scholarly journals Dectin-2 Is a Pattern Recognition Receptor for Fungi That Couples with the Fc Receptor γ Chain to Induce Innate Immune Responses

2006 ◽  
Vol 281 (50) ◽  
pp. 38854-38866 ◽  
Author(s):  
Kota Sato ◽  
Xiao-li Yang ◽  
Tatsuo Yudate ◽  
Jin-Sung Chung ◽  
Jianming Wu ◽  
...  
Keyword(s):  
Pattern Recognition ◽  
Immune Responses ◽  
Fc Receptor ◽  
Pattern Recognition Receptor ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Recognition Receptor

Pattern recognition receptor-mediated innate immune responses in seminal vesicle epithelial cell and their impacts on cellular function†

2019 ◽  
Vol 101 (4) ◽  
pp. 733-747 ◽  
Author(s):  
Maolei Gong ◽  
Fei Wang ◽  
Weihua Liu ◽  
Ran Chen ◽  
Han Wu ◽  
...  
Keyword(s):  
Pattern Recognition ◽  
Epithelial Cells ◽  
Immune Responses ◽  
Pattern Recognition Receptors ◽  
Seminal Vesicles ◽  
Pattern Recognition Receptor ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Toll Like Receptor ◽  
Recognition Receptor

Abstract The seminal vesicles can be infected by microorganisms, thereby resulting in vesiculitis and impairment in male fertility. Innate immune responses in seminal vesicles cells to microbial infections, which facilitate vesiculitis, have yet to be investigated. The present study aims to elucidate pattern recognition receptor–mediated innate immune responses in seminal vesicles epithelial cells. Various pattern recognition receptors, including Toll-like receptor 3, Toll-like receptor 4, cytosolic ribonucleic acid, and deoxyribonucleic acid sensors, are abundantly expressed in seminal vesicles epithelial cells. These pattern recognition receptors can recognize their respective ligands, thus activating nuclear factor kappa B and interferon regulatory factor 3. The pattern recognition receptor signaling induces expression of pro-inflammatory cytokines, such as tumor necrosis factor alpha (Tnfa) and interleukin 6 (Il6), chemokines monocyte chemoattractant protein-1 (Mcp1) and C–X–C motif chemokine 10 (Cxcl10), and type 1 interferons Ifna and Ifnb. Moreover, pattern recognition receptor-mediated innate immune responses up-regulated the expression of microsomal prostaglandin E synthase and cyclooxygenase 2, but they down-regulated semenogelin-1 expression. These results provide novel insights into the mechanism underlying vesiculitis and its impact on the functions of the seminal vesicles.

Pattern Recognition Receptor-initiated Innate Immune Responses in mouse Prostatic Epithelial Cells

2021 ◽  
Author(s):  
Xiaoqin Yu ◽  
Ran Chen ◽  
Fei Wang ◽  
Weihua Liu ◽  
Wenjing Zhang ◽  
...  
Keyword(s):  
Pattern Recognition ◽  
Epithelial Cells ◽  
Immune Responses ◽  
Pattern Recognition Receptor ◽  
Innate Immune ◽  
Poly I:C ◽  
Innate Immune Responses ◽  
Local Inflammation ◽  
Recognition Receptor

Abstract Three major pathogenic states of the prostate, including benign prostatic hyperplasia, prostate cancer, and prostatitis, are related to the local inflammation. However, the mechanisms underlying the initiation of prostate inflammation remain largely unknown. Given that the innate immune responses of the tissue-specific cells to microbial infection or auto-antigens contribute to local inflammation, this study focused on pattern recognition receptor (PRR)-initiated innate immune responses in mouse prostatic epithelial cells (PECs). Primary mouse PECs abundantly expressed Toll-like receptor 3 (TLR3), TLR4, TLR5, melanoma differentiation-associated protein 5 (MDA5) and p204. These PRRs can be activated by their respective ligands: lipopolysaccharide (LPS) and flagellin of Gram-negative bacteria for TLR4 and TLR5, polyinosinic-polycytidylic acid (poly(I:C)) for TLR3 and MDA5, and herpes simplex virus DNA analog (HSV60) for p204. LPS and flagellin predominantly induced the expression of inflammatory cytokines, including TNFA, IL6, MCP1, and CXCL10. Poly(I:C) and HSV60 predominantly induced the expression of type 1 interferons (IFNA and IFNB) and antiviral proteins: Mx GTPase 1, 2′,5′-oligoadenylate synthetase 1, and IFN-stimulated gene 15. The replication of mumps virus in PECs was inhibited by type 1 IFN signaling. These findings provide insights into the mechanisms underlying innate immune response in the prostate.

scholarly journals Peptidomimetic 1-Benzyl-5-methyl-4-(n-octylamino)pyrimidin-2(1H)-one Showed Cardioprotection Effect in a Myocardial Ischemia (MI) Mouse Model

Proceedings ◽  
2019 ◽  
Vol 22 (1) ◽  
pp. 72
Author(s):  
Lena Trifonov ◽  
Vadim Nudelman ◽  
Michael Zhenin ◽  
Guy Cohen ◽  
Krzysztof Jozwiak ◽  
...  
Keyword(s):  
Immune Response ◽  
Pattern Recognition ◽  
Myocardial Ischemia ◽  
Mouse Model ◽  
Innate Immune Response ◽  
Pattern Recognition Receptor ◽  
Innate Immune ◽  
Microbial Pathogens ◽  
Toll Like Receptors ◽  
Recognition Receptor

TLR4, a member of the toll-like receptors (TLRs) family, serves as a pattern recognition receptor in the innate immune response to different microbial pathogens. [...]

scholarly journals SlPRA1A/RAB attenuate EIX immune responses via degradation of LeEIX2 pattern recognition receptor

2018 ◽  
Vol 13 (5) ◽  
pp. e1467689 ◽  
Author(s):  
L. Pizarro ◽  
M. Leibman-Markus ◽  
S. Schuster ◽  
M. Bar ◽  
A. Avni
Keyword(s):  
Pattern Recognition ◽  
Immune Responses ◽  
Pattern Recognition Receptor ◽  
Recognition Receptor

scholarly journals Interplay of protease-activated receptors and NOD pattern recognition receptors in epithelial innate immune responses to bacteria

2010 ◽  
Vol 131 (2) ◽  
pp. 113-119 ◽  
Author(s):  
Whasun O. Chung ◽  
Jonathan Y. An ◽  
Lei Yin ◽  
Beth M. Hacker ◽  
Maryam G. Rohani ◽  
...  
Keyword(s):  
Pattern Recognition ◽  
Immune Responses ◽  
Pattern Recognition Receptors ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Protease Activated Receptors

scholarly journals The Many Roles of Galectin-3, a Multifaceted Molecule, in Innate Immune Responses against Pathogens

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Laura Díaz-Alvarez ◽  
Enrique Ortega
Keyword(s):  
Immune Responses ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Terminal Protein ◽  
Molecular Pattern ◽  
Evolutionarily Conserved ◽  
Carbohydrate Recognition Domains ◽  
Galectin 3 ◽  
The Many ◽  
Recognition Receptor

Galectins are a group of evolutionarily conserved proteins with the ability to bindβ-galactosides through characteristic carbohydrate-recognition domains (CRD). Galectin-3 is structurally unique among all galectins as it contains a C-terminal CRD linked to an N-terminal protein-binding domain, being the only chimeric galectin. Galectin-3 participates in many functions, both intra- and extracellularly. Among them, a prominent role for Galectin-3 in inflammation has been recognized. Galectin-3 has also been shown to directly bind to pathogens and to have various effects on the functions of the cells of the innate immune system. Thanks to these two properties, Galectin-3 participates in several ways in the innate immune response against invading pathogens. Galectin-3 has been proposed to function not only as a pattern-recognition receptor (PRR) but also as a danger-associated molecular pattern (DAMP). In this review, we analyze the various roles that have been assigned to Galectin-3, both as a PRR and as a DAMP, in the context of immune responses against pathogenic microorganisms.

scholarly journals Selectively expressing SARS-CoV-2 Spike protein S1 subunit in cardiomyocytes induces cardiac hypertrophy in mice.

2021 ◽  
Author(s):  
Steven G. Negron ◽  
Chase W. Kessinger ◽  
Bing Xu ◽  
William T. Pu ◽  
Zhiqiang Lin
Keyword(s):  
Immune Responses ◽  
Cardiac Injury ◽  
Innate Immune ◽  
Spike Protein ◽  
Innate Immune Responses ◽  
Toll Like Receptor 4 ◽  
Cardiac Inflammation ◽  
Leucine Rich Repeats ◽  
Recognition Receptor

Cardiac injury is common in hospitalized COVID-19 patients and portends poorer prognosis and higher mortality. To better understand how SARS-CoV-2 (CoV-2) damages the heart, it is critical to elucidate the biology of CoV-2 encoded proteins, each of which may play multiple pathological roles. For example, CoV-2 Spike glycoprotein (CoV-2-S) not only engages ACE2 to mediate virus infection, but also directly impairs endothelial function and can trigger innate immune responses in cultured murine macrophages. Here we tested the hypothesis that CoV-2-S damages the heart by activating cardiomyocyte (CM) innate immune responses. HCoV-NL63 is another human coronavirus with a Spike protein (NL63-S) that also engages ACE2 for virus entry but is known to only cause moderate respiratory symptoms. We found that CoV-2-S and not NL63-S interacted with Toll-like receptor 4 (TLR4), a crucial pattern recognition receptor that responsible for detecting pathogen and initiating innate immune responses. Our data show that the S1 subunit of CoV-2-S (CoV-2-S1) interacts with the extracellular leucine rich repeats-containing domain of TLR4 and activates NF-kB. To investigate the possible pathological role of CoV-2-S1 in the heart, we generated a construct that expresses membrane-localized CoV-2-S1 (S1-TM). AAV9-mediated, selective expression of the S1-TM in CMs caused heart dysfunction, induced hypertrophic remodeling, and elicited cardiac inflammation. Since CoV-2-S does not interact with murine ACE2, our study presents a novel ACE2-independent pathological role of CoV-2-S, and suggests that the circulating CoV-2-S1 is a TLR4-recognizable alarmin that may harm the CMs by triggering their innate immune responses.

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