Role of the CD1a molecule in the superantigen-induced activation of MHC class II negative human thymocytes

Bacterial superantigens (Sag) are potent activators of T cells. This T-cell activation has been described as an MHC class II dependent phenomenon. We have observed that human thymocytes depleted of MHC class II positive cells are still able to proliferate in response to the staphylococcal enterotoxin A (SEA). This proliferation was clearly inhibited by the addition of monoclonal antibodies directed against the CD1a molecule. In contrast, monoclonal antibodies directed against the CD1b and CD1c molecules have no effect on the Sag-induced activation of the CD2 (+) MHC class II (−) thymocytes. We next examined the ability of the CD1a molecule to transmit transmembrane signals. Results obtained indicate that CD1a ligation on these thymocytes induced tyrosine phosphorylation of the p56 lck tyrosine kinase. Signal transduction via CD1a is further confirmed by the observation of a significant intracellular calcium flux (Ca i ++) in thymocytes following CD1a engagement. These data demonstrate that CD1a ligation induces a signal transduction pathway which has a potential role in the bacterial superantigen-induced activation of human CD2 (+) MHC class II (−) thymocytes.