Apoptosis-Linked Gene 2-Deficient Mice Exhibit Normal T-Cell Development and Function

Author:

Jang Ihn Kyung1,Hu Renju1,Lacaná Emanuela2,D'Adamio Luciano3,Gu Hua1

Affiliation:

1. Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 20852

2. Division of Hematologic Products, Center for Biological Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892

3. Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York 10461

Abstract

ABSTRACT The apoptosis-linked gene product, ALG-2, is a member of the family of intracellular Ca 2+ -binding proteins and a part of the apoptotic machinery controlled by T-cell receptor (TCR), Fas, and glucocorticoid signals. To explore the physiologic function of ALG-2 in T-cell development and function, we generated mice harboring a null mutation in the alg - 2 gene. The alg - 2 null mutant mice were viable and fertile and showed neither gross developmental abnormality nor immune dysfunction. Analyses of apoptotic responses of ALG-2-deficient T cells demonstrated that ALG-2 deficiency failed to block apoptosis induced by TCR, Fas, or dexamethasone signals. These findings indicate that ALG-2 is physiologically dispensable for apoptotic responses induced by the above signaling pathways and suggest that other functionally redundant proteins might exist in mammalian cells.

Publisher

American Society for Microbiology

Subject

Cell Biology,Molecular Biology

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