Induction of interleukin 2 (IL2) and interferon‐γ and enhancement of IL2 receptor expression by a CD26 monoclonal antibody

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Abstract
The ability of the 134‐2C2 monoclonal antibody (mAb; CD26) to transmit an activation signal and to affect T cell proliferation has been studied. The 134‐2C2 mAb, although not being mitogenic by itself, is able to increase the proliferation of purified T cells in the presence of exogenous interleukin 2 (IL2) or phorbol 12‐myristate 13‐acetate (PMA). No effect of our mAb was observed on the proliferation of T cells induced by other stimuli such as Sepharose‐bound CD3 mAb, phytohemagglutinin or calcium ionophore. Since the co‐stimulatory effect of 134‐2C2 mAb on PMA‐induced T cell proliferation was strongly inhibited by an anti‐Tac antibody, its involvement on the IL2/IL2 receptor pathway was investigated. An increased IL2 secretion in T cells cultured with PMA plus 134‐2C2 mAb was observed and Northern blot analysis showed that the mAb 134‐2C2 acts synergistically with PMA favoring the induction of both IL2 and interferon‐γ mRNA synthesis, as well as the enhancement of IL2 receptor and transferrin receptor mRNA expression. Studies on mechanisms implicated in signal transduction showed that 134‐2C2 mAb modifies neither intracellular calcium levels nor phosphoinositide breakdown. Additionally, no effect was exerted on protein kinase C translocation. These data suggest that the CD26 antigen is involved in T cell activation in an IL2/IL2 receptor‐dependent pathway.

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