Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

FcR gamma chain deletion results in pleiotrophic effector cell defects.

Cell | Feb 11, 1994

http://www.ncbi.nlm.nih.gov/pubmed/8313472

The gamma subunit of immunoglobulin Fc receptors is an essential component of the high-affinity receptor for IgG (Fc gamma RIII) and is associated with the high-affinity receptor for IgG (Fc gamma RI) 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 gamma 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 gamma 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.

Pubmed ID: 8313472 RIS Download

Mesh terms: Animals | Base Sequence | Blotting, Southern | Cells, Cultured | Chimera | Cytotoxicity, Immunologic | DNA | DNA Primers | Female | Flow Cytometry | Gene Deletion | Genotype | Interleukin-4 | Macromolecular Substances | Macrophages, Peritoneal | Male | Mast Cells | Mice | Mice, Inbred C57BL | Mice, Transgenic | Molecular Sequence Data | Passive Cutaneous Anaphylaxis | Phagocytosis | Polymerase Chain Reaction | Prostaglandin D2 | RNA, Messenger | Receptors, IgE | Receptors, IgG | Spleen | Stem Cells | T-Lymphocytes

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

None

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.