RESUMO
More than 20 years ago, the 'danger theory' was proposed which explains why potent immune responses with no microbial components are elicited against tissue transplants, injuries, tumours and autoimmune diseases. It states that the immune system can distinguish between dangerous and innocuous endogenous signals. In response to trauma or other types of tissue and cell damage, certain molecules that function inside the cell are released or secreted from damaged or dying cells. Such mechanisms initiate an immune response in the absence of infection. These immunostimulatory molecules were named damage-associated molecular patterns (DAMPs). In this article, we will review the available data on the influence of select DAMPs on lung cancer cells and tumour microenvironments. We will also summarize the current information regarding the interactions between lung cancer-associated DAMPs and their toll-like receptors.
