The following is a summary ofPlasma cell but not CD20-mediated B-cell depletion protects from bleomycin-induced lung fibrosis” published in the November 2022 issue of Respiratory by Prêle et al.

Idiopathic pulmonary fibrosis (IPF), is a type of interstitial lung disease that is associated with persistent inflammation and tissue remodelling. This condition ultimately results in fibrosis, decreased pulmonary function, respiratory failure, and death. Bleomycin (Blm)-induced lung fibrosis in mice replicates several clinical features of human idiopathic pulmonary fibrosis (IPF), including prominent lymphoid aggregates consisting primarily of B-cells that accumulate in the lung adjacent to areas of active fibrosis. Bleomycin (Blm) is a bleomycin derivative. 

In a previous study, researchers demonstrated that the presence of B-cells is necessary for the progression of Blm-induced lung fibrosis in mice. Investigators examined the effects of anti-CD20 B-cell ablation therapy to selectively remove mature B-cells from the immune system and inhibit Blm-induced lung fibrosis. Their goal was to determine the therapeutic potential of inhibiting B-cell function in pulmonary fibrosis. This was accomplished by studying the effects of the therapy. However, immunological phenotyping of peripheral blood and lung resident cells revealed that anti-CD20-treated animals preserved a significant frequency of CD19+ CD138+  plasma cells. B-cell ablation using anti-CD20 did not improve fibrosis in this paradigm. 

It was interesting to see that large amounts of CD138+ cells were also found in the lung tissue of patients with IPF. This finding was consistent with the mouse model. When mice were given bortezomib, a drug that eliminates plasma cells, the level of Blm-induced lung fibrosis was reduced. This finding suggests that plasma cells are crucial effector cells in the formation and progression of pulmonary fibrosis.