Consequently, our findings in IPF patients that (i) increased proportions of circulating plasmablasts and (IgA-)memory B-cells with (ii) enhanced BTK expression, (iii) augmented pulmonary Tfh-cell activation, and (iv) enhanced plasma autoreactive IgA are present indicate an important role for B-cells in IPF pathogenesis. Here, CD79A is linked to idiopathic pulmonary fibrosis.