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Anti-Mac-1 selectively inhibits the mouse and human type three complement receptor.

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Beller, D I, Springer, T A, Schreiber, R D·1982·The Journal of experimental medicine

Abstract

Anti-Mac-1 (M1/70), a rat monoclonal antibody that reacts with mouse and human macrophages, polymorphonuclear leukocytes (PMNL), and natural killer cells, selectively inhibited complement receptor-mediated rosetting by murine macrophages and human PMNL. Preincubation of macrophages with anti-Mac-1 inhibited formation of rosettes with sheep erythrocytes bearing IgM antibody and murine C3 fragments. No inhibition was observed when other monoclonal antibodies that react with macrophages (such as anti-Ly5, anti-H-2, or anti-pan-leukocyte) were tested at 10-fold higher concentrations. Anti-Mac-1 did not affect macrophage Fc receptor-mediated rosetting. Erythrocytes bearing homogeneous human C3 fragments C3b (EC3b) or C3bi (EC3bi) were used to test the specificity of the murine macrophage and human PMNL complement receptor inhibited by anti-Mac-1. In both cases, anti-Mac-1 inhibited CR3-mediated rosetting of EC3bi but not CR1-dependent rosetting of EC3b. The results show that Mac-1 is either identical to CR3 or closely associated with CR3 function. This is one of the first cases in which a monoclonal antibody-defined differentiation antigen has been associated with a specific cell surface function.

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Metadata

Authors
Beller, D. I., Springer, T. A., & Schreiber, R. D.
Venue
The Journal of experimental medicine
Published
1982-10-01
Volume
156
Issue
4
Pages
1000-1009
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W2105074038
Cited by
606
References
0
FWCI
21.22
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Anti-Mac-1 selectively inhibits the mouse and human type three complement receptor. https://app.cochat.ai/papers/10.1084/jem.156.4.1000
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Beller, D. I., Springer, T. A., & Schreiber, R. D. (1982). Anti-Mac-1 selectively inhibits the mouse and human type three complement receptor. The Journal of experimental medicine. https://doi.org/10.1084/jem.156.4.1000

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.