C1q, the first component of the classical pathway of the complement system, interacts with various cell types and triggers a variety of cell-specific cellular responses, such as oxidative burst, chemotaxis, phagocytosis, etc. Different biological responses are attributed to the interaction of C1q with more than one putative cell-surface C1q receptor/C1q-binding protein. Previously, it has been shown that C1q-mediated oxidative burst by neutrophils is not linked to G-protein-coupled fMet-Leu-Phe-mediated response. In the present study, we have investigated neutrophil migration brought about by C1q and tried to identify the signal-transduction pathways involved in the chemotactic response. We found that C1q stimulated neutrophil migration in a dose-dependent manner, primarily by enhancing chemotaxis (directed movement) rather than chemokinesis (random movement). This C1q-induced chemotaxis could be abolished by an inhibitor of G-proteins (pertussis toxin) and PtdIns(3,4,5)P3 kinase (wortmannin and LY294002). The collagen tail of C1q appeared to mediate chemotaxis. gC1qR, a C1q-binding protein, has recently been reported to participate in C1q-mediated chemotaxis of murine mast cells and human eosinophils. We observed that gC1qR enhanced binding of free C1q to adherent neutrophils and promoted C1q-mediated chemotaxis of neutrophils by nearly seven-fold. Our results suggests C1q-mediated chemotaxis involves gC1qR as well as G-protein-coupled signal-transduction mechanisms operating downstream to neutrophil chemotaxis.
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February 1998
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Research Article|
February 15 1998
C1q-mediated chemotaxis by human neutrophils: involvement of gClqR and G-protein signalling mechanisms
E. A. Leonora LEIGH;
E. A. Leonora LEIGH
*MRC Immunochemistry Unit, Department of Biochemistry, University of Oxford, Oxford OX1 3QU, U.K.
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Berhane GHEBREHIWET;
Berhane GHEBREHIWET
†Department of Medicine, State University of New York, Stony Brook, NY 11794, U.S.A., and Department of Pathology, State University of New York, Stony Brook, NY 11794, U.S.A.
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P. S. Tim PERERA;
P. S. Tim PERERA
‡Yamanouchi Research Institute, Littlemore Park, Oxford OX4 4SX, U.K.
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N. Ian BIRD;
N. Ian BIRD
‡Yamanouchi Research Institute, Littlemore Park, Oxford OX4 4SX, U.K.
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Peter STRONG;
Peter STRONG
*MRC Immunochemistry Unit, Department of Biochemistry, University of Oxford, Oxford OX1 3QU, U.K.
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Uday KISHORE;
Uday KISHORE
*MRC Immunochemistry Unit, Department of Biochemistry, University of Oxford, Oxford OX1 3QU, U.K.
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B. M. Kenneth REID;
B. M. Kenneth REID
*MRC Immunochemistry Unit, Department of Biochemistry, University of Oxford, Oxford OX1 3QU, U.K.
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Paul EGGLETON
Paul EGGLETON
1
*MRC Immunochemistry Unit, Department of Biochemistry, University of Oxford, Oxford OX1 3QU, U.K.
1To whom correspondence should be addressed.
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Publisher: Portland Press Ltd
Received:
September 09 1997
Accepted:
October 08 1997
Online ISSN: 1470-8728
Print ISSN: 0264-6021
The Biochemical Society, London © 1998
1998
Biochem J (1998) 330 (1): 247–254.
Article history
Received:
September 09 1997
Accepted:
October 08 1997
Citation
E. A. Leonora LEIGH, Berhane GHEBREHIWET, P. S. Tim PERERA, N. Ian BIRD, Peter STRONG, Uday KISHORE, B. M. Kenneth REID, Paul EGGLETON; C1q-mediated chemotaxis by human neutrophils: involvement of gClqR and G-protein signalling mechanisms. Biochem J 15 February 1998; 330 (1): 247–254. doi: https://doi.org/10.1042/bj3300247
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