scholarly journals A bacterial carbohydrate links innate and adaptive responses through Toll-like receptor 2

2006 ◽  
Vol 203 (13) ◽  
pp. 2853-2863 ◽  
Author(s):  
Qun Wang ◽  
Rachel M. McLoughlin ◽  
Brian A. Cobb ◽  
Marie Charrel-Dennis ◽  
Kathleen J. Zaleski ◽  
...  
Keyword(s):  
Interferon Γ ◽  
Cd4 T Cell ◽  
Toll Like Receptor ◽  
Adaptive Responses ◽  
Intraabdominal Abscess ◽  
Germ Free ◽  
Th2 Cell ◽  
Th1 Cytokine ◽  
Toll Like Receptor 2 ◽  
Cell Balance

Commensalism is critical to a healthy Th1/Th2 cell balance. Polysaccharide A (PSA), which is produced by the intestinal commensal Bacteroides fragilis, activates CD4+ T cells, resulting in a Th1 response correcting the Th2 cell skew of germ-free mice. We identify Toll-like receptors as crucial to the convergence of innate and adaptive responses stimulated by PSA. Optimization of the Th1 cytokine interferon-γ in PSA-stimulated dendritic cell–CD4+ T cell co-cultures depends on both Toll-like receptor (TLR) 2 and antigen presentation. Synergy between the innate and adaptive responses was also shown when TLR2−/− mice exhibited impaired intraabdominal abscess formation in response to B. fragilis. Commensal bacteria, using molecules like PSA, potentially modulate the Th1/Th2 cell balance and the response to infection by coordinating both the innate and adaptive pathways.

scholarly journals Upregulated Expression of Toll-Like Receptor 7 in Peripheral Blood Basophils of Patients With Allergic Rhinitis

2021 ◽  
pp. 194589242199303
Author(s):  
Lihong Wang ◽  
Mengmeng Zhan ◽  
Junling Wang ◽  
Dong Chen ◽  
Nan Zhao ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Mrna Levels ◽  
Toll Like Receptor ◽  
Cell Functions ◽  
Th2 Cell ◽  
Hla Dr ◽  
Ku812 Cells ◽  
Th1 Cytokine ◽  
Der P1 ◽  
Blood Granulocyte

Background Recently, it has been reported that Toll-like receptor 7 (TLR7) agonists can improve allergic rhinitis (AR) symptoms by up-regulation of Th1 cytokine release and suppression of Th2 cell functions. However, little is known of the expression of TLR7 in basophils of AR. Objective To explore the expression of TLR7 in basophils of AR, and influence of allergens on TLR7 expression. Methods The expression levels of TLR7 in basophils of patients with AR were determined by flow cytometry, and the influence of allergens on TLR7 expression was examined by real time (q) PCR. Results The percentages of TLR7+CCR3+ cells ( P < 0.001 and P = 0.011), TLR7+CD123+HLA-DR− cells ( P = 0 .016 and P = 0.042) and TLR7+CCR3+CD123+HLA-DR− cells ( P = 0.046 and P = 0.035) in blood granulocyte and mononucleated cell populations of the patients with AR were increased, respectively compared with HC subjects. TLR7 MFI on CCR3+ cells ( P = 0.050 and P = 0.043), CD123+HLA-DR− cells ( P < 0.001 and P = 0.002) and CCR3+CD123+HLA-DR− cells ( P < 0.001 and P = 0.003) were enhanced compared with HC subjects. Allergens Der p1 and OVA provoked upregulation of TLR7 expression at both protein and mRNA levels and IL-13 production in KU812 cells. House Dust Mite extract (HDME), Artemisia sieversiana wild allergen extract (ASWE), IL-31, IL-33, IL-37, and TSLP provoked elevation of IL-6 release from KU812 cells following 2 h incubation period. Conclusions The percentage of TLR7+ basophils and TLR7 expression intensity in a single basophil are both increased in the blood of patients with AR, indicating that basophils likely contribute to the pathogenesis of AR via TLR7.

Toll-Like Receptor–2 Agonist–Allergen Coupling Efficiently Redirects Th2 Cell Responses and Inhibits Allergic Airway Eosinophilia

2012 ◽  
Vol 47 (6) ◽  
pp. 852-863 ◽  
Author(s):  
Jayendra Kumar Krishnaswamy ◽  
Adan Chari Jirmo ◽  
Abdul Mannan Baru ◽  
Thomas Ebensen ◽  
Carlos A. Guzmán ◽  
...  
Keyword(s):  
Toll Like Receptor ◽  
Airway Eosinophilia ◽  
Cell Responses ◽  
Th2 Cell ◽  
Toll Like Receptor 2

scholarly journals Patency ofLitomosoides sigmodontisinfection depends on Toll-like receptor 4 whereas Toll-like receptor 2 signalling influences filarial-specific CD4+T-cell responses

Immunology ◽  
2016 ◽  
Vol 147 (4) ◽  
pp. 429-442 ◽  
Author(s):  
Maria B. Rodrigo ◽  
Sandy Schulz ◽  
Vanessa Krupp ◽  
Manuel Ritter ◽  
Katharina Wiszniewsky ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Responses ◽  
Cd4 T Cell ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Cell Responses ◽  
Toll Like Receptor 2

Human Langerhans cells selectively activated via Toll-like receptor 2 agonists acquire migratory and CD4+ T cell stimulatory capacity

2008 ◽  
Vol 83 (5) ◽  
pp. 1118-1127 ◽  
Author(s):  
Matthias Peiser ◽  
Juliana Koeck ◽  
Carsten J. Kirschning ◽  
Burghardt Wittig ◽  
Reinhard Wanner
Keyword(s):  
T Cell ◽  
Langerhans Cells ◽  
Cd4 T Cell ◽  
Toll Like Receptor ◽  
Stimulatory Capacity ◽  
Toll Like Receptor 2 ◽  
Cell Stimulatory Capacity

scholarly journals Microbe-Mediated Activation of Toll-like Receptor 2 Drives PDL1 Expression in HNSCC

Cancers ◽  
2021 ◽  
Vol 13 (19) ◽  
pp. 4782
Author(s):  
Jacqueline E Mann ◽  
Megan L Ludwig ◽  
Aditi Kulkarni ◽  
Erin B Scheftz ◽  
Isabel R Murray ◽  
...  
Keyword(s):  
Immune Evasion ◽  
Interferon Γ ◽  
Multiple Models ◽  
Toll Like Receptor ◽  
Cell Line Model ◽  
Genome Wide ◽  
A Genome ◽  
Toll Like Receptor 2 ◽  
Future Work ◽  
Stimulation Of

As immunotherapies targeting the PDL1 checkpoint have become a mainstay of treatment for a subset of head and neck squamous cell carcinoma (HNSCC) patients, a detailed understanding of the mechanisms underlying PDL1-mediated immune evasion is needed. To elucidate factors regulating expression of PDL1 in HNSCC cells, a genome-wide CRISPR profiling approach was implemented to identify genes and pathways conferring altered PDL1 expression in an HNSCC cell line model. Our screen nominated several candidate PDL1 drivers, including Toll-like Receptor 2 (TLR2). Depletion of TLR2 blocks interferon-γ-induced PDL1 expression, and stimulation of TLR2 with either Staphylococcus aureus or a bacterial lipopeptide mimetic, Pam3CSK4, enhanced PDL1 expression in multiple models. The data herein demonstrate a role for TLR2 in modulating the expression of PDL1 in HNSCC models and suggest that microbiota may directly modulate immunosuppression in cancer cells. Our study represents a step toward disentangling the diverse pathways and stimuli regulating PDL1 expression in HNSCC and underscores a need for future work to characterize the complex microbiome in HNSCC patients treated with immunotherapy.

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