Abstract
Radiation therapy for thoracic neoplasms is limited by the risk of radiation lung injury. Acute pneumonitis is thought to result in a perpetual cascade of cytokines production post-irradiation, which recruits macrophage, lymphocyte, neutrophil, and mast inflammatory cells, leading to eventual pulmonary fibrosis. It is unclear which is the key cellular mediator in this pathologic inflammatory milieu, and what are the crucial modulating immune interactions. Subsets of T cells can have either pro-inflammatory function (T helper and cytotoxic T cells), or immunosuppressive effects (T regulatory cells).
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