Effector or target cell selection mediated by C3 bridges

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Potential effector cells (including stimulated lymphocytes and cultured monocytes) and potential target cells of NK and AK type cytotoxic reactions (including several lymphoblastoid cell lines) cleave the third complement component (C3). As a result of expression of C3bA sites such cells are able to bind covalently the activated C3b through its metastable binding site and thereby become "armed" by the C3b. This permits C3b-bridge formation between these cells and CR1-bearing cells. The "effector selection" (i.e. when C3b is bound covalently to potential target cells) or "target selection" (when C3b is covalently bound to C3bA sites on potential effector cells) mediated by C3b bridges results in enhanced killing capacity. Macrophages activate and bind C3b as well; but the covalent binding of C3b by these cells inhibits Fc receptor mediated ADCC type killing.

Original languageEnglish
Pages (from-to)243-248
Number of pages6
JournalImmunology Letters
Volume14
Issue number3
DOIs
Publication statusPublished - 1987

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Antibody-Dependent Cell Cytotoxicity
Complement C3
Fc Receptors
Natural Killer Cells
Monocytes
Macrophages
Binding Sites
Lymphocytes
Cell Line

Keywords

  • Antibody dependent cellular cytotoxicity
  • Associative recognition
  • C3
  • Natural killer

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Effector or target cell selection mediated by C3 bridges. / Gergely, J.; Erdei, A.; Sármay, G.; Klein, Eva.

In: Immunology Letters, Vol. 14, No. 3, 1987, p. 243-248.

Research output: Contribution to journalArticle

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AU - Erdei, A.

AU - Sármay, G.

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AB - Potential effector cells (including stimulated lymphocytes and cultured monocytes) and potential target cells of NK and AK type cytotoxic reactions (including several lymphoblastoid cell lines) cleave the third complement component (C3). As a result of expression of C3bA sites such cells are able to bind covalently the activated C3b through its metastable binding site and thereby become "armed" by the C3b. This permits C3b-bridge formation between these cells and CR1-bearing cells. The "effector selection" (i.e. when C3b is bound covalently to potential target cells) or "target selection" (when C3b is covalently bound to C3bA sites on potential effector cells) mediated by C3b bridges results in enhanced killing capacity. Macrophages activate and bind C3b as well; but the covalent binding of C3b by these cells inhibits Fc receptor mediated ADCC type killing.

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