Radiation therapy is one of the most common treatment strategies for thorax
malignancies. One of the considerable limitations of this
therapy is its toxicity to normal tissue. The lung is the major dose-limiting organ for
radiotherapy. That is because ionizing radiation produces
reactive oxygen species that induce lesions, and not only is
tumor tissue damaged, but overwhelming inflammatory lung damage can occur in the alveolar epithelium and capillary endothelium. This damage may result in radiation-induced
pneumonitis and/or
fibrosis. While describing the lung response to irradiation generally, the main focus of this review is on
cytokines and their roles and functions within the individual stages. We discuss the relationship between radiation and
cytokines and their direct and indirect effects on the formation and development of
radiation injuries. Although this topic has been intensively studied and discussed for years, we still do not completely understand the roles of
cytokines. Experimental data on
cytokine involvement are fragmented across a large number of experimental studies; hence, the need for this review of the current knowledge.
Cytokines are considered not only as molecular factors involved in the signaling network in
pathological processes, but also for their diagnostic potential. A concentrated effort has been made to identify the significant immune system
proteins showing positive correlation between serum levels and tissue damages. Elucidating the correlations between the extent and nature of radiation-induced
pulmonary injuries and the levels of one or more key
cytokines that initiate and control those damages may improve the efficacy of
radiotherapy in
cancer treatment and ultimately the well-being of patients.