Signaling for death of lymphoid cells.

Current opinion in immunology ·Vol. 5 ·No. 3 ·1993-06-00 ·Pages 368-73

King LB, Ashwell JD

Abstract

The induction of programmed cell death in lymphocytes is a common response to a wide variety of physiological and pharmacological stimuli. While there is still much to be learned about the transmembrane signals that lead to programmed cell death, progress has been made in identifying new cell surface molecules (e.g. APO-1/Fas) that may regulate the physiological induction of lymphocyte death, molecules whose expression inhibits apoptosis (e.g. Bcl-2), and the antagonism of activation-induced cell death in T-cell hybridomas and thymocytes by members of the steroid receptor superfamily.

MeSH Terms

Animals Antigens, Surface/physiology Apoptosis/physiology Autoimmunity Calcium/physiology Granzymes Humans Lymphocyte Activation/physiology Lymphocytes/cytology Mice Models, Biological Protein Kinase C/physiology Proto-Oncogene Proteins/physiology Proto-Oncogene Proteins c-bcl-2 Proto-Oncogene Proteins c-myc/biosynthesis,genetics Receptors, Glucocorticoid/physiology Serine Endopeptidases/physiology Signal Transduction/physiology Transcription Factors/physiology Transcription, Genetic Tretinoin/pharmacology fas Receptor

Chemicals

Antigens, Surface Proto-Oncogene Proteins Proto-Oncogene Proteins c-bcl-2 Proto-Oncogene Proteins c-myc Receptors, Glucocorticoid Transcription Factors fas Receptor Tretinoin Protein Kinase C Granzymes Serine Endopeptidases GZMA protein, human Calcium

Authors & Affiliations

2 authors, click to expand affiliations / ORCID

King L B

National Cancer Institute, National Institutes of Health, Bethesda.

Ashwell J D

Article Info

Journal

Current opinion in immunology

Abbr.

Curr Opin Immunol

ISSN

0952-7915

DOI

10.1016/0952-7915(93)90055-w

Published

1993-06-00

Pages

368-73

Language

English

Region

England

NLM ID

8900118

Subset

External Links

PubMed source DOI: 10.1016/0952-7915(93)90055-w View journal details

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