Rapid αß T-cell responses orchestrate innate immunity in response to Staphylococcal enterotoxin A.

In the generation of a traditional immune response against invading pathogens, innate cells guide T cells by programming their differentiation. However, here we demonstrate that αß T cells have an essential role in priming innate immunity in the lung after Staphylococcus aureus enterotoxin A (SEA) inhalation. We found that SEA induces waves of cellular activation, cytokine production, and migration into the lung tissue and airways. However, this innate response was completely inhibited in the absence of αß T cells. Specifically, we found that interleukin (IL)-17A was required for the recruitment of neutrophils and monocytes into the lung. The cellular source of IL-17A was γδ T cells, which increased their IL-17A production following SEA but only in an αß T-cell-dependent manner. Thus, rapid T-cell activation orchestrates innate immunity and may be a new point of therapeutic intervention for acute lung injury.

Are Th17 cells in the gut pathogenic or protective?

Th17 cells are abundant in multiple chronic inflammatory and autoimmune diseases. Clinical trials with antibodies to interleukin (IL)-17A, one of the Th17-cell signature cytokines, have recently reported therapeutic benefit in multiple patient populations; however, in Crohn's disease the role of Th17 cells and IL-17A appears to be more complicated. The development of different subsets of Th17 cells and their relative pathogenic activities with a focus on the gut environment will be discussed.