The BTK inhibitor ibrutinib may protect against pulmonary injury in COVID-19–infected patients

Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus–Infected Pneumonia in Wuhan, China

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Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China

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SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor

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Inhibiting Bruton’s tyrosine kinase rescues mice from lethal influenza-induced acute lung injury

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BTKCys481Serdrives ibrutinib resistance via ERK1/2 and protects BTKwild-typeMYD88-mutated cells by a paracrine mechanism

(2018) Jiaji G. Chen et al.   BLOOD

CXCL13 levels are elevated in patients with Waldenström macroglobulinemia, and are predictive of major response to ibrutinib

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M1 Means Kill; M2 Means Heal

(2017) Klaus Ley   JOURNAL OF IMMUNOLOGY

CXCL13 levels are elevated in patients with Waldenström macroglobulinemia, and are predictive of major response to ibrutinib

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HCK is a survival determinant transactivated by mutated MYD88, and a direct target of ibrutinib

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The Membrane Protein of Severe Acute Respiratory Syndrome Coronavirus Functions as a Novel Cytosolic Pathogen-Associated Molecular Pattern To Promote Beta Interferon Induction via a Toll-Like-Receptor-Related TRAF3-Independent Mechanism

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Ibrutinib modifies the function of monocyte/macrophage population in chronic lymphocytic leukemia

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Disruption of in vivo Chronic Lymphocytic Leukemia Tumor-Microenvironment Interactions by Ibrutinib - Findings from an Investigator-Initiated Phase II Study

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A mutation in MYD88 (L265P) supports the survival of lymphoplasmacytic cells by activation of Bruton tyrosine kinase in Waldenstrom macroglobulinemia

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Alveolar Epithelial Cells Are Critical in Protection of the Respiratory Tract by Secretion of Factors Able To Modulate the Activity of Pulmonary Macrophages and Directly Control Bacterial Growth

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Innate Immune Responses to Bacterial Ligands in the Peripheral Human Lung – Role of Alveolar Epithelial TLR Expression and Signalling

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