γδ T cells protect against lung fibrosis via IL-22

Inflammation-induced pulmonary fibrosis (PF) leads to irreversible loss of lung function and is a predictor of mortality in numerous lung diseases. Why some subjects with lung inflammation but not others develop PF is unclear. In a mouse model of hypersensitivity pneumonitis that progresses to lung fibrosis upon repeated exposure to the ubiquitous microorganism Bacillus subtilis, γδ T cells expand in the lung and inhibit collagen deposition. We show that a subset of these γδ cells represents the predominant source of the Th17 cytokine IL-22 in this model. Preventing expression of IL-22, either by mutating the aryl hydrocarbon receptor (AhR) or inhibiting AhR signaling, accelerated lung fibrosis. Direct blockade of IL-22 also enhanced collagen deposition in the lung, whereas administration of recombinant IL-22 inhibited lung fibrosis. Moreover, the presence of protective γδ T cells and IL-22 diminished recruitment of CD4+ T cells to lung. These data reveal a protective pathway that involves the inhibition of αβ T cells by regulatory IL-22–secreting γδ T cells

Single and Paired Point Defects in a 2D Wigner Crystal

Using the path-integral Monte Carlo method, we calculate the energy to form single and pair vacancies and interstitials in a two-dimensional Wigner crystal of electrons. We confirm that the lowest-lying energy defects of a 2D electron Wigner crystal are interstitials, with a creation energy roughly 2/3 that of a vacancy. The formation energy of the defects goes to zero near melting, suggesting that point defects might mediate the melting process. In addition, we find that the interaction between defects is strongly attractive, so that most defects will exist as bound pairs.Comment: 4 pages, 5 encapsulated figure