Arming Th17 Cells for Antifungal Host Defense

2013 ◽  
Vol 7 (2) ◽  
pp. 138-143 ◽  
Author(s):  
André Gladiator ◽  
Kerstin Trautwein-Weidner ◽  
Eva Bär ◽  
Salomé LeibundGut-Landmann
Keyword(s):  
Host Defense ◽  
Th17 Cells

scholarly journals Extracellular traps released by antimicrobial TH17 cells contribute to host defense

2020 ◽  
Author(s):  
George W. Agak ◽  
Alice Mouton ◽  
Rosane Teles ◽  
Thomas A. Weston ◽  
Marco Morselli ◽  
...  
Keyword(s):  
Host Defense ◽  
Th17 Cells ◽  
Extracellular Traps

scholarly journals IL-17A and Th17 Cells in Lung Inflammation: An Update on the Role of Th17 Cell Differentiation and IL-17R Signaling in Host Defense against Infection

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Hsing-Chuan Tsai ◽  
Sharlene Velichko ◽  
Li-Yin Hung ◽  
Reen Wu
Keyword(s):  
Cell Differentiation ◽  
Host Defense ◽  
Th17 Cell ◽  
Th17 Cells ◽  
Critical Role ◽  
Klebsiella Pneumonia ◽  
Antimicrobial Proteins ◽  
Cytokines And Chemokines ◽  
Th17 Cell Differentiation

The significance of Th17 cells and interleukin- (IL-)17A signaling in host defense and disease development has been demonstrated in various infection and autoimmune models. Numerous studies have indicated that Th17 cells and its signature cytokine IL-17A are critical to the airway’s immune response against various bacteria and fungal infection. Cytokines such as IL-23, which are involved in Th17 differentiation, play a critical role in controllingKlebsiella pneumonia(K. pneumonia) infection. IL-17A acts on nonimmune cells in infected tissues to strengthen innate immunity by inducing the expression of antimicrobial proteins, cytokines, and chemokines. Mice deficient in IL-17 receptor (IL-17R) expression are susceptible to infection by various pathogens. In this review, we summarize the recent advances in unraveling the mechanism behind Th17 cell differentiation, IL-17A/IL-17R signaling, and also the importance of IL-17A in pulmonary infection.

scholarly journals Th17 cells and mucosal host defense

2007 ◽  
Vol 19 (6) ◽  
pp. 377-382 ◽  
Author(s):  
Shean J. Aujla ◽  
Patricia J. Dubin ◽  
Jay K. Kolls
Keyword(s):  
Host Defense ◽  
Th17 Cells

scholarly journals Identification of Novel Molecular Markers of Human Th17 Cells

Cells ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 1611 ◽  
Author(s):  
Anna Sałkowska ◽  
Kaja Karaś ◽  
Iwona Karwaciak ◽  
Aurelia Walczak-Drzewiecka ◽  
Mariusz Krawczyk ◽  
...  
Keyword(s):  
Host Defense ◽  
Th17 Cell ◽  
Th17 Cells ◽  
Cathepsin L ◽  
Cell Type ◽  
Protein Levels ◽  
Pathological Conditions ◽  
Th17 Lymphocytes ◽  
New Information ◽  
Apolipoprotein D

Th17 cells are important players in host defense against pathogens such as Staphylococcus aureus, Candida albicans, and Bacillus anthracis. Th17 cell-mediated inflammation, under certain conditions in which balance in the immune system is disrupted, is the underlying pathogenic mechanism of certain autoimmune disorders, e.g., rheumatoid arthritis, Graves’ disease, multiple sclerosis, and psoriasis. In the present study, using transcriptomic profiling, we selected genes and analyzed the expression of these genes to find potential novel markers of Th17 lymphocytes. We found that APOD (apolipoprotein D); C1QL1 (complement component 1, Q subcomponent-like protein 1); and CTSL (cathepsin L) are expressed at significantly higher mRNA and protein levels in Th17 cells than in the Th1, Th2, and Treg subtypes. Interestingly, these genes and the proteins they encode are well associated with the function of Th17 cells, as these cells produce inflammation, which is linked with atherosclerosis and angiogenesis. Furthermore, we found that high expression of these genes in Th17 cells is associated with the acetylation of H2BK12 within their promoters. Thus, our results provide new information regarding this cell type. Based on these results, we also hope to better identify pathological conditions of clinical significance caused by Th17 cells.

scholarly journals Th17 cells and IL-17 receptor signaling are essential for mucosal host defense against oral candidiasis

2009 ◽  
Vol 206 (2) ◽  
pp. 299-311 ◽  
Author(s):  
Heather R. Conti ◽  
Fang Shen ◽  
Namrata Nayyar ◽  
Eileen Stocum ◽  
Jianing N. Sun ◽  
...  
Keyword(s):  
Host Defense ◽  
Th17 Cells ◽  
Oral Candidiasis ◽  
Gene Profiling ◽  
Anatomical Location ◽  
T Helper 1 ◽  
Signature Genes ◽  
Mucosal Candidiasis ◽  
Disseminated Disease

The commensal fungus Candida albicans causes oropharyngeal candidiasis (OPC; thrush) in settings of immunodeficiency. Although disseminated, vaginal, and oral candidiasis are all caused by C. albicans species, host defense against C. albicans varies by anatomical location. T helper 1 (Th1) cells have long been implicated in defense against candidiasis, whereas the role of Th17 cells remains controversial. IL-17 mediates inflammatory pathology in a gastric model of mucosal candidiasis, but is host protective in disseminated disease. Here, we directly compared Th1 and Th17 function in a model of OPC. Th17-deficient (IL-23p19−/−) and IL-17R–deficient (IL-17RA−/−) mice experienced severe OPC, whereas Th1-deficient (IL-12p35−/−) mice showed low fungal burdens and no overt disease. Neutrophil recruitment was impaired in IL-23p19−/− and IL-17RA−/−, but not IL-12−/−, mice, and TCR-αβ cells were more important than TCR-γδ cells. Surprisingly, mice deficient in the Th17 cytokine IL-22 were only mildly susceptible to OPC, indicating that IL-17 rather than IL-22 is vital in defense against oral candidiasis. Gene profiling of oral mucosal tissue showed strong induction of Th17 signature genes, including CXC chemokines and β defensin-3. Saliva from Th17-deficient, but not Th1-deficient, mice exhibited reduced candidacidal activity. Thus, the Th17 lineage, acting largely through IL-17, confers the dominant response to oral candidiasis through neutrophils and antimicrobial factors.

scholarly journals NLRP1B and NLRP3 control the host response following colonization by the commensal protist Tritrichomonas musculis.

2021 ◽  
Author(s):  
Pailin Chiaranunt ◽  
Kyle Burrows ◽  
Louis Ngai ◽  
Eric Y Cao ◽  
Helen Liang ◽  
...  
Keyword(s):  
Host Defense ◽  
Th17 Cell ◽  
Th17 Cells ◽  
Host Response ◽  
Cell Activation ◽  
Intestinal Protozoa ◽  
Host Protection ◽  
Salmonella Infections ◽  
Immune Changes ◽  
Microbial Host

Commensal intestinal protozoa, unlike their pathogenic relatives, are neglected members of the mammalian microbiome. These microbes have a significant impact on host intestinal immune homeostasis, typically by elevating anti-microbial host defense. Tritrichomonas musculis (T. mu), a protozoan gut commensal, strengthens the intestinal host defense against enteric Salmonella infections through Asc- and Il1r1-dependent Th1 and Th17 cell activation. However, the underlying inflammasomes mediating this effect remain unknown. Here, we report that colonization with T. mu results in an increase in luminal extracellular ATP, elevated levels of IL-1b, and increased numbers of IL-18 receptor-expressing Th1 and Th17 cells in the colon. Mice deficient in either Nlrp1b or Nlrp3 failed to display these protozoan-driven immune changes and lost resistance to enteric Salmonella infections even in the presence of T. mu. These findings demonstrate that T. mu-mediated host protection requires sensors of extra and intracellular ATP to confer full resistance to enteric Salmonella infections.

scholarly journals Respective IL-17A production by γδ T and Th17 cells and its implication in host defense against chlamydial lung infection

2016 ◽  
Vol 14 (10) ◽  
pp. 850-861 ◽  
Author(s):  
Hong Bai ◽  
Xiaoling Gao ◽  
Lei Zhao ◽  
Ying Peng ◽  
Jie Yang ◽  
...  
Keyword(s):  
Host Defense ◽  
Th17 Cells ◽  
Lung Infection

scholarly journals Th17 cells provide direct protective effects that limit stomach parasite burden following orogastric mucosal Trypanosoma cruzi infection

2020 ◽  
Author(s):  
Catherine W. Cai ◽  
Christopher S. Eickhoff ◽  
Krystal A. Meza ◽  
Jennifer R. Blase ◽  
Rebecca E. Audette ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Nadph Oxidase ◽  
Host Defense ◽  
Mucosal Immunity ◽  
Oxidase Activity ◽  
Th17 Cells ◽  
Vaccine Development ◽  
Protective Mechanism ◽  
Macrophage Infection ◽  
Nadph Oxidase Activity

AbstractTrypanosoma cruzi is the intracellular parasite of Chagas disease, a chronic condition characterized by cardiac and gastrointestinal morbidity. Protective immunity requires CD4+ T cells, and Th1 cells and IFN-γ are important players in host defense. More recently, Th17 cells and IL-17 have been shown to exert protective functions in systemic T. cruzi infection. However, it remains unclear whether Th17 cells and IL-17A protect against mucosal infection, which is an important cause of human outbreaks. We found that IL-17RA knock-out (KO) mice are highly susceptible to orogastric infection, indicating an important function for this cytokine in mucosal immunity to T. cruzi. To investigate the specific role of Th17 cells for mucosal immunity, we reconstituted RAG1 KO mice with T. cruzi-specific T cell receptor transgenic Th17 cells prior to orogastric T. cruzi challenges. We found that Th17 cells provided protection against gastric mucosal T. cruzi infection, indicated by significantly lower stomach parasite burdens. In vitro macrophage infection assays revealed that protection by Th17 cells is reversed with IL-17A neutralization or loss of macrophage NADPH oxidase activity. Consistent with this, in vivo, mice lacking functional NADPH oxidase were not protected by Th17 cell transfer. These data are the first report that Th17 cells protect against mucosal T. cruzi infection, and identify a novel protective mechanism involving the induction of NADPH oxidase activity in macrophages by IL-17A. These studies provide important insights for Chagas vaccine development, and more broadly, increase our understanding of the diverse roles of Th17 cells in host defense.

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