Indicating that the accumulation of immune cells in A13-treated lungs at peak EAE is not inducing pulmonary fibrosis, analysis of immunostained tissue sections revealed only a marginal elevation in collagen type I and immune cell cluster-containing areas of EAE showed no accumulation of α-smooth muscle actin (αSMA) in A13-treated samples relative to naïve lung (Supplementary Fig. 14a). This evidence concerns the gene ACTA1 and pulmonary fibrosis.