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TLR7

Official Full Name
toll like receptor 7
Organism
Homo sapiens
GeneID
51284
Background
The protein encoded by this gene is a member of the Toll-like receptor (TLR) family which plays a fundamental role in pathogen recognition and activation of innate immunity. TLRs are highly conserved from Drosophila to humans and share structural and functional similarities. The human TLR family comprises 11 members. They recognize pathogen-associated molecular patterns (PAMPs) that are expressed on infectious agents, and mediate the production of cytokines necessary for the development of effective immunity. For the recognition of structural components in foreign microorganisms, the various TLRs exhibit different patterns of expression as well; in this way for example, TLR-3, -7, and -8 are essential in the recognition of single-stranded RNA viruses. TLR7 senses single-stranded RNA oligonucleotides containing guanosine- and uridine-rich sequences from RNA viruses, a recognition occuring in the endosomes of plasmacytoid dendritic cells and B cells. This gene is predominantly expressed in lung, placenta, and spleen, and is phylogenetically related and lies in close proximity to another family member, TLR8, on chromosome X. [provided by RefSeq, Aug 2020]
Synonyms
IMD74; SLEB17; TLR7-like;
Bio Chemical Class
Toll-like receptor
Protein Sequence
MVFPMWTLKRQILILFNIILISKLLGARWFPKTLPCDVTLDVPKNHVIVDCTDKHLTEIPGGIPTNTTNLTLTINHIPDISPASFHRLDHLVEIDFRCNCVPIPLGSKNNMCIKRLQIKPRSFSGLTYLKSLYLDGNQLLEIPQGLPPSLQLLSLEANNIFSIRKENLTELANIEILYLGQNCYYRNPCYVSYSIEKDAFLNLTKLKVLSLKDNNVTAVPTVLPSTLTELYLYNNMIAKIQEDDFNNLNQLQILDLSGNCPRCYNAPFPCAPCKNNSPLQIPVNAFDALTELKVLRLHSNSLQHVPPRWFKNINKLQELDLSQNFLAKEIGDAKFLHFLPSLIQLDLSFNFELQVYRASMNLSQAFSSLKSLKILRIRGYVFKELKSFNLSPLHNLQNLEVLDLGTNFIKIANLSMFKQFKRLKVIDLSVNKISPSGDSSEVGFCSNARTSVESYEPQVLEQLHYFRYDKYARSCRFKNKEASFMSVNESCYKYGQTLDLSKNSIFFVKSSDFQHLSFLKCLNLSGNLISQTLNGSEFQPLAELRYLDFSNNRLDLLHSTAFEELHKLEVLDISSNSHYFQSEGITHMLNFTKNLKVLQKLMMNDNDISSSTSRTMESESLRTLEFRGNHLDVLWREGDNRYLQLFKNLLKLEELDISKNSLSFLPSGVFDGMPPNLKNLSLAKNGLKSFSWKKLQCLKNLETLDLSHNQLTTVPERLSNCSRSLKNLILKNNQIRSLTKYFLQDAFQLRYLDLSSNKIQMIQKTSFPENVLNNLKMLLLHHNRFLCTCDAVWFVWWVNHTEVTIPYLATDVTCVGPGAHKGQSVISLDLYTCELDLTNLILFSLSISVSLFLMVMMTASHLYFWDVWYIYHFCKAKIKGYQRLISPDCCYDAFIVYDTKDPAVTEWVLAELVAKLEDPREKHFNLCLEERDWLPGQPVLENLSQSIQLSKKTVFVMTDKYAKTENFKIAFYLSHQRLMDEKVDVIILIFLEKPFQKSKFLQLRKRLCGSSVLEWPTNPQAHPYFWQCLKNALATDNHVAYSQVFKETV
Open
Disease
Asthma, Autoimmune disease, Bladder cancer, Diabetes mellitus, Diffuse large B-cell lymphoma, Epidermal dysplasias, Hepatitis virus infection, Herpes simplex infection, Human immunodeficiency virus disease, Immune system disease, Liver cancer, Lung cancer, Lupus erythematosus, Malaria, Melanoma, Mycosis fungoides, Psoriasis, Skin cancer, Solid tumour/cancer, Squamous cell carcinoma, Vasomotor/allergic rhinitis
Approved Drug
2 +
Clinical Trial Drug
20 +
Discontinued Drug
3 +

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Detailed Information

The TLR7 gene is located on the X chromosome (Xp22.2) and encodes a protein that is a member of the Toll-like receptor (TLR) family. The protein consists of an extracellular recognition domain, rich in leucine repeats (LRR), a transmembrane region, and an intracellular TIR (Toll/IL-1 receptor) signaling domain. TLR7 is primarily expressed in plasmacytoid dendritic cells (pDCs), B cells, and monocytes, localized in the endosomal membranes, where it functions as a crucial receptor for recognizing single-stranded RNA (ssRNA) and its derivatives, such as guanosine analogs. The activation of TLR7 is dependent on endosomal acidification and the collaborative action of RNA-processing enzymes, RNase T2/RNase 2, which cleave long-chain RNA into fragments containing GU/UR motifs, allowing for their binding in the ligand-binding pocket of TLR7.

Physiological Roles of TLR7 in Immune Regulation

TLR7 plays a critical role in initiating antiviral immunity. Upon recognizing RNA viruses like influenza or coronaviruses, TLR7 activation in pDCs induces the production of type I interferons (IFN-α/β), which are key in activating natural killer cells and enhancing antigen presentation. For instance, in COVID-19, TLR7 detects the viral RNA of SARS-CoV-2 and triggers an early interferon response, which is essential for clearing the virus from the body. Beyond antiviral defense, TLR7 has a significant impact on autoimmune diseases, particularly those with gender disparities. Systemic lupus erythematosus (SLE) affects females at a much higher rate than males (approximately 9:1), and this has been linked to the phenomenon of X chromosome escape of TLR7 expression. In females, the expression of both X-linked alleles of TLR7 leads to higher protein levels, which increases the sensitivity of immune cells to self-RNA, such as ribonucleoproteins, and results in excessive IFN-α production. This mechanism contributes to the breakdown of B cell tolerance and the development of autoimmunity. Notably, functional mutations in TLR7, such as R28G, have been shown to directly cause pediatric SLE, underscoring TLR7's central role in autoimmune pathogenesis.

Figure 1. TLR7 signaling in lupus B cells.Figure 1. TLR7 signaling in lupus B cells. (Satterthwaite AB. et al., 2021)

Disease Associations and Genetic Susceptibility

Variants in TLR7 exhibit a unique disease-associated pattern that includes both loss-of-function (LOF) and gain-of-function (GOF) mutations, leading to distinct immune dysregulation:

Loss-of-function mutations in TLR7, such as N215S, can result in the receptor's inability to respond to ligands, which is associated with more severe infections. A recent study conducted in Spain (2025) found that males with rare TLR7 mutations were at a significantly higher risk of developing severe COVID-19 pneumonia and requiring ICU admission. The mechanism behind this is that the LOF mutations delay the IFN-I response, which leads to uncontrolled viral replication and a cytokine storm, a hallmark of severe infection.

Gain-of-function mutations in TLR7, such as R28G, have been linked to several autoimmune diseases, including SLE and rheumatoid arthritis. These mutations increase the receptor's recognition of self-RNA, promoting the activation of extrafollicular B cells and the production of autoantibodies, thus exacerbating disease severity. This heightened sensitivity to self-RNA can drive chronic inflammation and tissue damage.

Common polymorphisms in TLR7, such as Q11L (rs179008) and c.4-151A>G (rs179009), have clinical implications by regulating TLR7 expression levels. These polymorphisms have been associated with an increased risk of requiring oxygen therapy, with an odds ratio (OR) of 3.01 (P=0.003), suggesting their role in individualized risk assessment, especially for respiratory diseases.

Targeted Therapeutic Strategies for TLR7 Modulation

Given TLR7's dual role in both immune defense and autoimmunity, therapeutic strategies targeting this receptor must carefully balance immune activation and suppression. Several approaches are being explored:

Antagonists for Autoimmune Diseases: Small molecule antagonists such as M5049 have shown efficacy in reducing anti-dsDNA antibody titers in SLE patients, and phase II clinical trials are underway. A derivative of Artemisinin, called SM934, developed by the Chinese Academy of Sciences, inhibits the interaction between TLR7 and IRAK4, effectively reducing IFN-α production. This molecule is also being evaluated in lupus trials.

Agonists for Cancer Immunotherapy: TLR7 agonists, like 24e/25a, developed by Tsinghua University's Liao Xuebin team, have been shown to reshape the tumor microenvironment in colorectal cancer models. These agonists increase the infiltration of M1 macrophages and CD8+ T cells, and promote a favorable Teff/Treg ratio, enhancing anti-tumor immunity. When combined with PD-1 antibodies, these agonists can induce complete tumor regression in 30% of animal models.

Gender-Specific Therapies: Gender-specific approaches to TLR7-targeted therapy have shown promise. For female patients with SLE, low-dose TLR7 antagonists might be more effective, whereas male patients suffering from severe infections may benefit from early intervention with TLR7 agonists, such as Resiquimod, to enhance their immune response against pathogens.

Challenges and Future Directions

The primary challenge in developing TLR7-targeted therapies lies in distinguishing between self-RNA and pathogen-derived RNA. Several strategies are being explored to overcome this:

Ligand-Specific Engineering: One approach is to design allosteric agonists that specifically bind to viral RNA motifs, such as 5'-triphosphates, thereby avoiding autoimmune activation. This would ensure that only viral infections are targeted while preserving self-tolerance.

Cell-Type Specific Delivery: Targeting TLR7 ligands specifically to tumor-draining lymph nodes or pDCs using nanocarriers could limit systemic inflammation and prevent the risk of generalized immune activation.

Combination Therapies: Combining TLR7 agonists with other immune-modulating therapies, such as anti-CD20 antibodies, could effectively deplete autoreactive B cells, but such combinations must be carefully monitored to avoid over-suppressing the immune system, which may increase susceptibility to infections.

Reference

  1. Song Y, Zhou W. Role of TLR7 in the pathogenesis of primary Sjögren's syndrome. Clin Exp Rheumatol. 2024 Dec;42(12):2513-2519.

  2. Satterthwaite AB. TLR7 Signaling in Lupus B Cells: New Insights into Synergizing Factors and Downstream Signals. Curr Rheumatol Rep. 2021 Nov 24;23(11):80.

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