rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
1989-3-13
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pubmed:abstractText |
Several chymotryptic-type protease inhibitors were found to inhibit both anti-CD3 mAb- and PHA-induced rise in Ca2+ and IL-2 production in Jurkat T cells. The magnitude of inhibition was a function of the effectors used to stimulate Ca2+ entry and depended on the concentration of the inhibitors. Neither tryptic-type protease inhibitors nor an elastase substrate prevented anti-CD3 mAb- or PHA-induced Ca2+ rise in Jurkat cells. The inhibitory effect of N-alpha-p-tosyl-L-phenylalanine chloromethyl-ketone on anti-CD3 mAb- and PHA-induced rise in Ca2+ resulted from a rapid increase in Ca2+ efflux. The inhibitors which were effective on Ca2+ mobilization also inhibited IL-2 production initiated by an anti-CD3 mAb in the presence of 12-O-tetradecanoylphorbol-13-acetate, and to a lesser extent by PHA or the calcium ionophore A23187. No inhibition of IL-2 production was observed when tryptic-type protease inhibitors or the elastase inhibitor were used. In addition, membrane preparations from Jurkat cells were found to hydrolyze the chymotryptic substrate Suc-Ala-Ala-Phe-paranitroaniline, an effect markedly inhibited by N-alpha-p-tosyl-L-phenylalanine chloromethylketone. Moreover, this inhibitor protected one potential endogenous substrate (Mr 38 kDa) from proteolysis. Taken together, these observations show that chymotryptic-type protease inhibitors block the responses generated by the binding of anti-CD3 mAb to Jurkat cells, and suggest that a chymotryptic-like membrane protease contributes to T cell activation.
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/Calcimycin,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Chymotrypsin,
http://linkedlifedata.com/resource/pubmed/chemical/Egtazic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Immunosuppressive Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Phytohemagglutinins,
http://linkedlifedata.com/resource/pubmed/chemical/Protease Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell,
http://linkedlifedata.com/resource/pubmed/chemical/Tosylphenylalanyl Chloromethyl...
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0022-1767
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
142
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1253-9
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:2521661-Antibodies, Monoclonal,
pubmed-meshheading:2521661-Antigens, CD3,
pubmed-meshheading:2521661-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:2521661-Calcimycin,
pubmed-meshheading:2521661-Calcium,
pubmed-meshheading:2521661-Cell Line,
pubmed-meshheading:2521661-Cell Membrane,
pubmed-meshheading:2521661-Chymotrypsin,
pubmed-meshheading:2521661-Dose-Response Relationship, Immunologic,
pubmed-meshheading:2521661-Egtazic Acid,
pubmed-meshheading:2521661-Humans,
pubmed-meshheading:2521661-Hydrolysis,
pubmed-meshheading:2521661-Immunosuppressive Agents,
pubmed-meshheading:2521661-Interleukin-2,
pubmed-meshheading:2521661-Lymphocyte Activation,
pubmed-meshheading:2521661-Membrane Proteins,
pubmed-meshheading:2521661-Molecular Weight,
pubmed-meshheading:2521661-Phytohemagglutinins,
pubmed-meshheading:2521661-Protease Inhibitors,
pubmed-meshheading:2521661-Receptors, Antigen, T-Cell,
pubmed-meshheading:2521661-T-Lymphocytes,
pubmed-meshheading:2521661-Tosylphenylalanyl Chloromethyl Ketone
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pubmed:year |
1989
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pubmed:articleTitle |
Chymotryptic-type protease inhibitors block the increase in Ca2+ and Il-2 production in activated Jurkat T cells.
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pubmed:affiliation |
Institut National de la Santé et de la Recherche Médicale U210, Nice, France.
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pubmed:publicationType |
Journal Article
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