慢性B淋巴细胞增殖性疾病根据免疫表型可分为不同亚型,免疫表型在各亚型的诊断及鉴别诊断中发挥着重要作用,典型(慢性)B淋巴细胞白血病免疫表型为CD5+、CD23+、FMC(flinders medical centre)7+;而毛细胞白血病特异性高表达CD22、CD25、C...慢性B淋巴细胞增殖性疾病根据免疫表型可分为不同亚型,免疫表型在各亚型的诊断及鉴别诊断中发挥着重要作用,典型(慢性)B淋巴细胞白血病免疫表型为CD5+、CD23+、FMC(flinders medical centre)7+;而毛细胞白血病特异性高表达CD22、CD25、CD103和CD11c;滤泡性淋巴瘤主要表达CD20、CD10、CD22、CD79a,不表达CD5;套细胞淋巴瘤则过度表达CD5+、FMC7+、Bcl-2+、细胞周期蛋白(cyclinD1+);典型瓦氏巨球蛋白血症不表达CD5及CD23,而变异型则表达;边缘区B细胞淋巴瘤的典型免疫表型为CD5-、CD10-、CD23-、cyclinD1-。对于不典型的慢性B淋巴细胞增殖性疾病需结合病理学、遗传学、分子生物学诊断,从而指导临床治疗及预后。展开更多
IL-4 is an important B cell survival and growth factor. IL-4 induced the tyrosine phosphorylation of IRS2 in resting B lymphocytes and in LPS- or CD40L-activated blasts. Phosphorylated IRS2 coprecipitated with the p85...IL-4 is an important B cell survival and growth factor. IL-4 induced the tyrosine phosphorylation of IRS2 in resting B lymphocytes and in LPS- or CD40L-activated blasts. Phosphorylated IRS2 coprecipitated with the p85 subunit of PI 3’ kinase in both resting and activated cells. By contrast, association of phosphorylated IRS2 with GRB2 was not detected in resting B cells after IL-4 treatment although both proteins were expressed. However, IL-4 induced association of IRS2 with GRB2 in B cell blasts. The pattern of IL-4- induced recruitment of p85 and GRB2 to IRS2 observed in B cells derived from STAT6 null mice was identical to that observed for normal mice. While IL-4 alone does not induce activation of MEK, a MEKI inhibitor suppressed the IL-4-induced proliferative response of LPS-activated B cell blasts. These results demonstrate that costimulation of splenic B cells alters IL-4-induced signal transduction independent of STAT6 leading to proliferation. Furthermore, proliferation induced by IL-4 in LPS-activated blasts is dependent upon the MAP kinase pathway.展开更多
文摘慢性B淋巴细胞增殖性疾病根据免疫表型可分为不同亚型,免疫表型在各亚型的诊断及鉴别诊断中发挥着重要作用,典型(慢性)B淋巴细胞白血病免疫表型为CD5+、CD23+、FMC(flinders medical centre)7+;而毛细胞白血病特异性高表达CD22、CD25、CD103和CD11c;滤泡性淋巴瘤主要表达CD20、CD10、CD22、CD79a,不表达CD5;套细胞淋巴瘤则过度表达CD5+、FMC7+、Bcl-2+、细胞周期蛋白(cyclinD1+);典型瓦氏巨球蛋白血症不表达CD5及CD23,而变异型则表达;边缘区B细胞淋巴瘤的典型免疫表型为CD5-、CD10-、CD23-、cyclinD1-。对于不典型的慢性B淋巴细胞增殖性疾病需结合病理学、遗传学、分子生物学诊断,从而指导临床治疗及预后。
文摘IL-4 is an important B cell survival and growth factor. IL-4 induced the tyrosine phosphorylation of IRS2 in resting B lymphocytes and in LPS- or CD40L-activated blasts. Phosphorylated IRS2 coprecipitated with the p85 subunit of PI 3’ kinase in both resting and activated cells. By contrast, association of phosphorylated IRS2 with GRB2 was not detected in resting B cells after IL-4 treatment although both proteins were expressed. However, IL-4 induced association of IRS2 with GRB2 in B cell blasts. The pattern of IL-4- induced recruitment of p85 and GRB2 to IRS2 observed in B cells derived from STAT6 null mice was identical to that observed for normal mice. While IL-4 alone does not induce activation of MEK, a MEKI inhibitor suppressed the IL-4-induced proliferative response of LPS-activated B cell blasts. These results demonstrate that costimulation of splenic B cells alters IL-4-induced signal transduction independent of STAT6 leading to proliferation. Furthermore, proliferation induced by IL-4 in LPS-activated blasts is dependent upon the MAP kinase pathway.
