; P Eggleton
Journal:  Biochem J       Date:  1998-02-15       Impact factor: 3.857

3.  Molecular modelling of human complement subcomponent C1q and its complex with C1r2C1s2 derived from neutron-scattering curves and hydrodynamic properties.

Authors:  S J Perkins
Journal:  Biochem J       Date:  1985-05-15       Impact factor: 3.857

4.  Complement subcomponent C1q secreted by cultured human monocytes has subunit structure identical with that of serum C1q.

Authors:  A J Tenner; D B Volkin
Journal:  Biochem J       Date:  1986-01-15       Impact factor: 3.857

5.  Serum levels of RHP and of unbound C1q in rheumatoid arthritis and systemic lupus erythematosus.

Authors:  C L Rosano; N Parhami; K E Hechemy; C Hurwitz
Journal:  Inflammation       Date:  1988-08       Impact factor: 4.092

6.  Characterization of C1q-binding material released from the membranes of Raji and U937 cells by limited proteolysis with trypsin.

Authors:  A Erdei; K B Reid
Journal:  Biochem J       Date:  1988-10-15       Impact factor: 3.857

7.  Receptors for complement components in inflammation.

Authors:  A Sobel; C Blanc; A Cattaneo; M Moisy; M Lopez-Trascasa; J J Bourgarit; Y Gabay
Journal:  Agents Actions       Date:  1983-08

8.  Identification of a gC1q-binding protein (gC1q-R) on the surface of human neutrophils. Subcellular localization and binding properties in comparison with the cC1q-R.

Authors:  P Eggleton; B Ghebrehiwet; K N Sastry; J P Coburn; K S Zaner; K B Reid; A I Tauber
Journal:  J Clin Invest       Date:  1995-04       Impact factor: 14.808

9.  Evidence for intrinsic cellular defects of 'complement' receptor-mediated phagocytosis in patients with systemic lupus erythematosus (SLE).

Authors:  N P Hurst; G Nuki; T Wallington
Journal:  Clin Exp Immunol       Date:  1984-02       Impact factor: 4.330

10.  Fluid-phase interaction of C1 inhibitor (C1 Inh) and the subcomponents C1r and C1s of the first component of complement, C1.

Authors:  S Chesne; C L Villiers; G J Arlaud; M B Lacroix; M G Colomb
Journal:  Biochem J       Date:  1982-01-01       Impact factor: 3.857

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