Interstitial lung disease, a term for a group of disorders, causes lung fibrosis, is mostly
refractory to treatments and has a high death rate. After diagnosis the survival is up to 3 years but
in some cases the patients live much longer. It involves a heterogenous group of lung diseases that
exhibit progressive and irreversible destruction of the lung due to the formation of scars. This results
in lung malfunction, disruption of gas exchange, and eventual death because of respiratory
failure. The etiology of lung fibrosis is mostly unknown with a few exceptions. The major characteristics
of the disease are comprised of injury of epithelial type II cells, increased apoptosis, chronic
inflammation, monocytic and lymphocytic infiltration, accumulation of myofibroblasts, and inability
to repair damaged tissue properly. These events result in abnormal collagen deposition and
scarring. The inflammation process is mild, and the disease is primarily fibrotic driven. Immunosuppressants
do not treat the disease but the evidence is evolving that both innate and acquired immune
responses a well as the cytokines contribute to at least early progression of the disease. Furthermore,
mediators of inflammation including cytokines are involved throughout the process of
lung fibrosis. The diverse clinical outcome of the disease is due to different pattern of inflammatory
markers. Nonetheless, the development of novel therapeutic strategies requires better understanding
of the role of the immune response. This review highlights the role of the immune response in
interstitial lung disease and considers the therapeutic strategies based on these observations. For
this review several literature data sources were used to assess the role of the immune response in interstitial
lung disease and to evaluate the possible therapeutic strategies for the disease.
The role of glycolysis in immune response