The role of T-cells in radiation pneumonitis after bone marrow transplantation

Radiation pneumonitis is a frequent complication of bone marrow transplantation. In limiting the effective dose that can be given, it decreases the chances of cancer cell destruction and of graft acceptance. The incidence of radiation pneumonitis is increased if graft-versus-host disease or infection is present, presumably due to an interaction between T-cell-mediated and radiation-mediated damage. Even in the absence of graft-versus-host disease and infection, we have found that syngeneic T-cells can contribute to radiation pneumonitis in a bone marrow transplant setting. The incidence of radiation pneumonitis was higher after whole-body irradiation and bone marrow transplantation than after whole-thorax irradiation. In the former situation, but not the latter, prior thymectomy decreased the incidence of radiation pneumonitis. It is hypothesized that autoreactive T-cells escape induction of self-tolerance during regression of the immune system after whole-body irradiation and, because autoregulatory cells are eliminated, they can contribute to radiation pneumonitis. If this concept is correct, it provides another possible explanation for the sensitivity of the lung to post-transplant pneumonitis and suggests new strategies to limit the incidence of this serious transplant-related complication.