z-logo
Premium
Recognition of apoptotic cells by human macrophages: inhibition by a monocyte/macrophage‐specific monoclonal antibody
Author(s) -
Flora Pauline K.,
Gregory Christopher D.
Publication year - 1994
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830241109
Subject(s) - biology , monoclonal antibody , macrophage , monocyte , apoptosis , microbiology and biotechnology , immunology , antibody , genetics , in vitro
Abstract Cells undergoing death by apoptosis are rapidly engulfed by phagocytes in vivo , a highly efficient process which prevents leakage of potentially dangerous intracellular contents from dying cells to neighboring tissue. We have tested a panel of monoclonal antibodies (mAb) specifying a range of human monocyte/macrophage surface antigens for their capacity to inhibit the in vitro recognition of apoptotic cells by human peripheral blood monocyte‐derived macrophages. The results identify the antigen defined by the 61D3 mAb, a widely‐used marker of monocyte/macrophage lineage cells, as an important mediator of apoptotic cell recognition. In our system, apoptotic, but not viable, cells were recognized by the cultured macrophages and 61D3 was found to inhibit the recognition of all apoptotic cell types tested, including Ca 2+ ionophore‐treated or growth factor‐depleted B and T lymphocyte lines, tonsillar germinal center B cells, irradiated peripheral blood lymphocytes and senescing neutrophils. Furthermore, the apoptotic cell recognition pathway specified by 61D3 could be distinguished from that involving the macrophage α v β 3 vitronectin receptor which has been shown previously to play an important role in the recognition of apoptotic cells. These results provide further evidence that the mechanisms underlying rapid clearance of apoptotic cells involve multiple phagocyte receptors.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here