scholarly journals Targeting Mycobacterium tuberculosis Antigens to Dendritic Cells via the DC-Specific-ICAM3-Grabbing-Nonintegrin Receptor Induces Strong T-Helper 1 Immune Responses

2018 ◽  
Vol 9 ◽  
Author(s):  
Lis Noelia Velasquez ◽  
Philipp Stüve ◽  
Maria Virginia Gentilini ◽  
Maxine Swallow ◽  
Judith Bartel ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Mycobacterium Tuberculosis ◽  
Immune Responses ◽  
T Helper ◽  
T Helper 1

scholarly journals The Selenoprotein MsrB1 Instructs Dendritic Cells to Induce T-Helper 1 Immune Responses

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 1021
Author(s):  
Ho-Jae Lee ◽  
Joon Seok Park ◽  
Hyun Jung Yoo ◽  
Hae Min Lee ◽  
Byung Cheon Lee ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
T Cell ◽  
Immune Responses ◽  
Therapeutic Potential ◽  
Methionine Sulfoxide Reductase ◽  
Interleukin 12 ◽  
T Helper ◽  
T Helper 1

Immune activation associates with the intracellular generation of reactive oxygen species (ROS). To elicit effective immune responses, ROS levels must be balanced. Emerging evidence shows that ROS-mediated signal transduction can be regulated by selenoproteins such as methionine sulfoxide reductase B1 (MsrB1). However, how the selenoprotein shapes immunity remains poorly understood. Here, we demonstrated that MsrB1 plays a crucial role in the ability of dendritic cells (DCs) to provide the antigen presentation and costimulation that are needed for cluster of differentiation antigen four (CD4) T-cell priming in mice. We found that MsrB1 regulated signal transducer and activator of transcription-6 (STAT6) phosphorylation in DCs. Moreover, both in vitro and in vivo, MsrB1 potentiated the lipopolysaccharide (LPS)-induced Interleukin-12 (IL-12) production by DCs and drove T-helper 1 (Th1) differentiation after immunization. We propose that MsrB1 activates the STAT6 pathway in DCs, thereby inducing the DC maturation and IL-12 production that promotes Th1 differentiation. Additionally, we showed that MsrB1 promoted follicular helper T-cell (Tfh) differentiation when mice were immunized with sheep red blood cells. This study unveils as yet unappreciated roles of the MsrB1 selenoprotein in the innate control of adaptive immunity. Targeting MsrB1 may have therapeutic potential in terms of controlling immune reactions.

scholarly journals Interleukin-26 activates macrophages and facilitates killing of Mycobacterium tuberculosis

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Heike C. Hawerkamp ◽  
Lasse van Geelen ◽  
Jan Korte ◽  
Jeremy Di Domizio ◽  
Marc Swidergall ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Mycobacterium Tuberculosis ◽  
Innate Immune ◽  
Toll Like Receptor ◽  
T Helper ◽  
T Helper 1 ◽  
Cytokine Induction ◽  
Tnf Α ◽  
Necrosis Factor

Abstract Tuberculosis-causing Mycobacterium tuberculosis (Mtb) is transmitted via airborne droplets followed by a primary infection of macrophages and dendritic cells. During the activation of host defence mechanisms also neutrophils and T helper 1 (TH1) and TH17 cells are recruited to the site of infection. The TH17 cell-derived interleukin (IL)-17 in turn induces the cathelicidin LL37 which shows direct antimycobacterial effects. Here, we investigated the role of IL-26, a TH1- and TH17-associated cytokine that exhibits antimicrobial activity. We found that both IL-26 mRNA and protein are strongly increased in tuberculous lymph nodes. Furthermore, IL-26 is able to directly kill Mtb and decrease the infection rate in macrophages. Binding of IL-26 to lipoarabinomannan might be one important mechanism in extracellular killing of Mtb. Macrophages and dendritic cells respond to IL-26 with secretion of tumor necrosis factor (TNF)-α and chemokines such as CCL20, CXCL2 and CXCL8. In dendritic cells but not in macrophages cytokine induction by IL-26 is partly mediated via Toll like receptor (TLR) 2. Taken together, IL-26 strengthens the defense against Mtb in two ways: firstly, directly due to its antimycobacterial properties and secondly indirectly by activating innate immune mechanisms.

Signaling through Toll-like receptor 3 and Dectin-1 potentiates the capability of human monocyte-derived dendritic cells to promote T-helper 1 and T-helper 17 immune responses

Cytotherapy ◽  
2012 ◽  
Vol 14 (5) ◽  
pp. 598-607 ◽  
Author(s):  
Ana Dragicevic ◽  
Tanja Dzopalic ◽  
Sasa Vasilijic ◽  
Dragana Vucevic ◽  
Sergej Tomic ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Immune Responses ◽  
Human Monocyte ◽  
Toll Like Receptor ◽  
T Helper ◽  
T Helper 1 ◽  
T Helper 17

scholarly journals CD86 and IL-12p70 Are Key Players for T Helper 1 Polarization and Natural Killer Cell Activation by Toll-Like Receptor-Induced Dendritic Cells

PLoS ONE ◽  
2012 ◽  
Vol 7 (9) ◽  
pp. e44266 ◽  
Author(s):  
Felix S. Lichtenegger ◽  
Katharina Mueller ◽  
Bettina Otte ◽  
Barbara Beck ◽  
Wolfgang Hiddemann ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Natural Killer Cell ◽  
Natural Killer ◽  
Cell Activation ◽  
Killer Cell ◽  
Toll Like Receptor ◽  
T Helper ◽  
T Helper 1 ◽  
Natural Killer Cell Activation ◽  
Key Players

Monocyte-derived dendritic cells early exposed to Mycobacterium tuberculosis induce an enhanced T helper 17 response and transfer mycobacterial antigens

2016 ◽  
Vol 306 (7) ◽  
pp. 541-553 ◽  
Author(s):  
Luciana Balboa ◽  
Denise Kviatcovsky ◽  
Pablo Schierloh ◽  
Marina García ◽  
Silvia de la Barrera ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Mycobacterium Tuberculosis ◽  
T Helper ◽  
T Helper 17 ◽  
Mycobacterial Antigens

scholarly journals CpG Oligodeoxynucleotides Act as Adjuvants that Switch on T Helper 1 (Th1) Immunity

1997 ◽  
Vol 186 (10) ◽  
pp. 1623-1631 ◽  
Author(s):  
Rose S. Chu ◽  
Oleg S. Targoni ◽  
Arthur M. Krieg ◽  
Paul V. Lehmann ◽  
Clifford V. Harding
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Cpg Odn ◽  
T Helper ◽  
T Helper 1 ◽  
Cpg Oligodeoxynucleotides ◽  
Cytokine Pattern ◽  
Incomplete Freund’S Adjuvant ◽  
Ifn Γ ◽  
Hen Egg

Synthetic oligodeoxynucleotides (ODN) that contain unmethylated CpG motifs (CpG ODN) induce macrophages to secrete IL-12, which induces interferon (IFN)-γ secretion by natural killer (NK) cells. Since these cytokines can induce T helper 1 (Th1) differentiation, we examined the effects of coadministered CpG ODN on the differentiation of Th responses to hen egg lysozyme (HEL). In both BALB/c (Th2-biased) and B10.D2 (Th1-biased) mice, immunization with HEL in incomplete Freund's adjuvant (IFA) resulted in Th2-dominated immune responses characterized by HEL-specific secretion of IL-5 but not IFN-γ. In contrast, immunization with IFA-HEL plus CpG ODN switched the immune response to a Th1-dominated cytokine pattern, with high levels of HEL-specific IFN-γ secretion and decreased HEL-specific IL-5 production. IFA-HEL plus CpG ODN also induced anti-HEL IgG2a (a Th1-associated isotype), which was not induced by IFA-HEL alone. Control non–CpG ODN did not induce IFN-γ or IgG2a, excepting lesser increases in B10.D2 (Th1-biased) mice. Thus, CpG ODN provide a signal to switch on Th1-dominated responses to coadministered antigen and are potential adjuvants for human vaccines to elicit protective Th1 immunity.

MicroRNAs in the regulation of immune cell functions – implications for atherosclerotic vascular disease

2012 ◽  
Vol 107 (04) ◽  
pp. 626-633 ◽  
Author(s):  
Alma Zernecke
Keyword(s):  
Dendritic Cells ◽  
Immune Responses ◽  
Molecular Mechanisms ◽  
Immune Cell ◽  
Chronic Inflammatory Disease ◽  
Vascular Pathology ◽  
Lipid Uptake ◽  
T Helper ◽  
Atherosclerotic Vascular Disease ◽  
Cell Functions

SummaryRegarded as a chronic inflammatory disease of the vessel wall, the development of atherosclerotic lesions is shaped by immune responses and their regulation. Macrophages and dendritic cells are positioned at the crossroad of innate and adaptive immune responses by sensing atherogenic danger signals and by taking up and presenting antigens. T helper cells and auto-antibodies produced by B cells, together with their cytokine responses in turn modulate atheroprogression. In addition, platelets contribute to atherosclerosis by multiple pathways. microRNAs (miRNAs) that post-transcriptionally regulate gene expression may thus critically control immune cell differentiation and functions during plaque evolution. This review summarises the role of miRNAs in regulating lipid uptake and expression of inflammatory mediators in monocytes/macrophages and dendritic cells, in lymphocyte functions with a focus on T helper cell responses, as well as in platelet biology, and the implications of altering these functions in vascular pathology and atherosclerosis. T systematically survey miRNA functions in controlling molecular mechanisms and immune responses in atherosclerosis holds potential for the development of novel miRNA-based strategies for therapies targeting inflammation and immunity in atherosclerosis.

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