Gagro A, Rabatić S
Institute of Immunology, Zagreb, Croatia.
Eur J Immunol. 1994 May;24(5):1109-14. doi: 10.1002/eji.1830240515.
Interaction of CD4+ T cells and B cells is necessary for IgE production. It has been recently demonstrated that cell surface antigen CD21 is a ligand for CD23 (Fc epsilon RII) and that the pairing of these molecules may participate in the control of IgE production. In this study we investigated the effect of the Dermatophagoides pteronyssinus (Dpt) allergen and recombinant interleukin(rIL)-4 on the expression of CD21 and CD23 on T and B cells of asthmatic patients allergic to Dpt and of healthy controls. Peripheral blood mononuclear cells (PBMC) were incubated alone or with Dpt allergen (100 biological units/ml) and/or rIL-4 (100 U/ml) for up to 7 days. The flow-cytometric analysis of double-fluorescence staining revealed that Dpt allergen and/or rIL-4 induced CD23 on CD4+ T lymphocytes only in allergic patients. The allergen-induced CD23 on T cells is de novo synthesized antigen since no induction of CD23 on T cells was observed in cultures with 0.4 microgram/ml actinomycin D. Moreover, 100 U/ml of interferon-gamma inhibited the induction of CD23 on CD4+ T cells. T cells obtained from healthy donors did not express CD23 or CD21 antigen upon incubation with allergen and/or rIL-4. Although rIL-4 also induced CD23 in controls, the expression was only observed on CD20+ cells. The allergen alone induced a significant elevation of the mean fluorescence intensity of both CD21 and CD23 only in allergic individuals. When the cell proliferation was analyzed, a slightly increased stimulation index upon cultivation of PBMC was obtained from non-allergic donors as well, but less than in allergic patients. The co-expression of major histocompatibility complex class II molecules and CD23 on CD4+ T lymphocytes in allergic patients, as assessed by the three-color immunofluorescence analysis, indicates that these cells were activated. We conclude that CD4+ T lymphocytes possess a unique capability to express CD23 upon exposure to allergen. Moreover, the allergen-mediated induction of CD23 on T cells observed only in allergic patients may be the reason for the increase of IgE production. This would not occur in non-allergic individuals as there is no CD23 expression on T cells.
CD4+ T细胞与B细胞的相互作用对于IgE的产生是必需的。最近有研究表明，细胞表面抗原CD21是CD23（FcεRII）的配体，这些分子的配对可能参与了对IgE产生的调控。在本研究中，我们调查了尘螨变应原和重组白细胞介素（rIL）-4对尘螨过敏的哮喘患者及健康对照者的T细胞和B细胞上CD21和CD23表达的影响。外周血单个核细胞（PBMC）单独培养或与尘螨变应原（100生物单位/毫升）和/或rIL-4（100单位/毫升）一起培养长达7天。双荧光染色的流式细胞术分析显示，尘螨变应原和/或rIL-4仅在过敏患者的CD4+ T淋巴细胞上诱导CD23表达。变应原诱导T细胞上的CD23是从头合成的抗原，因为在含有0.4微克/毫升放线菌素D的培养物中未观察到T细胞上CD23的诱导。此外，100单位/毫升干扰素-γ抑制CD4+ T细胞上CD23的诱导。从健康供体获得的T细胞在与变应原和/或rIL-4孵育后不表达CD23或CD21抗原。尽管rIL-4在对照中也诱导CD23表达，但仅在CD20+细胞上观察到。仅变应原就仅在过敏个体中诱导CD21和CD23平均荧光强度显著升高。当分析细胞增殖时，非过敏供体的PBMC培养后刺激指数也略有增加，但低于过敏患者。通过三色免疫荧光分析评估，过敏患者CD4+ T淋巴细胞上主要组织相容性复合体II类分子与CD23的共表达表明这些细胞被激活。我们得出结论，CD + T淋巴细胞在暴露于变应原时具有独特的表达CD23的能力。此外，仅在过敏患者中观察到的变应原介导的T细胞上CD23的诱导可能是IgE产生增加的原因。在非过敏个体中不会发生这种情况，因为T细胞上没有CD23表达。
