NDLI: Induction of rapid T cell death and phagocytic activity by Fas-deficient lpr macrophages.

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Induction of rapid T cell death and phagocytic activity by Fas-deficient lpr macrophages.

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Induction of rapid T cell death and phagocytic activity by Fas-deficient lpr macrophages.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Ishimaru, Naozumi Arakaki, Rieko Oura, Ritsuko Kudo, Yasusei Hayashi, Yoshio Yamada, Akiko Tanaka, Eiji
Description	Country affiliation: Japan Author Affiliation: Oura R ( Department of Oral Molecular Pathology, Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima 770-8504, Japan.)
Abstract	Peripheral T cells are maintained by the apoptosis of activated T cells through the Fas-Fas ligand system. Although it is well known that normal T cells fail to survive in the Fas-deficient immune condition, the molecular mechanism for the phenomenon has yet to be elucidated. In this study, we demonstrate that rapid cell death and clearance of normal T cells were induced by Fas-deficient lpr macrophages. Transfer of normal T cells into lpr mice revealed that Fas expression on donor T cells was promptly enhanced through the IFN-Î³/IFN-Î³R. In addition, Fas ligand expression and phagocytic activity of lpr macrophages were promoted through increased NF-κB activation. Controlling Fas expression on macrophages plays an essential role in maintaining T cell homeostasis in the peripheral immune system. Our data suggest a critical implication to the therapeutic strategies such as transplantation and immunotherapy for immune disorder or autoimmunity related to abnormal Fas expression.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1103794
Journal	The Journal of Immunology
Issue Number	2
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-01-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antigens, Cd95 Deficiency Macrophages Immunology Metabolism Phagocytosis T-lymphocytes Animals Cell Death Cell Movement Genetics Fas Ligand Protein Gene Expression Regulation Immunomodulation Mice Mice, Inbred Mrl Lpr Mice, Transgenic Nf-kappa B Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Induction of Rapid T Cell Death and Phagocytic Activity by Fas-Deficient lpr Macrophages

Fas (CD95) expression and death-mediating function are induced by CD4 cross-linking on CD4+ T cells.

Fas-independent death of activated CD4(+) T lymphocytes induced by CTLA-4 crosslinking.

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Programmed death ligand 1 regulates a critical checkpoint for autoimmune myocarditis and pneumonitis in MRL mice.

B cell-derived IL-10 does not regulate spontaneous systemic autoimmunity in MRL.Fas(lpr) mice.

Deficient leptin signaling ameliorates systemic lupus erythematosus lesions in MRL/Mp-Fas lpr mice.

Correction of accelerated autoimmune disease by early replacement of the mutated lpr gene with the normal Fas apoptosis gene in the T cells of transgenic MRL-lpr/lpr mice.

Rapid B cell apoptosis induced by antigen receptor ligation does not require Fas (CD95/APO-1), the adaptor protein FADD/MORT1 or CrmA-sensitive caspases but is defective in both MRL-+/+ and MRL-lpr/lpr mice

Induction of rapid T cell death and phagocytic activity by Fas-deficient lpr macrophages.

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Induction of Rapid T Cell Death and Phagocytic Activity by Fas-Deficient lpr Macrophages

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Induction of rapid T cell death and phagocytic activity by Fas-deficient lpr macrophages.