Identifying the Patterns of Pattern Recognition Receptors

Hill, Andrea A.; Diehl, Gretchen E.

doi:10.1016/j.immuni.2018.08.027

Cited by 11 publications

(7 citation statements)

References 9 publications

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“…Myeloid lineage cells express pattern recognition receptors (PRRs) 4 that recognize both pathogen- and damage-associated molecular patterns (PAMPs and DAMPs, respectively), which are broadly shared across kingdoms 5 and initiate polarized T helper (Th) cell responses. 4 , 6 Dendritic cell–expressed PRRs (e.g., TLR4) and diverse C-type lectin receptors have been implicated in recognizing allergen-associated PAMPs.…”

Section: Introductionmentioning

confidence: 99%

Environmental allergens trigger type 2 inflammation through ripoptosome activation

Brusilovsky

Rochman

et al. 2021

Nat Immunol

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Environmental allergens including fungi, insects and mites trigger type 2 immunity; however, the innate sensing mechanisms and initial signaling events remain unclear. Herein, we demonstrate that allergens trigger RIPK1-caspase 8 ripoptosome activation in epithelial cells. The active caspase 8 subsequently engages caspases 3 and 7, which directly mediate intracellular maturation and release of IL-33, a pro-atopy, innate immunity, alarmin cytokine. Mature IL-33 maintained functional interaction with the cognate ST2 receptor and elicited potent pro-atopy inflammatory activity in vitro and in vivo. Inhibiting caspase 8 pharmacologically and deleting murine Il33 and Casp8 each attenuated allergic inflammation in vivo. Clinical data substantiated ripoptosome activation and IL-33 maturation as likely contributors to human allergic inflammation. Our findings reveal an epithelial barrier, allergen-sensing mechanism that converges on the ripoptosome as an intracellular molecular signaling platform triggering type 2 innate immune responses. These findings have significant implications for understanding and treating human allergic diseases.

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Section: Introductionmentioning

confidence: 99%

Environmental allergens trigger type 2 inflammation through ripoptosome activation

Brusilovsky

Rochman

et al. 2021

Nat Immunol

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“…In our results, microscopic examination of TLR-2 immunostained sections revealed positive TLR-2 reaction in normal epithelial cells of the control group. Hill and Diehl [24] declared that, in humans, TLR expression is mainly expressed in immune cells, where it drives immune responses and is less widespread in epithelial cells where it offers a barrier against pathogens.…”

Section: Discussionmentioning

confidence: 99%

The effect of smoking on clinical presentation and expression of TLR-2 and CD34 in Oral lichen Planus patients: clinical and immunohistochemical study

2020

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Background: Oral lichen planus is a chronic inflammatory disease which is considered as a potential precancerous condition. Numerous studies have confirmed that inflammation is a strong risk factor for cancer development. Smoking is associated with potentially malignant disorders of the oral and oropharyngeal mucosa. The adverse consequences of smoking in various pathologies are mediated by its effects on the immune-inflammatory system. Little is known about the influence of cigarette smoke content on the course of OLP and inflammatory response. Methods: Twenty oral lichen planus smoker patients, 20 oral lichen planus non-smoker patients and 20 control patients were included in this work. Pain and clinical scores were calculated for each patient. Image analysis to calculate area percent for TLR-2 and CD34 immuno-expression was performed. Data was tabulated and statistically analyzed. Results: The present study showed no statistically significant difference in clinical and pain scores between the smoker and non-smoker groups. However, there was a significant difference in area percent values for TLR-2 and CD34 immuno-expression between the smoker and the non-smoker groups. Conclusion: Smoking enhanced TLR-2 and CD34 expression in OLP which are considered as inflammatory mediators and are contributing factors in the pathogenesis of oral lichen planus.

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“…, via encapsulation or surface presentation) is an important strategy to induce maturation of DCs, which can improve PRR recognition and antigen processing. 37,89 The majority of commonly used PRR ligands for vaccine applications have been demonstrated to work well with NP formulations to improve vaccine efficacy. 90,91 These ligands include TLR-3 agonist poly(I : C), TLR-4 agonist MPLA, TLR-7/8 agonist imiquimod, TLR-9 agonist CpG-ODN and STNG agonist, which can trigger the maturation of DCs and the expression of co-stimulatory molecules.…”

Section: Polymeric Nps For Ex Vivo Subunit Cancer Vaccinesmentioning

confidence: 99%