Ferrer J M, Iglesias J, Hernández M, Matamoros N
Immunology Section, Hospital Son Dureta, Palma de Mallorca, Spain.
Clin Exp Immunol. 1995 Nov;102(2):286-9. doi: 10.1111/j.1365-2249.1995.tb03779.x.
The failure of B cells from CVI patients to secrete normal amounts of antibodies has been attributed either to an intrinsic B cell defect or to a lack of cooperation from T cells. In an attempt to improve the definition of the origin of this defect in one of the main cellular compartments, we studied the ability of helper CD4 cells and their CD4 CD45RO subpopulation from CVI patients to secrete interleukins (IL-2 and IL-4) in response to mitogen stimulation. We found that CD4 and CD4 CD45RO cells from some patients secrete abnormal amounts of interleukins (in general low levels of IL-2 and high levels of IL-4) upon stimulation with pokeweed mitogen (PWM). These irregularities may contribute to the defective differentiation of B cells in these patients.
常见可变免疫缺陷(CVI)患者的B细胞无法分泌正常量的抗体,这要么归因于B细胞内在缺陷,要么归因于T细胞缺乏协同作用。为了更好地界定这一缺陷在主要细胞区室之一中的起源,我们研究了CVI患者的辅助性CD4细胞及其CD4 CD45RO亚群在有丝分裂原刺激下分泌白细胞介素(IL-2和IL-4)的能力。我们发现,来自部分患者的CD4和CD4 CD45RO细胞在用商陆有丝分裂原(PWM)刺激后会分泌异常量的白细胞介素(一般IL-2水平低而IL-4水平高)。这些异常情况可能导致这些患者B细胞分化存在缺陷。