NDLI: The Fas protein is expressed at high levels on CD4+CD8+ thymocytes and activated mature lymphocytes in normal mice but not in the lupus-prone strain, MRL lpr/lpr.

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The Fas protein is expressed at high levels on CD4+CD8+ thymocytes and activated mature lymphocytes in normal mice but not in the lupus-prone strain, MRL lpr/lpr.

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The Fas protein is expressed at high levels on CD4+CD8+ thymocytes and activated mature lymphocytes in normal mice but not in the lupus-prone strain, MRL lpr/lpr.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Brot, N. Elkon, K. B. Drappa, J.
Description	Author Affiliation: Drappa J ( Hospital for Special Surgery, Cornell University Medical College, New York, NY 10021.);
Abstract	The lymphoproliferation (lpr) mutation in the MRL strain of mice is caused by the insertion of the early transposable element ETn in the Fas gene. The insertion causes a striking decrease in Fas mRNA expression and is associated clinically with marked acceleration of the lupus-like disease. To further explore the role of the Fas protein in T-cell selection in the thymus and tolerance in the peripheral immune system, we produced a monospecific polyclonal anti-murine Fas antibody that binds to a polymorphic region of the protein. Fas protein expression was detected on approximately 90% of BALB/c and MRL +/+ thymocytes, and the expression was highest on CD4+CD8+ thymocytes, the stage at which most thymocytes die by apoptosis. In contrast to the high level of expression of Fas on thymocytes, Fas was detected on < 10% of normal splenic T cells. After activation of splenic T cells with Con A or anti-CD3 and interleukin 2, Fas expression increased approximately 10-fold. Fas expression on splenic B cells was also markedly up-regulated after activation with lipopolysaccharide or anti-mu antibodies. The Fas protein was not detected on resting or activated lymphocytes obtained from MRL lpr/lpr mice. Together, these findings suggest that Fas plays a role in both thymic selection and T-cell survival in the periphery and that the accelerated autoimmunity in MRL lpr/lpr mice results from a defect in both of these pathways.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	21
Volume Number	90
Language	English
Publisher	National Academy of Sciences
Publisher Date	1993-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antigens, CD4 Immunology Antigens, CD8 Antigens, Surface Biosynthesis Lupus Erythematosus, Systemic Lymphocyte Activation T-Lymphocyte Subsets Metabolism Amino Acid Sequence Animals Antigens, CD95 Cells, Cultured Flow Cytometry Genetics Mice Mice, Inbred BALB C Mice, Inbred CBA Mice, Mutant Strains Mice, SCID Molecular Sequence Data Polymerase Chain Reaction Protein Biosynthesis RNA, Messenger Spleen Transcription, Genetic Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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