Regulation of epithelial immunity by IL-17 family cytokines

2012 ◽  
Vol 33 (7) ◽  
pp. 343-349 ◽  
Author(s):  
Rajita Pappu ◽  
Sascha Rutz ◽  
Wenjun Ouyang
Keyword(s):  
The Lancet ◽  
1988 ◽  
Vol 332 (8612) ◽  
pp. 652-654 ◽  
Author(s):  
S.E. Barton ◽  
D. Jenkins ◽  
J. Cuzick ◽  
P.H. Maddox ◽  
R. Edwards ◽  
...  

2014 ◽  
Vol 10 (8) ◽  
pp. e1004257 ◽  
Author(s):  
Julian R. Naglik ◽  
Jonathan P. Richardson ◽  
David L. Moyes

2018 ◽  
Vol 314 (2) ◽  
pp. G247-G255 ◽  
Author(s):  
Cristina Pardo-Camacho ◽  
Ana M González-Castro ◽  
Bruno K Rodiño-Janeiro ◽  
Marc Pigrau ◽  
María Vicario

As the largest interface between the outside and internal milieu, the intestinal epithelium constitutes the first structural component facing potential luminal threats to homeostasis. This single-cell layer is the epicenter of a tightly regulated communication network between external and internal factors that converge to prime defensive responses aimed at limiting antigen penetration and the maintenance of intestinal barrier function. The defensive role developed by intestinal epithelial cells (IEC) relies largely on the variety of receptors they express at both extracellular (apical and basolateral) and intracellular compartments, and the capacity of IEC to communicate with immune and nervous systems. IEC recognize pathogen-associated molecules by innate receptors that promote the production of mucus, antimicrobial substances, and immune mediators. Epithelial cells are key to oral tolerance maintenance and also participate in adaptive immunity through the expression of immunoglobulin (Ig) receptors and by promoting local Ig class switch recombination. In IEC, different types of antigens can be sensed by multiple immune receptors that share signaling pathways to assure effective responses. Regulated defensive activity maintains intestinal homeostasis, whereas a breakdown in the control of epithelial immunity can increase the intestinal passage of luminal content and microbial invasion, leading to inflammation and tissue damage. In this review, we provide an updated overview of the type of immune receptors present in the human intestinal epithelium and the responses generated to promote effective barrier function and maintain mucosal homeostasis.


2021 ◽  
Vol 118 (10) ◽  
pp. e2020922118
Author(s):  
Seonghan Jang ◽  
Peter Mergaert ◽  
Tsubasa Ohbayashi ◽  
Kota Ishigami ◽  
Shuji Shigenobu ◽  
...  

Most animals harbor a gut microbiota that consists of potentially pathogenic, commensal, and mutualistic microorganisms. Dual oxidase (Duox) is a well described enzyme involved in gut mucosal immunity by the production of reactive oxygen species (ROS) that antagonizes pathogenic bacteria and maintains gut homeostasis in insects. However, despite its nonspecific harmful activity on microorganisms, little is known about the role of Duox in the maintenance of mutualistic gut symbionts. Here we show that, in the bean bug Riptortus pedestris, Duox-dependent ROS did not directly contribute to epithelial immunity in the midgut in response to its mutualistic gut symbiont, Burkholderia insecticola. Instead, we found that the expression of Duox is tracheae-specific and its down-regulation by RNAi results in the loss of dityrosine cross-links in the tracheal protein matrix and a collapse of the respiratory system. We further demonstrated that the establishment of symbiosis is a strong oxygen sink triggering the formation of an extensive network of tracheae enveloping the midgut symbiotic organ as well as other organs, and that tracheal breakdown by Duox RNAi provokes a disruption of the gut symbiosis. Down-regulation of the hypoxia-responsive transcription factor Sima or the regulators of tracheae formation Trachealess and Branchless produces similar phenotypes. Thus, in addition to known roles in immunity and in the formation of dityrosine networks in diverse extracellular matrices, Duox is also a crucial enzyme for tracheal integrity, which is crucial to sustain mutualistic symbionts and gut homeostasis. We expect that this is a conserved function in insects.


2015 ◽  
Vol 291 (2) ◽  
pp. 998-1013 ◽  
Author(s):  
Raina N. Fichorova ◽  
Hidemi S. Yamamoto ◽  
Titilayo Fashemi ◽  
Evan Foley ◽  
Stanthia Ryan ◽  
...  
Keyword(s):  

2000 ◽  
Vol 192 (5) ◽  
pp. 705-718 ◽  
Author(s):  
Marie-Caroline Dieu-Nosjean ◽  
Catherine Massacrier ◽  
Bernhard Homey ◽  
Béatrice Vanbervliet ◽  
Jean-Jacques Pin ◽  
...  

Dendritic cells (DCs) form a network comprising different populations that initiate and differentially regulate immune responses. Langerhans cells (LCs) represent a unique population of DCs colonizing epithelium, and we present here observations suggesting that macrophage inflammatory protein (MIP)-3α plays a central role in LC precursor recruitment into the epithelium during inflammation. (a) Among DC populations, MIP-3α was the most potent chemokine inducing the selective migration of in vitro–generated CD34+ hematopoietic progenitor cell–derived LC precursors and skin LCs in accordance with the restricted MIP-3α receptor (CC chemokine receptor 6) expression to these cells. (b) MIP-3α was mainly produced by epithelial cells, and the migration of LC precursors induced by the supernatant of activated skin keratinocytes was completely blocked with an antibody against MIP-3α. (c) In vivo, MIP-3α was selectively produced at sites of inflammation as illustrated in tonsils and lesional psoriatic skin where MIP-3α upregulation appeared associated with an increase in LC turnover. (d) Finally, the secretion of MIP-3α was strongly upregulated by cells of epithelial origin after inflammatory stimuli (interleukin 1β plus tumor necrosis factor α) or T cell signals. Results of this study suggest a major role of MIP-3α in epithelial colonization by LCs under inflammatory conditions and immune disorders, and might open new ways to control epithelial immunity.


2017 ◽  
Vol 9 (4) ◽  
pp. 333-342 ◽  
Author(s):  
Mathilde Gendrin ◽  
Fanny Turlure ◽  
Faye H. Rodgers ◽  
Anna Cohuet ◽  
Isabelle Morlais ◽  
...  

Peptidoglycan recognition proteins (PGRPs) form a family of immune regulators that is conserved from insects to mammals. In the malaria vector mosquito Anophelescoluzzii, the peptidoglycan receptor PGRPLC activates the immune-deficiency (Imd) pathway limiting both the microbiota load and Plasmodium infection. Here, we carried out an RNA interference screen to examine the role of all 7 Anopheles PGRPs in infections with Plasmodium berghei and P. falciparum. We show that, in addition to PGRPLC, PGRPLA and PGRPS2/PGRPS3 also participate in antiparasitic defenses, and that PGRPLB promotes mosquito permissiveness to P. falciparum. We also demonstrate that following a mosquito blood feeding, which promotes growth of the gut microbiota, PGRPLA and PGRPLB positively and negatively regulate the activation of the Imd pathway, respectively. Our data demonstrate that PGRPs are important regulators of the mosquito epithelial immunity and vector competence.


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