New study finds blocking histones using antibodies alleviates lung fibrosis

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New study finds blocking histones using antibodies alleviates lung fibrosis
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Lung fibrosis is a debilitating disease affecting nearly 250,000 people in the U.S. alone with 50,000 new cases reported each year. There is currently no cure and limited available treatment options, underscoring the pressing need to better understand why people get this disease.

β 1 , from platelets. TGFβ1 in turn blocks the release of another mediator, interleukin-27 , from specialized immune cells called macrophages. This inhibition prevents IL-27 from suppressing fibrosis.

"Although histones have previously been implicated in fibrosis, how they mediate the development of the disease is not completely understood. Our findings provide novel mechanistic insights into how the altered interactions between different cell types contributes to histone-mediated fibrosis development," explain Arjun Sharma, one of the first authors, and Markus Bosmann, MD, the corresponding author and associate professor of medicine and pathology & laboratory medicine.

Further experiments including screening lung airway fluid to assess levels of immune mediators after blocking histones, tissue staining and genetic deletion, all identified TGFβ1 and IL-27 as key downstream molecular mediators of histones during fibrosis."This study helps bridge a crucial knowledge gap by elucidating the role of three key proteins—histones, TGFβ1, and IL-27 in fibrosis development, opening up avenues for new therapies," says Bosmann.

Riehl, Dennis R. et al, Externalized histones fuel pulmonary fibrosis via a platelet-macrophage circuit of TGFβ1 and IL-27,

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