Intestinal Tuft-2 Cells Exert Antimicrobial Immunity Via Sensing Bacterial Metabolite N-Undecanoylglycine by Vomeronasal Receptor Vmn2r26

2021 ◽  
Author(s):  
Zhen Xiong ◽  
Jingjing Geng ◽  
Xiaoxiao Zhu ◽  
Yuwei Xu ◽  
Dongdong Fan ◽  
...  
Keyword(s):  
Vomeronasal Receptor ◽  
Antimicrobial Immunity

scholarly journals From immune to olfactory expression: neofunctionalization of formyl peptide receptors

2021 ◽  
Vol 383 (1) ◽  
pp. 387-393
Author(s):  
Madlaina Boillat ◽  
Alan Carleton ◽  
Ivan Rodriguez
Keyword(s):  
Expression Patterns ◽  
Vomeronasal Organ ◽  
Formyl Peptide Receptor ◽  
Regulatory Sequence ◽  
Powerful Source ◽  
Peptide Receptor ◽  
Gene Shuffling ◽  
Evolutionary Innovation ◽  
Vomeronasal Receptor ◽  
Formyl Peptide

Abstract Variations in gene expression patterns represent a powerful source of evolutionary innovation. In a rodent living about 70 million years ago, a genomic accident led an immune formyl peptide receptor (FPR) gene to hijack a vomeronasal receptor regulatory sequence. This gene shuffling event forced an immune pathogen sensor to transition into an olfactory chemoreceptor, which thus moved from sensing the internal world to probing the outside world. We here discuss the evolution of the FPR gene family, the events that led to their neofunctionalization in the vomeronasal organ and the functions of immune and vomeronasal FPRs.

Expression of Cell-Mediated Antimicrobial Immunity by Mouse Trophoblast Monolayers

1983 ◽  
Vol 147 (6) ◽  
pp. 1006-1010 ◽  
Author(s):  
C. S. Pavia
Keyword(s):  
Antimicrobial Immunity

Immunosensation: Neuroimmune Cross Talk in the Skin

2021 ◽  
Vol 39 (1) ◽  
Author(s):  
Masato Tamari ◽  
Aaron M. Ver Heul ◽  
Brian S. Kim
Keyword(s):  
Immune System ◽  
Host Immunity ◽  
The Body ◽  
Annual Review ◽  
Publication Date ◽  
Protective Behaviors ◽  
Evolutionarily Conserved ◽  
Structural Barrier ◽  
Thermal Stimuli ◽  
Antimicrobial Immunity

Classically, skin was considered a mere structural barrier protecting organisms from a diversity of environmental insults. In recent decades, the cutaneous immune system has become recognized as a complex immunologic barrier involved in both antimicrobial immunity and homeostatic processes like wound healing. To sense a variety of chemical, mechanical, and thermal stimuli, the skin harbors one of the most sophisticated sensory networks in the body. However, recent studies suggest that the cutaneous nervous system is highly integrated with the immune system to encode specific sensations into evolutionarily conserved protective behaviors. In addition to directly sensing pathogens, neurons employ novel neuroimmune mechanisms to provide host immunity. Therefore, given that sensation underlies various physiologies through increasingly complex reflex arcs, a much more dynamic picture is emerging of the skin as a truly systemic organ with highly coordinated physical, immunologic, and neural functions in barrier immunology. Expected final online publication date for the Annual Review of Immunology, Volume 39 is April 2021. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

Regulated proteolysis of p62/SQSTM1 enables differential control of autophagy and nutrient sensing

2018 ◽  
Vol 11 (559) ◽  
pp. eaat6903 ◽  
Author(s):  
Julia Sanchez-Garrido ◽  
Vanessa Sancho-Shimizu ◽  
Avinash R. Shenoy
Keyword(s):  
Nutrient Sensing ◽  
Caspase 8 ◽  
Rimmed Vacuoles ◽  
Sequestosome 1 ◽  
Inflammatory Conditions ◽  
Mtorc1 Signaling ◽  
Differential Control ◽  
Antimicrobial Immunity ◽  
Lateral Sclerosis

The multidomain scaffold protein p62 (also called sequestosome-1) is involved in autophagy, antimicrobial immunity, and oncogenesis. Mutations in SQSTM1, which encodes p62, are linked to hereditary inflammatory conditions such as Paget’s disease of the bone, frontotemporal dementia (FTD), amyotrophic lateral sclerosis, and distal myopathy with rimmed vacuoles. Here, we report that p62 was proteolytically trimmed by the protease caspase-8 into a stable protein, which we called p62TRM. We found that p62TRM, but not full-length p62, was involved in nutrient sensing and homeostasis through the mechanistic target of rapamycin complex 1 (mTORC1). The kinase RIPK1 and caspase-8 controlled p62TRM production and thus promoted mTORC1 signaling. An FTD-linked p62 D329G polymorphism and a rare D329H variant could not be proteolyzed by caspase-8, and these noncleavable variants failed to activate mTORC1, thereby revealing the detrimental effect of these mutations. These findings on the role of p62TRM provide new insights into SQSTM1-linked diseases and mTORC1 signaling.

scholarly journals The RNA helicase DDX3X is an essential mediator of innate antimicrobial immunity

2018 ◽  
Vol 14 (11) ◽  
pp. e1007397 ◽  
Author(s):  
Daniel Szappanos ◽  
Roland Tschismarov ◽  
Thomas Perlot ◽  
Sandra Westermayer ◽  
Katrin Fischer ◽  
...  
Keyword(s):  
Rna Helicase ◽  
Antimicrobial Immunity

Fos-Like Immunoreactivity in the Vomeronasal Receptor Neurons of Mice

1999 ◽  
pp. 535-547
Author(s):  
Woochan Jang ◽  
H. David ◽  
J. A. Maruniak ◽  
Eric Walters
Keyword(s):  
Vomeronasal Receptor ◽  
Receptor Neurons

scholarly journals microRNA-210 and microRNA-3570 Negatively Regulate NF-κB-Mediated Inflammatory Responses by Targeting RIPK2 in Teleost Fish

2021 ◽  
Vol 12 ◽  
Author(s):  
Hui Su ◽  
Renjie Chang ◽  
Weiwei Zheng ◽  
Yuena Sun ◽  
Tianjun Xu
Keyword(s):  
Immune Response ◽  
Signaling Pathway ◽  
Innate Immune Response ◽  
Inflammatory Responses ◽  
Innate Immune ◽  
Regulatory Role ◽  
Inflammatory Cytokine Production ◽  
Immune Genes ◽  
Lower Vertebrates ◽  
Antimicrobial Immunity

Pathogen infection can cause the production of inflammatory cytokines, which are key mediators that cause the host’s innate immune response. Therefore, proper regulation of immune genes associated with inflammation is essential for immune response. Among them, microRNAs (miRNAs) as gene regulator have been widely reported to be involved in the innate immune response of mammals. However, the regulatory network in which miRNAs are involved in the development of inflammation is largely unknown in lower vertebrates. Here, we identified two miRNAs from miiuy croaker (Miichthys miiuy), miR-210 and miR-3570, which play a negative regulatory role in host antibacterial immunity. We found that the expressions of miR-210 and miR-3570 were significantly upregulated under the stimulation of Gram-negative bacterium vibrio harveyi and LPS (lipopolysaccharide). Induced miR-210 and miR-3570 inhibit inflammatory cytokine production by targeting RIPK2, thereby avoiding excessive inflammation. In particular, we found that miR-210 and miR-3570 negatively regulate antimicrobial immunity by regulating the RIPK2-mediated NF-κB signaling pathway. The collective results indicated that both miRNAs are used as negative feedback regulators to regulate RIPK2-mediated NF-κB signaling pathway and thus play a regulatory role in bacteria-induced inflammatory response.

scholarly journals Type III Interferons: Emerging Roles in Autoimmunity

2021 ◽  
Vol 12 ◽  
Author(s):  
Sindhu Manivasagam ◽  
Robyn S. Klein
Keyword(s):  
Immune Cells ◽  
T Cell Differentiation ◽  
Cd4 T Cell ◽  
Th1 Cells ◽  
Type Iii ◽  
Adaptive Immune ◽  
Adaptive Immune Cells ◽  
Cellular Specificity ◽  
Epithelial Barriers ◽  
Antimicrobial Immunity

Type III interferons (IFNs) or the lambda IFNs (IFNLs or IFN-λs) are antimicrobial cytokines that play key roles in immune host defense at endothelial and epithelial barriers. IFNLs signal via their heterodimeric receptor, comprised of two subunits, IFNLR1 and interleukin (IL)10Rβ, which defines the cellular specificity of the responses to the cytokines. Recent studies show that IFNL signaling regulates CD4+ T cell differentiation, favoring Th1 cells, which has led to the identification of IFNL as a putative therapeutic target for autoimmune diseases. Here, we summarize the IFNL signaling pathways during antimicrobial immunity, IFNL-mediated immunomodulation of both innate and adaptive immune cells, and induction of autoimmunity.

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