TLR7 Signaling in Lupus B Cells: New Insights into Synergizing Factors and Downstream Signals
Purpose of the Review Systemic lupus erythematosus (SLE) is driven by nucleic acid-containing antigens that stimulate endosomal TLRs. We review new advances in our understanding of how TLR7 signaling in B cells drives autoimmunity. Recent Findings Pathogenic B cell responses to TLR7 engagement are s...
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| Published in | Current rheumatology reports Vol. 23; no. 11; p. 80 |
|---|---|
| Main Author | |
| Format | Journal Article |
| Language | English |
| Published |
New York
Springer US
24.11.2021
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Purpose of the Review
Systemic lupus erythematosus (SLE) is driven by nucleic acid-containing antigens that stimulate endosomal TLRs. We review new advances in our understanding of how TLR7 signaling in B cells drives autoimmunity.
Recent Findings
Pathogenic B cell responses to TLR7 engagement are shaped by the disease-associated cytokine environment. TLR7, IFNγ, and IL-21 together promote the formation of autoreactive germinal centers and the ABC/DN2 B cell subset. BAFF and type 1 IFNs enhance autoantibody production from transitional B cells in concert with TLR7. TLR7 signaling components STAT1, BANK1, IRF5, SLC15A4, and CXorf21/TASL are associated genetically with SLE and important for lupus development in mice, while role of T-bet is controversial. Proper control of TLR7 trafficking by UNC93B1, syntenin-1, and αvβ3 integrin is critical for preventing autoimmunity.
Summary
A better understanding of TLR7 signaling has revealed potential new therapeutic approaches for SLE, several of which are being tested in animal models or clinical trials. |
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| AbstractList | Purpose of the Review
Systemic lupus erythematosus (SLE) is driven by nucleic acid-containing antigens that stimulate endosomal TLRs. We review new advances in our understanding of how TLR7 signaling in B cells drives autoimmunity.
Recent Findings
Pathogenic B cell responses to TLR7 engagement are shaped by the disease-associated cytokine environment. TLR7, IFNγ, and IL-21 together promote the formation of autoreactive germinal centers and the ABC/DN2 B cell subset. BAFF and type 1 IFNs enhance autoantibody production from transitional B cells in concert with TLR7. TLR7 signaling components STAT1, BANK1, IRF5, SLC15A4, and CXorf21/TASL are associated genetically with SLE and important for lupus development in mice, while role of T-bet is controversial. Proper control of TLR7 trafficking by UNC93B1, syntenin-1, and αvβ3 integrin is critical for preventing autoimmunity.
Summary
A better understanding of TLR7 signaling has revealed potential new therapeutic approaches for SLE, several of which are being tested in animal models or clinical trials. PURPOSE OF THE REVIEWSystemic lupus erythematosus (SLE) is driven by nucleic acid-containing antigens that stimulate endosomal TLRs. We review new advances in our understanding of how TLR7 signaling in B cells drives autoimmunity. RECENT FINDINGSPathogenic B cell responses to TLR7 engagement are shaped by the disease-associated cytokine environment. TLR7, IFNγ, and IL-21 together promote the formation of autoreactive germinal centers and the ABC/DN2 B cell subset. BAFF and type 1 IFNs enhance autoantibody production from transitional B cells in concert with TLR7. TLR7 signaling components STAT1, BANK1, IRF5, SLC15A4, and CXorf21/TASL are associated genetically with SLE and important for lupus development in mice, while role of T-bet is controversial. Proper control of TLR7 trafficking by UNC93B1, syntenin-1, and αvβ3 integrin is critical for preventing autoimmunity. A better understanding of TLR7 signaling has revealed potential new therapeutic approaches for SLE, several of which are being tested in animal models or clinical trials. Systemic lupus erythematosus (SLE) is driven by nucleic acid-containing antigens that stimulate endosomal TLRs. We review new advances in our understanding of how TLR7 signaling in B cells drives autoimmunity. Pathogenic B cell responses to TLR7 engagement are shaped by the disease-associated cytokine environment. TLR7, IFNγ, and IL-21 together promote the formation of autoreactive germinal centers and the ABC/DN2 B cell subset. BAFF and type 1 IFNs enhance autoantibody production from transitional B cells in concert with TLR7. TLR7 signaling components STAT1, BANK1, IRF5, SLC15A4, and CXorf21/TASL are associated genetically with SLE and important for lupus development in mice, while role of T-bet is controversial. Proper control of TLR7 trafficking by UNC93B1, syntenin-1, and αvβ3 integrin is critical for preventing autoimmunity. A better understanding of TLR7 signaling has revealed potential new therapeutic approaches for SLE, several of which are being tested in animal models or clinical trials. |
| ArticleNumber | 80 |
| Author | Satterthwaite, Anne B. |
| AuthorAffiliation | 1 Department of Internal Medicine, Rheumatic Diseases Division and Department of Immunology, UT Southwestern Medical Center, Dallas, TX 75390 USA |
| AuthorAffiliation_xml | – name: 1 Department of Internal Medicine, Rheumatic Diseases Division and Department of Immunology, UT Southwestern Medical Center, Dallas, TX 75390 USA |
| Author_xml | – sequence: 1 givenname: Anne B. surname: Satterthwaite fullname: Satterthwaite, Anne B. email: anne.satterthwaite@utsouthwestern.edu organization: Department of Internal Medicine, Rheumatic Diseases Division and Department of Immunology, UT Southwestern Medical Center |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34817709$$D View this record in MEDLINE/PubMed |
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| Keywords | Lupus Signaling Transcription factors TLR7 B cells Cytokines |
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Systemic lupus erythematosus (SLE) is driven by nucleic acid-containing antigens that stimulate endosomal TLRs. We review new advances in... Systemic lupus erythematosus (SLE) is driven by nucleic acid-containing antigens that stimulate endosomal TLRs. We review new advances in our understanding of... PURPOSE OF THE REVIEWSystemic lupus erythematosus (SLE) is driven by nucleic acid-containing antigens that stimulate endosomal TLRs. We review new advances in... |
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| SubjectTerms | Animals Autoimmunity B-Lymphocytes - metabolism Humans Interferon Regulatory Factors Lupus Erythematosus, Systemic Medicine Medicine & Public Health Mice Rheumatology Section Editor Signal Transduction Systemic Lupus Erythematosus (G Tsokos Toll-Like Receptor 7 - metabolism Topical Collection on Systemic Lupus Erythematosus |
| Title | TLR7 Signaling in Lupus B Cells: New Insights into Synergizing Factors and Downstream Signals |
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