FcR γ chain deletion results in pleiotrophic effector cell defects Journal Article


Authors: Takai, T.; Li, M.; Sylvestre, D.; Clynes, R.; Ravetch, J. V.
Article Title: FcR γ chain deletion results in pleiotrophic effector cell defects
Abstract: The γ subunit of immunoglobulin Fc receptors is an essential component of the high-affinity receptor for IgE (FcεRI) and the low-affinity receptor for IgG (FcγRIII) and is associated with the high-affinity receptor for IgG (FcγRI) and the T cell receptor-CD3 complex. It is required for both receptor assembly and signal transduction. Targeted disruption of this subunit results in immunocompromised mice. Activated macrophages from γ chain-deficient mice unexpectedly lack the ability to phagocytose antibody-coated particles, despite normal binding. Defects in NK cell-mediated antibody-dependent cytotoxicity and mast cell-mediated allergic responses are evident in these animals, establishing the indispensable role of FcRs in these responses. However, loss of γ chain does not appear to perturb T cell development, since both thymic and peripheral T cell populations appear normal. These mice thus represent an important tool for evaluating the role of these receptors in humoral and cellular immune responses. © 1994.
Keywords: gene deletion; nonhuman; flow cytometry; mutant protein; polymerase chain reaction; t-lymphocytes; animal cell; mouse; animal; mice; cells, cultured; spleen; genotype; mice, inbred c57bl; animalia; mice, transgenic; chimera; dna; molecular sequence data; rna, messenger; stem cells; natural killer cell; base sequence; fc receptor; cytotoxicity, immunologic; receptors, igg; dna primers; immune deficiency; phagocytosis; antibody dependent cellular cytotoxicity; interleukin-4; mast cell; mast cells; receptors, ige; macrophage activation; blotting, southern; receptor subunit; male; female; priority journal; article; support, non-u.s. gov't; support, u.s. gov't, p.h.s.; macromolecular systems; macrophages, peritoneal; passive cutaneous anaphylaxis; prostaglandin d2
Journal Title: Cell
Volume: 76
Issue: 3
ISSN: 0092-8674
Publisher: Cell Press  
Date Published: 1994-02-11
Start Page: 519
End Page: 529
Language: English
DOI: 10.1016/0092-8674(94)90115-5
PROVIDER: scopus
PUBMED: 8313472
DOI/URL:
Notes: Source: Scopus
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  1. Raphael A Clynes
    6 Clynes
  2. Jeffrey V. Ravetch
    72 Ravetch