The innate immune brakes of the lung

Respiratory mucosal surfaces are continuously exposed to not only innocuous non-self antigens but also pathogen-associated molecular patterns (PAMPs) originating from environmental or symbiotic microbes. According to either self/non-self or danger models, this should systematically result in homeostasis breakdown and the development of immune responses directed to inhaled harmless antigens, such as T helper type (Th)2-mediated asthmatic reactions, which is fortunately not the case in most people. This discrepancy implies the existence, in the lung, of regulatory mechanisms that tightly control immune homeostasis. Although such mechanisms have been poorly investigated in comparison to the ones that trigger immune responses, a better understanding of them could be useful in the development of new therapeutic strategies against lung diseases (e.g., asthma). Here, we review current knowledge on innate immune cells that prevent the development of aberrant immune responses in the lung, thereby contributing to mucosal homeostasis.

Automated summary

Respiratory mucosal surfaces are continuously exposed to innocuous non-self antigens and pathogen-associated molecular patterns (PAMPs). Despite the potential for immune responses, there are regulatory mechanisms in the lung that tightly control immune homeostasis and prevent the development of aberrant immune responses. Understanding these mechanisms could lead to the development of new therapeutic strategies for lung diseases like asthma.