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Hemolytically inactive C5b67 complex: an agonist of polymorphonuclear leukocytes
C Wang1, S Barbashov, R M Jack
1Charles A. Dana Research Institute, Beth Israel Hospital, Boston, MA 02215, USA.
Blood
|May 1, 1995
Summary
Hemolytically inactive C5b67 (iC5b67) activates human polymorphonuclear leukocytes (PMN) chemotaxis and calcium signaling. This complement fragment impacts PMN function, involving G-proteins and calcium in its signaling pathway.
Area of Science:
- Immunology
- Complement System
- Leukocyte Biology
Background:
- The complement system plays a crucial role in innate and adaptive immunity.
- Complement fragments, like C5b67, are known to activate immune cells.
- Understanding the specific functions of complement components is vital for immunology research.
Purpose of the Study:
- To investigate the functional activity of hemolytically inactive C5b67 (iC5b67) on human polymorphonuclear leukocytes (PMN).
- To elucidate the signaling pathways involved in iC5b67-mediated PMN responses.
- To determine if iC5b67 acts through known complement receptors or signaling cascades.
Main Methods:
- Formation of iC5b67 from purified human complement components.
- Assays for PMN chemotaxis, calcium (Ca2+) fluxes, and superoxide production.
- Analysis of CR1 and CR3 expression, and use of insolubilized anti-C7 for activity removal.
- Pertussis toxin pretreatment to investigate G-protein involvement.
Main Results:
- iC5b67 stimulated PMN chemotaxis and Ca2+ fluxes at nanomolar concentrations.
- iC5b67 inhibited superoxide production and did not upregulate CR1 and CR3.
- iC5b67 signaling involved G-proteins and Ca2+, sharing pathways with C5a and FMLP.
Conclusions:
- Hemolytically inactive C5b67 is a potent agonist for human PMN functional responses.
- iC5b67 induces specific PMN activities, distinct from its lytic function.
- The findings highlight a novel role for complement fragments in modulating leukocyte behavior and signaling.