[en] The full text of the publication follows. Purpose: The purpose of this study was to analyze the radiosensitivity of human lymphocytes. T cells, whether activated or not, seems to be a good model to study the radiosensitivity of normal tissues. To clarify the mechanism of action of these radiations, we study genes modulation that provides a response to alpha particles. Materials and methods: Lymphocytes from healthy donors were isolated and half were subjected to polyclonal activation monitored by expression of CD25. Both the non-activated T lymphocytes (NATL) and activated lymphocytes (ATL) were incubated with BSA-CHX-DTPA coupled to ²¹³Bi (185 kBq/ml) or with BSA-SAB coupled to ²¹¹At (74 kBq/ml). Tests were performed on the cells of four different donors to assess mortality, redox activity, cell cycle distribution and DNA double strands breaks. Gene expression was investigated using the DNA micro-arrays. Results: Forty-eight hours after irradiation with ²¹³Bi (185 kBq/ml), mortality was 29.9 ±2.2% for NATL and 12.4 ± 7.6% for ATL. With ²¹¹At (74 kBq/ml), mortality was 44.3 ± 8.8% for NATL and 16.5 ± 8.2% for ATL. For the two alpha radionuclides irradiation, the cell cycle distribution of NATL remained quiescent and alpha irradiation did not trigger their activation; for ATL, irradiation gets blocked in G2/M. An increase of 15% in the number of DNA double strands was observed in two populations of lymphocytes at 42 hours when T cells were irradiated with ²¹³Bi, but the increase is less important when T cells were irradiated with ²¹¹At. Six genes were up regulated at least 1,5-fold: CDKN1A, DRAM, FAS, MDM2, PLK2, TNFRSF10B. Conclusion: In conclusion, we identified molecular and cellular mechanisms that cells trigger after alpha irradiation. Preliminary data indicate the involvement of pathways of apoptosis, autophagy and cell cycle. (authors)