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The role of Bruton’s tyrosine kinase in autoimmunity and implications for therapy
Open accessAbstract
Bruton's tyrosine kinase (BTK) mediates B cell signaling and is also present in innate immune cells but not T cells. BTK propagates B cell receptor (BCR) responses to antigen-engagement as well as to stimulation via CD40, toll-like receptors (TLRs), Fc receptors (FCRs) and chemokine receptors. Importantly, BTK can modulate signaling, acting as a "rheostat" rather than an "on-off" switch; thus, overexpression leads to autoimmunity while decreased levels improve autoimmune disease outcomes. Autoreactive B cells depend upon BTK for survival to a greater degree than normal B cells, reflected as loss of autoantibodies with maintenance of total antibody levels when BTK is absent. This review describes contributions of BTK to immune tolerance, including studies testing BTK-inhibitors for treatment of autoimmune diseases.
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“Importantly, BTK transduces constitutive signaling downstream of the BCR in many B-cell malignancies, so BTK has long been considered an attractive target for treating these diseases.”
From Bruton tyrosine kinase degradation as a therapeutic strategy for cancer (2019) · cites this paper as [1]
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Metadata
- Authors
- Crofford, L. J., Nyhoff, L. E., Sheehan, J. H., & Kendall, P. L.
- Affiliations
- Vanderbilt University (US)
- Corresponding author
- Crofford, Leslie J.
- Venue
- Expert Review of Clinical Immunology
- Publisher
- Informa UK Limited
- Published
- 2016-03-04
- Volume
- 12
- Issue
- 7
- Pages
- 763-773
- ISSN
- 1744-666X (ISSN-L)
- 1744-8409
- PMC
- PMC5070917
- OpenAlex
- W2258682798
- Cited by
- 142
- References
- 136
- Citations by year
- 2026: 9 · 2025: 15 · 2024: 13 · 2023: 18 · 2022: 29 · 2021: 21 · 2020: 9 · 2019: 13 · 2018: 8 · 2017: 5 · 2016: 2
- FWCI
- 0.90
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Expert Review of Clinical Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (NIAMS R01 AR049010, NIDDK R01 DK84246)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Immunodeficiency and Autoimmune Disorders
- Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
- Keywords
- Bruton's tyrosine kinase, autoimmunity, B cell signaling, B cell receptor signaling, CD40 signaling, Toll-like receptors, Fc receptors, chemokine receptors, autoreactive B cells, autoantibodies, immune tolerance, BTK inhibitors, autoimmune disease therapy
- MeSH terms
- Agammaglobulinaemia Tyrosine Kinase, Animals, Anti-Inflammatory Agents, Autoantibodies, Autoimmune Diseases, B-Lymphocytes, Humans, Immune Tolerance, Lymphocyte Activation, Protein-Tyrosine Kinases, Receptors, Antigen, B-Cell, Signal Transduction, Autoimmunity
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