PubMed:25675201 JSONTXT

{"project":"wangzhuo19_800_2","denotations":[{"id":"T1","span":{"begin":38,"end":47},"obj":"CI"},{"id":"T2","span":{"begin":107,"end":116},"obj":"CI"},{"id":"T3","span":{"begin":211,"end":220},"obj":"CI"},{"id":"T4","span":{"begin":438,"end":447},"obj":"CI"},{"id":"T5","span":{"begin":350,"end":359},"obj":"CI"},{"id":"T6","span":{"begin":1046,"end":1055},"obj":"CI"},{"id":"T7","span":{"begin":1716,"end":1725},"obj":"CI"},{"id":"T8","span":{"begin":1820,"end":1829},"obj":"CI"},{"id":"T9","span":{"begin":1363,"end":1372},"obj":"CI"}],"text":"Cytokine Release After Treatment With Rituximab in Renal Transplant Recipients.\nBACKGROUND: Treatment with rituximab may be accompanied by a systemic cytokine release. We studied the effects of a single dose of rituximab on cytokine levels in transplant patients and examined the underlying mechanism.\nMETHODS: Twenty renal transplant recipients (10 rituximab-treated, 10 placebo-treated) were recruited from a randomized clinical trial. Rituximab or placebo was infused during surgery, and blood samples were taken before, during, and after surgery and analyzed for interleukin (IL)-2, IL-4, IL-6, IL-10, IL-12, IL-17, interferon-γ, macrophage inflammatory protein (MIP)-1β, transforming growth factor-β, and tumor necrosis factor-α. in vitro, healthy donor peripheral blood mononuclear cells, purified B cells, monocytes, natural killer (NK) cells, or combinations thereof were incubated with rituximab, rituximab-F(ab')2, or medium and MIP-1β, IL-10, interferon-γ, and tumor necrosis factor-α levels were measured in the supernatant.\nRESULTS: Rituximab-treated patients had higher serum levels of IL-10 (101 ± 35 pg/mL vs 41 ± 9 pg/mL; P \u003c 0.01) and MIP-1β (950 ± 418 pg/mL vs 125 ± 32 pg/mL; P \u003c 0.001) compared to placebo-treated patients at 2 hours after start of infusion. There was no difference in the level of other cytokines. In vitro, the addition of rituximab, but not rituximab-F(ab')2 fragments, only led to significantly increased levels of MIP-1β in co-cultures of B and NK cells. Levels of MIP-1β were higher in patients with a high affinity Fc-receptor compared to those with a lower affinity FcγRIIIa (1356 ± 184 pg/mL vs 679 ± 273 pg/mL; P \u003c 0.01).\nCONCLUSIONS: In addition to B-cell depletion, rituximab can modulate the immune response by inducing cytokine secretion, especially IL-10 and MIP-1β. Rituximab-induced MIP-1β secretion depends on the combined presence of B cells and FcR-bearing cells, especially NK cells."}

{"project":"Zierdiyeerkenaili_800_2","denotations":[{"id":"T1","span":{"begin":38,"end":47},"obj":"CI"},{"id":"T2","span":{"begin":107,"end":116},"obj":"CI"},{"id":"T3","span":{"begin":211,"end":220},"obj":"CI"},{"id":"T4","span":{"begin":350,"end":359},"obj":"CI"},{"id":"T5","span":{"begin":895,"end":904},"obj":"CI"},{"id":"T6","span":{"begin":906,"end":915},"obj":"CI"},{"id":"T7","span":{"begin":1363,"end":1372},"obj":"CI"},{"id":"T8","span":{"begin":1382,"end":1391},"obj":"CI"},{"id":"T9","span":{"begin":1716,"end":1725},"obj":"CI"},{"id":"T10","span":{"begin":318,"end":345},"obj":"DP"},{"id":"T11","span":{"begin":51,"end":78},"obj":"DP"},{"id":"T12","span":{"begin":1046,"end":1055},"obj":"CI"},{"id":"T13","span":{"begin":438,"end":447},"obj":"CI"},{"id":"T14","span":{"begin":1820,"end":1829},"obj":"CI"}],"text":"Cytokine Release After Treatment With Rituximab in Renal Transplant Recipients.\nBACKGROUND: Treatment with rituximab may be accompanied by a systemic cytokine release. We studied the effects of a single dose of rituximab on cytokine levels in transplant patients and examined the underlying mechanism.\nMETHODS: Twenty renal transplant recipients (10 rituximab-treated, 10 placebo-treated) were recruited from a randomized clinical trial. Rituximab or placebo was infused during surgery, and blood samples were taken before, during, and after surgery and analyzed for interleukin (IL)-2, IL-4, IL-6, IL-10, IL-12, IL-17, interferon-γ, macrophage inflammatory protein (MIP)-1β, transforming growth factor-β, and tumor necrosis factor-α. in vitro, healthy donor peripheral blood mononuclear cells, purified B cells, monocytes, natural killer (NK) cells, or combinations thereof were incubated with rituximab, rituximab-F(ab')2, or medium and MIP-1β, IL-10, interferon-γ, and tumor necrosis factor-α levels were measured in the supernatant.\nRESULTS: Rituximab-treated patients had higher serum levels of IL-10 (101 ± 35 pg/mL vs 41 ± 9 pg/mL; P \u003c 0.01) and MIP-1β (950 ± 418 pg/mL vs 125 ± 32 pg/mL; P \u003c 0.001) compared to placebo-treated patients at 2 hours after start of infusion. There was no difference in the level of other cytokines. In vitro, the addition of rituximab, but not rituximab-F(ab')2 fragments, only led to significantly increased levels of MIP-1β in co-cultures of B and NK cells. Levels of MIP-1β were higher in patients with a high affinity Fc-receptor compared to those with a lower affinity FcγRIIIa (1356 ± 184 pg/mL vs 679 ± 273 pg/mL; P \u003c 0.01).\nCONCLUSIONS: In addition to B-cell depletion, rituximab can modulate the immune response by inducing cytokine secretion, especially IL-10 and MIP-1β. Rituximab-induced MIP-1β secretion depends on the combined presence of B cells and FcR-bearing cells, especially NK cells."}

{"project":"chenxin_473849_800_3","denotations":[{"id":"T16","span":{"begin":1382,"end":1399},"obj":"CI"},{"id":"T2","span":{"begin":350,"end":359},"obj":"CI"},{"id":"T3","span":{"begin":107,"end":116},"obj":"CI"},{"id":"T4","span":{"begin":211,"end":220},"obj":"CI"},{"id":"T5","span":{"begin":895,"end":904},"obj":"CI"},{"id":"T7","span":{"begin":1363,"end":1372},"obj":"CI"},{"id":"T9","span":{"begin":1716,"end":1725},"obj":"CI"},{"id":"T11","span":{"begin":38,"end":47},"obj":"CI"},{"id":"T12","span":{"begin":438,"end":447},"obj":"CI"},{"id":"T13","span":{"begin":1046,"end":1055},"obj":"CI"},{"id":"T14","span":{"begin":1820,"end":1829},"obj":"CI"},{"id":"T15","span":{"begin":906,"end":923},"obj":"CI"}],"text":"Cytokine Release After Treatment With Rituximab in Renal Transplant Recipients.\nBACKGROUND: Treatment with rituximab may be accompanied by a systemic cytokine release. We studied the effects of a single dose of rituximab on cytokine levels in transplant patients and examined the underlying mechanism.\nMETHODS: Twenty renal transplant recipients (10 rituximab-treated, 10 placebo-treated) were recruited from a randomized clinical trial. Rituximab or placebo was infused during surgery, and blood samples were taken before, during, and after surgery and analyzed for interleukin (IL)-2, IL-4, IL-6, IL-10, IL-12, IL-17, interferon-γ, macrophage inflammatory protein (MIP)-1β, transforming growth factor-β, and tumor necrosis factor-α. in vitro, healthy donor peripheral blood mononuclear cells, purified B cells, monocytes, natural killer (NK) cells, or combinations thereof were incubated with rituximab, rituximab-F(ab')2, or medium and MIP-1β, IL-10, interferon-γ, and tumor necrosis factor-α levels were measured in the supernatant.\nRESULTS: Rituximab-treated patients had higher serum levels of IL-10 (101 ± 35 pg/mL vs 41 ± 9 pg/mL; P \u003c 0.01) and MIP-1β (950 ± 418 pg/mL vs 125 ± 32 pg/mL; P \u003c 0.001) compared to placebo-treated patients at 2 hours after start of infusion. There was no difference in the level of other cytokines. In vitro, the addition of rituximab, but not rituximab-F(ab')2 fragments, only led to significantly increased levels of MIP-1β in co-cultures of B and NK cells. Levels of MIP-1β were higher in patients with a high affinity Fc-receptor compared to those with a lower affinity FcγRIIIa (1356 ± 184 pg/mL vs 679 ± 273 pg/mL; P \u003c 0.01).\nCONCLUSIONS: In addition to B-cell depletion, rituximab can modulate the immune response by inducing cytokine secretion, especially IL-10 and MIP-1β. Rituximab-induced MIP-1β secretion depends on the combined presence of B cells and FcR-bearing cells, especially NK cells."}

{"project":"yaoziqian_800_2","denotations":[{"id":"T1","span":{"begin":38,"end":47},"obj":"CI"},{"id":"T2","span":{"begin":51,"end":78},"obj":"something"},{"id":"T3","span":{"begin":211,"end":220},"obj":"CI"},{"id":"T4","span":{"begin":318,"end":345},"obj":"CI"},{"id":"T5","span":{"begin":438,"end":447},"obj":"CI"},{"id":"T6","span":{"begin":1046,"end":1055},"obj":"CI"},{"id":"T7","span":{"begin":1363,"end":1372},"obj":"CI"},{"id":"T8","span":{"begin":1382,"end":1391},"obj":"CI"},{"id":"T9","span":{"begin":1820,"end":1829},"obj":"CI"},{"id":"T10","span":{"begin":1716,"end":1725},"obj":"CI"},{"id":"T11","span":{"begin":906,"end":915},"obj":"CI"},{"id":"T12","span":{"begin":895,"end":904},"obj":"CI"}],"text":"Cytokine Release After Treatment With Rituximab in Renal Transplant Recipients.\nBACKGROUND: Treatment with rituximab may be accompanied by a systemic cytokine release. We studied the effects of a single dose of rituximab on cytokine levels in transplant patients and examined the underlying mechanism.\nMETHODS: Twenty renal transplant recipients (10 rituximab-treated, 10 placebo-treated) were recruited from a randomized clinical trial. Rituximab or placebo was infused during surgery, and blood samples were taken before, during, and after surgery and analyzed for interleukin (IL)-2, IL-4, IL-6, IL-10, IL-12, IL-17, interferon-γ, macrophage inflammatory protein (MIP)-1β, transforming growth factor-β, and tumor necrosis factor-α. in vitro, healthy donor peripheral blood mononuclear cells, purified B cells, monocytes, natural killer (NK) cells, or combinations thereof were incubated with rituximab, rituximab-F(ab')2, or medium and MIP-1β, IL-10, interferon-γ, and tumor necrosis factor-α levels were measured in the supernatant.\nRESULTS: Rituximab-treated patients had higher serum levels of IL-10 (101 ± 35 pg/mL vs 41 ± 9 pg/mL; P \u003c 0.01) and MIP-1β (950 ± 418 pg/mL vs 125 ± 32 pg/mL; P \u003c 0.001) compared to placebo-treated patients at 2 hours after start of infusion. There was no difference in the level of other cytokines. In vitro, the addition of rituximab, but not rituximab-F(ab')2 fragments, only led to significantly increased levels of MIP-1β in co-cultures of B and NK cells. Levels of MIP-1β were higher in patients with a high affinity Fc-receptor compared to those with a lower affinity FcγRIIIa (1356 ± 184 pg/mL vs 679 ± 273 pg/mL; P \u003c 0.01).\nCONCLUSIONS: In addition to B-cell depletion, rituximab can modulate the immune response by inducing cytokine secretion, especially IL-10 and MIP-1β. Rituximab-induced MIP-1β secretion depends on the combined presence of B cells and FcR-bearing cells, especially NK cells."}

{"project":"yangbin123xm_800_3","denotations":[{"id":"T1","span":{"begin":38,"end":47},"obj":"CI"},{"id":"T10","span":{"begin":1820,"end":1829},"obj":"CI"},{"id":"T2","span":{"begin":107,"end":116},"obj":"CI"},{"id":"T3","span":{"begin":211,"end":220},"obj":"CI"},{"id":"T4","span":{"begin":350,"end":359},"obj":"CI"},{"id":"T5","span":{"begin":438,"end":447},"obj":"CI"},{"id":"T6","span":{"begin":895,"end":904},"obj":"CI"},{"id":"T7","span":{"begin":1046,"end":1055},"obj":"CI"},{"id":"T8","span":{"begin":1363,"end":1372},"obj":"CI"},{"id":"T9","span":{"begin":1716,"end":1725},"obj":"CI"},{"id":"T11","span":{"begin":906,"end":923},"obj":"CI"},{"id":"T12","span":{"begin":1382,"end":1399},"obj":"CI"}],"text":"Cytokine Release After Treatment With Rituximab in Renal Transplant Recipients.\nBACKGROUND: Treatment with rituximab may be accompanied by a systemic cytokine release. We studied the effects of a single dose of rituximab on cytokine levels in transplant patients and examined the underlying mechanism.\nMETHODS: Twenty renal transplant recipients (10 rituximab-treated, 10 placebo-treated) were recruited from a randomized clinical trial. Rituximab or placebo was infused during surgery, and blood samples were taken before, during, and after surgery and analyzed for interleukin (IL)-2, IL-4, IL-6, IL-10, IL-12, IL-17, interferon-γ, macrophage inflammatory protein (MIP)-1β, transforming growth factor-β, and tumor necrosis factor-α. in vitro, healthy donor peripheral blood mononuclear cells, purified B cells, monocytes, natural killer (NK) cells, or combinations thereof were incubated with rituximab, rituximab-F(ab')2, or medium and MIP-1β, IL-10, interferon-γ, and tumor necrosis factor-α levels were measured in the supernatant.\nRESULTS: Rituximab-treated patients had higher serum levels of IL-10 (101 ± 35 pg/mL vs 41 ± 9 pg/mL; P \u003c 0.01) and MIP-1β (950 ± 418 pg/mL vs 125 ± 32 pg/mL; P \u003c 0.001) compared to placebo-treated patients at 2 hours after start of infusion. There was no difference in the level of other cytokines. In vitro, the addition of rituximab, but not rituximab-F(ab')2 fragments, only led to significantly increased levels of MIP-1β in co-cultures of B and NK cells. Levels of MIP-1β were higher in patients with a high affinity Fc-receptor compared to those with a lower affinity FcγRIIIa (1356 ± 184 pg/mL vs 679 ± 273 pg/mL; P \u003c 0.01).\nCONCLUSIONS: In addition to B-cell depletion, rituximab can modulate the immune response by inducing cytokine secretion, especially IL-10 and MIP-1β. Rituximab-induced MIP-1β secretion depends on the combined presence of B cells and FcR-bearing cells, especially NK cells."}