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Antigen-Dependent and -Independent IFN- Modulation by Penicillins

Elisabetta Padovan^1,*, Salome von Greyerz, Werner J. Pichler and Hans Ulrich Weltzien^*

^* Max Planck Institute for Immunobiology, Freiburg, Germany; and Institute of Immunology and Allergology, Inselspital, Bern, Switzerland

The activation of CD4⁺ T lymphocytes upon Ag stimulation plays a critical role in adverse immune responses including drug-specific hypersensitivity reactions. We examined the modulation of T cell phenotype induced by hapten-specific stimulation using the model of ß-lactam antibiotics such as penicillin G (Pen G), Pen V, and ampicillin (Amp). When PBMC of donors suffering from hypersensitivity reactions against ß-lactams were stimulated in vitro with different doses of Pen G, a preferential expansion of IL-4-producing TCRß⁺ cells was detected. A panel of T cell clones was then prepared from Pen G-specific lines after two cycles of restimulation with the hapten. For the majority of these clones, we found that high doses of Pen G induced optimal IL-4 secretion, whereas the amount of IFN- secreted was inversely correlated with the dose of Pen G, thus leading to a hapten-inducible shift of the fuctional phenotypes for some of the clones. Finally, Pen V and Amp were used to modulate different Ag-induced immune responses. We found that Amp had no influence on the cytokine pattern induced by specific Ag or mitogens. In contrast, Pen V inhibited the secretion of IFN-, but not IL-4, most likely by Ag-independent mechanisms. This last finding may open new applications for immune intervention in those diseases in which polarized Th1 responses are involved in the development of the pathology.

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