ALLERGEN-INDUCED CD23 ON CD4(-LYMPHOCYTES AND CD21 ON B-LYMPHOCYTES IN PATIENTS WITH ALLERGIC-ASTHMA - EVIDENCE AND REGULATION() T)

Interaction of CD3(+) T cells and B cells is necessary for IgE product ion. It has been recently demonstrated that cell surface antigen CD21 is a ligand for CD23 (Fc epsilon RII) and that the pairing of these mo lecules may participate in the control of IgE production. In this stud y we investigated the effect of the Dermatophagoides pteronyssinus (Dp t) allergen and recombinant interleukin(rIL)-4 on the expression of CD 21 and CD23 on T and B cells of asthmatic patients allergic to Dpt and of healthy controls. Peripheral blood mononuclear cells (PBMC) were i ncubated alone or with Dpt allergen (100 biological units/ml) and/or r IL-4 (100 U/ml) for up to 7 days. The now-cytometric analysis of doubl e-fluorescence staining revealed that Dpt allergen and/or rIL-4 induce d CD23 on CD4(+) T lymphocytes only in allergic patients. The allergen -induced CD23 on T cells is de novo synthesized antigen since no induc tion of CD23 on T cells was observed in cultures with 0.4 mu g/ml acti nomycin D. Moreover, 100 U/ml of interferon-gamma inhibited the induct ion of CD23 on CD4(+) T cells. T cells obtained from healthy donors di d not express CD23 or CD21 antigen upon incubation with allergen and/o r rIL-4. Although rIL-4 also induced CD23 in controls, the expression was only observed on CD20(+) cells. The allergen alone induced a signi ficant elevation of the mean fluorescence intensity of both CD21 and C D23 only in allergic individuals. When the cell proliferation was anal yzed, a slightly increased stimulation index upon cultivation of PBMC was obtained from non-allergic donors as well, but less than in allerg ic patients. The co-expression of major histocompability complex class LT molecules and CD23 on CD4(+) T lymphocytes in allergic patients, a s assessed by the three-color immunofluorescence analysis, indicates t hat 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 p roduction. This would not occur in non-allergic individuals as there i s no CD23 expression on T cells.