Document Detail

Prevention of anti-CD3 monoclonal antibody-induced thymic apoptosis by protein tyrosine kinase inhibitors.
MedLine Citation:
PMID:  7523495     Owner:  NLM     Status:  MEDLINE    
The thymus gland is crucial for the formation of thymocytes of diverse TCR specificity. Recent studies have demonstrated that deletion (negative selection) of autoreactive thymocytes occurs through the process of apoptosis in which TCR activates cell death by DNA fragmentation. In addition, in vitro stimulation of thymocytes with anti-CD3 mAb, calcium ionophore, or glucocorticoids results in DNA fragmentation followed by cell death. The availability of various substances capable of inhibiting activation-induced programmed cell death of thymocytes may be used as a tool to help identify several important events occurring during the process of apoptosis. We investigated the effect of protein tyrosine kinase (PTK) inhibitors, herbimycin A and genistein, on thymocyte apoptosis induced by stimulation of anti-CD3 mAb or glucocorticoid. Anti-CD3 mAb stimulation resulted in removal of CD4+CD8+ thymocytes by DNA fragmentation. However, in PTK inhibitor-pretreated thymocytes, there was a minimal deletion of double positive thymocytes. In contrast, PTK inhibitors did not prevent glucocorticoid-induced thymic apoptosis. Our results suggest that anti-CD3 mAb-induced thymic apoptosis depends on PTK activation via TCR, and that glucocorticoid-induced thymic apoptosis is PTK-independent.
K Migita; K Eguchi; Y Kawabe; A Mizokami; T Tsukada; S Nagataki
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  153     ISSN:  0022-1767     ISO Abbreviation:  J. Immunol.     Publication Date:  1994 Oct 
Date Detail:
Created Date:  1994-11-10     Completed Date:  1994-11-10     Revised Date:  2012-06-05    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  3457-65     Citation Subset:  AIM; IM    
First Department of Internal Medicine, Nagasaki University School of Medicine, Japan.
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MeSH Terms
Antigens, CD3 / physiology*
Clonal Deletion
Dexamethasone / pharmacology
Isoflavones / pharmacology
Lactams, Macrocyclic
Mice, Inbred BALB C
Protein-Tyrosine Kinases / antagonists & inhibitors*
Proto-Oncogene Proteins / antagonists & inhibitors
Proto-Oncogene Proteins c-fyn
Quinones / pharmacology
T-Lymphocyte Subsets / cytology,  drug effects
Thymus Gland / cytology*
Tyrosine / analogs & derivatives,  metabolism
Reg. No./Substance:
0/Antigens, CD3; 0/Benzoquinones; 0/Isoflavones; 0/Lactams, Macrocyclic; 0/Proto-Oncogene Proteins; 0/Quinones; 21820-51-9/Phosphotyrosine; 446-72-0/Genistein; 50-02-2/Dexamethasone; 55520-40-6/Tyrosine; 70563-58-5/herbimycin; EC Kinases; EC protein, mouse; EC Proteins c-fyn

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