RRC ID |
19384
|
Author |
Oura R, Arakaki R, Yamada A, Kudo Y, Tanaka E, Hayashi Y, Ishimaru N.
|
Title |
Induction of rapid T cell death and phagocytic activity by Fas-deficient lpr macrophages.
|
Journal |
J Immunol
|
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-γ/IFN-γR. 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.
|
Volume |
190(2)
|
Pages |
578-85
|
Published |
2013-1-15
|
DOI |
10.4049/jimmunol.1103794
|
PII |
jimmunol.1103794
|
PMID |
23255359
|
PMC |
PMC3539689
|
MeSH |
Animals
Cell Death / immunology
Cell Movement / genetics
Cell Movement / immunology
Fas Ligand Protein / genetics
Fas Ligand Protein / immunology
Gene Expression Regulation
Immunomodulation / genetics
Macrophages / immunology*
Macrophages / metabolism*
Mice
Mice, Inbred MRL lpr
Mice, Transgenic
NF-kappa B / metabolism
Phagocytosis / immunology*
T-Lymphocytes / immunology*
T-Lymphocytes / metabolism*
fas Receptor / deficiency*
|
IF |
4.886
|
Times Cited |
5
|
WOS Category
|
IMMUNOLOGY
|
Resource |
Mice |
RBRC00267 |