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Anti-Mac-1 selectively inhibits the mouse and human type three complement receptor
The Journal of Experimental Medicine
|October 1, 1982
Summary
The anti-Mac-1 antibody selectively inhibits complement receptor function in macrophages and neutrophils. This suggests Mac-1 is crucial for complement receptor 3 (CR3) activity.
Area of Science:
- Immunology
- Cell Biology
Background:
- Macrophages and polymorphonuclear leukocytes (PMNL) play key roles in immune responses.
- Complement receptors mediate crucial cellular functions, including phagocytosis and inflammation.
Purpose of the Study:
- To investigate the function of the Mac-1 antigen on immune cells.
- To determine if Mac-1 is involved in complement receptor-mediated interactions.
Main Methods:
- Utilized a rat monoclonal antibody, anti-Mac-1 (M1/70), to target the Mac-1 antigen.
- Assessed the antibody's effect on complement receptor-mediated rosetting of erythrocytes by murine macrophages and human PMNL.
- Tested specificity using erythrocytes coated with C3b (EC3b) and C3bi (EC3bi) fragments.
Main Results:
- Anti-Mac-1 selectively inhibited complement receptor-mediated rosetting by macrophages and PMNL.
- The antibody blocked rosetting with C3bi-coated erythrocytes (EC3bi), indicating involvement with CR3.
- No inhibition of Fc receptor-mediated rosetting was observed.
Conclusions:
- Mac-1 is either identical to or closely associated with the complement receptor 3 (CR3).
- This study provides early evidence linking a monoclonal antibody-defined differentiation antigen to a specific cell surface function.