SIRP-a triggers tolerogenic training of resident alveolar macrophages after inflammation, leading to immune paralysis and increased susceptibility to secondary pneumonia

The reprogramming of alveolar macropahges (AM) in mice after resolution of primary bacterial or viral pneumonia induced poor phagocytic capacity for several weeks. The tyrosine kinase-inhibitory receptor, SIRP-a, played a critical role in the establishment of the microenvironment that induced tolerogenic training. Overall design: Transcriptomic and epigenetic analyzes were made on uninfected mice (WT and SIRP-a KO) and 7 days after the infection was cured.