Pulmonary T and B cells are important for protection of this mucosal barrier site. While viral infections lead to the development of ectopic lymphoid structures highly similar to germinal centers in secondary lymphoid organs, little is known about how T/B cooperation occurs in the unstructured, diffuse tissue infiltrates characteristic of autoimmune diseases and non-viral infections. Using a mouse model of interstitial lung inflammation, Schacht et al. found that naive B cells are directly activated in the lung tissue. Despite the absence of any germinal center-like structures, the interaction of B cells with peripheral T helper cells resulted in efficient somatic hypermutation and class switching. Macrophages were critical as antigen-presenting cells for this process. Unique B cell repertoires indicated that the lung response was autonomous from the lung-draining lymph node. Only lung GC-like B cells were switched to IgA and had a broader repertoire, making them ideal candidates to produce broadly neutralizing immunoglobulins against respiratory pathogens.
