PubMed:9135552 JSONTXT

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{"project":"genia-medco-coref","denotations":[{"id":"C3","span":{"begin":101,"end":134},"obj":"NP"},{"id":"C4","span":{"begin":146,"end":174},"obj":"NP"},{"id":"C5","span":{"begin":175,"end":179},"obj":"NP"},{"id":"C6","span":{"begin":300,"end":311},"obj":"NP"},{"id":"C8","span":{"begin":473,"end":494},"obj":"NP"},{"id":"C9","span":{"begin":510,"end":539},"obj":"NP"},{"id":"C10","span":{"begin":590,"end":601},"obj":"NP"},{"id":"C11","span":{"begin":614,"end":687},"obj":"NP"},{"id":"C12","span":{"begin":729,"end":757},"obj":"NP"},{"id":"C13","span":{"begin":770,"end":782},"obj":"NP"},{"id":"C14","span":{"begin":904,"end":956},"obj":"NP"},{"id":"C15","span":{"begin":957,"end":962},"obj":"NP"},{"id":"C16","span":{"begin":1164,"end":1193},"obj":"NP"},{"id":"C17","span":{"begin":1197,"end":1209},"obj":"NP"},{"id":"C18","span":{"begin":1370,"end":1374},"obj":"NP"}],"relations":[{"id":"R1","pred":"coref-relat","subj":"C5","obj":"C4"},{"id":"R2","pred":"coref-ident","subj":"C6","obj":"C3"},{"id":"R3","pred":"coref-ident","subj":"C10","obj":"C6"},{"id":"R4","pred":"coref-ident","subj":"C12","obj":"C11"},{"id":"R5","pred":"coref-ident","subj":"C13","obj":"C9"},{"id":"R6","pred":"coref-relat","subj":"C15","obj":"C14"},{"id":"R7","pred":"coref-ident","subj":"C17","obj":"C8"},{"id":"R8","pred":"coref-ident","subj":"C18","obj":"C16"}],"text":"The tumour associated cell surface antigen A6H is costimulatory for human CD4+ but not CD8+ T cells.\nThe A6H monoclonal antibody (mAb) recognizes a 120,000-140,000 MW antigen that is expressed at similar densities on 85-90% of human CD4+ and CD8+ T cells and on renal cell carcinomas. The binding of the A6H mAb induced a costimulatory signal in anti-CD3 activated T cells. In the present report, we show that A6H costimulated cell proliferation and cytokine production in purified CD4+ T cells. Unexpectedly, the CD8+ T-cell subpopulation failed to respond. CD4+ T cells costimulated with the A6H mAb upregulated CD80, CD86, CD71, interleukin-2 (IL-2)R alpha, IL-2R beta and IL-2R gamma, while no corresponding up-regulation of these cell surface molecules was seen in CD8+ T cells. In order to investigate the nature of the A6H mAb costimulus at the transcriptional level we have examined induction of the transcription factors OCT-1, AP-1 and NF-kappa B which are known to be transcriptional regulators of several cytokine and cytokine receptor genes, including the IL-2 and IL-2R genes. Co-ligation of the A6H antigen and the CD3 complex induced expression of the transcription factor AP-1 in CD4+ T cells, whereas no increase in NF-kappa B and octamer-binding (Oct) proteins was seen compared to T cells stimulated with anti-CD3 alone. Furthermore, no induction of AP-1 was seen in A6H costimulated CD8+ T cells. These results suggests that both proximal steps in CD8+ T-cell activation as well as the later phases are unresponsive to A6H ligation. Molecular differences of the A6H molecule or distinct regulation of the A6H transduced AP-1 activation pathway may exist in CD4+ and CD8+ T cell subpopulations."}

{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":100},"obj":"Sentence"},{"id":"S2","span":{"begin":101,"end":284},"obj":"Sentence"},{"id":"S3","span":{"begin":285,"end":373},"obj":"Sentence"},{"id":"S4","span":{"begin":374,"end":495},"obj":"Sentence"},{"id":"S5","span":{"begin":496,"end":558},"obj":"Sentence"},{"id":"S6","span":{"begin":559,"end":783},"obj":"Sentence"},{"id":"S7","span":{"begin":784,"end":1090},"obj":"Sentence"},{"id":"S8","span":{"begin":1091,"end":1340},"obj":"Sentence"},{"id":"S9","span":{"begin":1341,"end":1417},"obj":"Sentence"},{"id":"S10","span":{"begin":1418,"end":1553},"obj":"Sentence"},{"id":"S11","span":{"begin":1554,"end":1714},"obj":"Sentence"}],"text":"The tumour associated cell surface antigen A6H is costimulatory for human CD4+ but not CD8+ T cells.\nThe A6H monoclonal antibody (mAb) recognizes a 120,000-140,000 MW antigen that is expressed at similar densities on 85-90% of human CD4+ and CD8+ T cells and on renal cell carcinomas. The binding of the A6H mAb induced a costimulatory signal in anti-CD3 activated T cells. In the present report, we show that A6H costimulated cell proliferation and cytokine production in purified CD4+ T cells. Unexpectedly, the CD8+ T-cell subpopulation failed to respond. CD4+ T cells costimulated with the A6H mAb upregulated CD80, CD86, CD71, interleukin-2 (IL-2)R alpha, IL-2R beta and IL-2R gamma, while no corresponding up-regulation of these cell surface molecules was seen in CD8+ T cells. In order to investigate the nature of the A6H mAb costimulus at the transcriptional level we have examined induction of the transcription factors OCT-1, AP-1 and NF-kappa B which are known to be transcriptional regulators of several cytokine and cytokine receptor genes, including the IL-2 and IL-2R genes. Co-ligation of the A6H antigen and the CD3 complex induced expression of the transcription factor AP-1 in CD4+ T cells, whereas no increase in NF-kappa B and octamer-binding (Oct) proteins was seen compared to T cells stimulated with anti-CD3 alone. Furthermore, no induction of AP-1 was seen in A6H costimulated CD8+ T cells. These results suggests that both proximal steps in CD8+ T-cell activation as well as the later phases are unresponsive to A6H ligation. Molecular differences of the A6H molecule or distinct regulation of the A6H transduced AP-1 activation pathway may exist in CD4+ and CD8+ T cell subpopulations."}

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