PubMed:10352258 JSONTXT

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{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":226},"obj":"Sentence"},{"id":"S2","span":{"begin":227,"end":497},"obj":"Sentence"},{"id":"S3","span":{"begin":498,"end":694},"obj":"Sentence"},{"id":"S4","span":{"begin":695,"end":866},"obj":"Sentence"},{"id":"S5","span":{"begin":867,"end":970},"obj":"Sentence"},{"id":"S6","span":{"begin":971,"end":1069},"obj":"Sentence"},{"id":"S7","span":{"begin":1070,"end":1297},"obj":"Sentence"}],"text":"In vivo inhibition of NF-kappa B in T-lineage cells leads to a dramatic decrease in cell proliferation and cytokine production and to increased cell apoptosis in response to mitogenic stimuli, but not to abnormal thymopoiesis.\nTo understand the role of NF-kappa B complexes in T cell development and activation, we have generated transgenic mice in which RelA and c-Rel complexes were selectively inhibited in the T-lineage cells by specific expression of a trans-dominant form of I kappa B alpha. Transgene expression did not affect the thymic development, but led to lowered numbers of splenic T cells and to a dramatic decrease in the ex vivo proliferative response of splenic T lymphocytes. Analysis of IL-2 and IL-2R alpha expression demonstrated that the perturbation of the proliferation response was not attributable to an abnormal expression of these genes. In contrast, expression of IL-4, IL-10, and IFN-gamma was strongly inhibited in the transgenic T cells. The proliferative deficiency of the transgenic T cells was associated with an increased apoptosis. These results point out the involvement of NF-kappa B/Rel family proteins in growth signaling pathways by either regulating proteins involved in the IL-2 signaling or by functionally interfering with the cell cycle progression."}

{"project":"genia-medco-coref","denotations":[{"id":"C1","span":{"begin":36,"end":51},"obj":"NP"},{"id":"C2","span":{"begin":134,"end":158},"obj":"NP"},{"id":"C3","span":{"begin":330,"end":345},"obj":"NP"},{"id":"C4","span":{"begin":349,"end":354},"obj":"NP"},{"id":"C5","span":{"begin":410,"end":429},"obj":"NP"},{"id":"C6","span":{"begin":947,"end":969},"obj":"NP"},{"id":"C7","span":{"begin":1003,"end":1025},"obj":"NP"},{"id":"C8","span":{"begin":1046,"end":1068},"obj":"NP"}],"relations":[{"id":"R1","pred":"coref-relat","subj":"C4","obj":"C3"},{"id":"R2","pred":"coref-ident","subj":"C5","obj":"C1"},{"id":"R3","pred":"coref-ident","subj":"C7","obj":"C6"},{"id":"R4","pred":"coref-ident","subj":"C8","obj":"C2"}],"text":"In vivo inhibition of NF-kappa B in T-lineage cells leads to a dramatic decrease in cell proliferation and cytokine production and to increased cell apoptosis in response to mitogenic stimuli, but not to abnormal thymopoiesis.\nTo understand the role of NF-kappa B complexes in T cell development and activation, we have generated transgenic mice in which RelA and c-Rel complexes were selectively inhibited in the T-lineage cells by specific expression of a trans-dominant form of I kappa B alpha. Transgene expression did not affect the thymic development, but led to lowered numbers of splenic T cells and to a dramatic decrease in the ex vivo proliferative response of splenic T lymphocytes. Analysis of IL-2 and IL-2R alpha expression demonstrated that the perturbation of the proliferation response was not attributable to an abnormal expression of these genes. In contrast, expression of IL-4, IL-10, and IFN-gamma was strongly inhibited in the transgenic T cells. The proliferative deficiency of the transgenic T cells was associated with an increased apoptosis. These results point out the involvement of NF-kappa B/Rel family proteins in growth signaling pathways by either regulating proteins involved in the IL-2 signaling or by functionally interfering with the cell cycle progression."}

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