| pubmed-article:7685106 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7685106 | lifeskim:mentions | umls-concept:C0081937 | lld:lifeskim |
| pubmed-article:7685106 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:7685106 | lifeskim:mentions | umls-concept:C2267219 | lld:lifeskim |
| pubmed-article:7685106 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:7685106 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:7685106 | pubmed:dateCreated | 1993-7-2 | lld:pubmed |
| pubmed-article:7685106 | pubmed:abstractText | T cells have been shown to express CD26, a known ectoenzyme with dipeptidyl peptidase IV (DPPIV; EC 3.4.14.5) activity in its extracellular domain. CD26 can also deliver a second costimulatory signal and contribute to T-cell activation. In an earlier study, we established CD26-transfected Jurkat T-cell lines and demonstrated that monoclonal antibody-mediated crosslinking of CD26 and CD3 induced interleukin 2 (IL-2) production. To determine the contribution of DPPIV enzymatic activity to the costimulatory activity of CD26, human CD26 cDNA was mutated so that active-site serine was replaced by alanine. The mutant CD26 antigen lacked DPPIV enzyme activity but still retained reactivity with three anti-CD26 monoclonal antibodies directed against distinct epitopes of CD26. After stimulation with a combination of anti-CD26 and anti-CD3 antibodies, wild-type CD26 (DPPIV+)-transfected Jurkat cells produced substantially more IL-2 than did mutant CD26 (DPPIV-) or CD26- control transfectants. Nevertheless, the mutant CD26-transfected cells still produced significantly more IL-2 than did CD26- control transfectants. These results suggest that DPPIV activity plays an important but not absolute role in the co-stimulatory activity of CD26 in this system. We also found that wild-type CD26 (DPPIV+) transfectants produced more IL-2 than mutant CD26 (DPPIV-)-transfected cells or CD26- control transfectants when triggered by stimuli not involving CD26, such as anti-CD3 and phorbol ester. These results suggest that the DPPIV activity of CD26 functions to augment the cellular responses of CD26-transfected Jurkat cells to external stimuli mediated by CD26 and/or the CD3/T-cell receptor complex, thus enhancing IL-2 production. | lld:pubmed |
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| pubmed-article:7685106 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:7685106 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7685106 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7685106 | pubmed:month | May | lld:pubmed |
| pubmed-article:7685106 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:7685106 | pubmed:author | pubmed-author:YaronAA | lld:pubmed |
| pubmed-article:7685106 | pubmed:author | pubmed-author:TanakaTT | lld:pubmed |
| pubmed-article:7685106 | pubmed:author | pubmed-author:SchlossmanS... | lld:pubmed |
| pubmed-article:7685106 | pubmed:author | pubmed-author:MorimotoCC | lld:pubmed |
| pubmed-article:7685106 | pubmed:author | pubmed-author:KameokaJJ | lld:pubmed |
| pubmed-article:7685106 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7685106 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:7685106 | pubmed:volume | 90 | lld:pubmed |
| pubmed-article:7685106 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7685106 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7685106 | pubmed:pagination | 4586-90 | lld:pubmed |
| pubmed-article:7685106 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:7685106 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:7685106 | pubmed:articleTitle | The costimulatory activity of the CD26 antigen requires dipeptidyl peptidase IV enzymatic activity. | lld:pubmed |
| pubmed-article:7685106 | pubmed:affiliation | Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA. | lld:pubmed |
| pubmed-article:7685106 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7685106 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:7685106 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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