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[en] Full text: UVB radiation (290-320 nm) is immunosuppressive by multiple mechanisms allowing the outgrowth of UV-induced tumours in both mouse and man. Furthermore, patients with non-melanoma skin cancers have a higher risk of death from other cancers which could be explained by UV-induced immunomodulation. The mechanism(s) of suppression by UVB depend on whether the sensitising antigen is applied to the irradiated site ('local') or to non-irradiated sites ('systemic'). In the former, the activity of UV-induced TNFα is important as it affects the migration of Langerhans cells to draining lymph nodes. In contrast, histamine from dermal mast cells is critical to the early events by which UVB can suppress systemic immune responses. The prevalence of dermal mast cells in 7 strains and substrains of mice correlates directly with their susceptibility to UVB-induced systemic immunosuppression. Furthermore, mast cell depleted mice (Wf/Wf) are resistant to UVB-induced systemic immunomodulation. However, they become susceptible after reconstitution of the site to be irradiated with bone marrow derived mast cell precursors. The mice also gain susceptibility to cis-urocanic acid-induced systemic immunomodulation. There is considerable evidence that histamine is the mast cell product critical to downstream immunosuppressive events. Firstly, physiological concentrations of histamine suppress contact hypersensitivity responses. Secondly, histamine receptor antagonists halve UVB-induced systemic immunosuppression. Thirdly, mice with different UVB-susceptibilities are equally susceptible to histamine-induced immunosuppression, and finally, histamine can suppress contact hypersensitivity responses in Wf/Wf mice. We suggest that histamine may be immunomodulatory by multiple pathways. Histamine can induce the production of immunosuppressive prostanoids from keratinocytes. A lymphocyte-derived, histamine-induced suppressor factor was reported in the 1970's. More recently histamine has been shown to stimulate IL-10 production by macrophages and to induce the production of type 2 cytokines from T cell clones. Such actions in draining lymph nodes may be responsible for the UVB-induced switch from a type 1 to type 2 cytokine response following antigen sensitisation

[en] The key to answering some fundamental radiation biology questions, such as the hazards of ionizing radiation, is the ability to detect each charged particle as it interacts with a cell. However, due to the stochastic nature of energy deposition and the random position of tracks, these effects cannot be stimulated in the laboratory using conventional broad-field exposures. The availability of microbeam, especially the single particle microbeam in the world, whereby individual cells can be irradiated with either a single or an exact number of particles provides a useful tool to address these questions. The author describes the rationale, historical, and nowadays development of microbeam facilities in the world, as well as their biological researches and future development