scholarly journals n-3 Fatty acids inhibit transcription of human IL-13: implications for development of T helper type 2 immune responses

2012 ◽  
Vol 109 (6) ◽  
pp. 990-1000 ◽  
Author(s):  
Emily MacLean ◽  
Norman Madsen ◽  
Harissios Vliagoftis ◽  
Catherine Field ◽  
Lisa Cameron
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Allergic Disease ◽  
Transcriptional Activation ◽  
Control Diet ◽  
Th2 Cells ◽  
T Helper ◽  
Helper Type

Fish oil supplementation during pregnancy has been associated with lower levels of cord blood IL-13, suggesting that the administration ofn-3 fatty acids may attenuate the development of allergic disease. The present study aimed to investigate the mechanism by whichn-3 fatty acid administration influences the production of IL-13. Pregnant BALB/c mice were fed nutritionally complete high-fat diets (15 %, w/w) with ann-3 fatty acid-enriched (DHA 1 %, w/w) or control diet (0 % DHA) immediately following delivery. Pups were exposed during suckling and weaned to the maternal diet for the remainder of the study. The production of IL-13, IL-4, IL-10 and interferon-γ from the splenocytes of ovalbumin (ova)-sensitised animals was assessed followingin vitroova stimulation or unstimulated conditions. Human T helper type 2 (Th2) cells were mitogen-stimulated in the presence or absence of DHA (10 μm) and assessed for IL-13 and IL-4 expression using intracellular flow cytometry. The influence on transcriptional activation was studied using a human IL-13 promoter reporter construct and electromobility shift assay. Ova-activated splenocytes from DHA-fed mice produced less IL-13 (57·2 (se21·7) pg/ml) and IL-4 (7·33 (se3·4) pg/ml) compared with cells from the animals fed the control diet (161·5 (se45·0),P< 0·05; 33·2 (se11·8),P< 0·05).In vitro, DHA inhibited the expression of IL-13 protein from human Th2 cells as well as transcriptional activation and binding of the transcription factors cyclic AMP response element binding and activating transcription factor 2 to the human IL-13 promoter. These data indicate the potential ofn-3 fatty acids to attenuate IL-13 expression, and suggest that they may subsequently reduce allergic sensitisation and the development of allergic disease.

The roles of immune cells in atherosclerotic calcification

Vascular ◽  
2021 ◽  
pp. 170853812110327
Author(s):  
Jingsong Cao ◽  
Xuyu Zu ◽  
Jianghua Liu
Keyword(s):  
B Cells ◽  
Immune Cells ◽  
Cardiovascular Events ◽  
Th2 Cells ◽  
Regulatory B Cells ◽  
T Helper ◽  
Relationship Of ◽  
The Relationship ◽  
Helper Type

Atherosclerosis is the leading cause of acute cardiovascular events, and vascular calcification is an important pathological phenomenon in atherosclerosis. Recently, many studies have shown that immune cells are closely associated with the development of atherosclerosis and calcification, but there are many conflicting viewpoints because of immune system complications, such as the pro-atherosclerotic and atheroprotective effects of regulatory B cells (Bregs), T helper type 2 (Th2) cells and T helper type 17 (Th17) cells. In this review, we summarize the studies on the roles of immune cells, especially lymphocytes and macrophages, in atherosclerotic calcification. Furthermore, we prepared graphs showing the relationship between T cells, B cells and macrophages and atherosclerotic calcification. Finally, we highlight some potential issues that are closely associated with the function of immune cells in atherosclerotic calcification. Based on current research results, this review summarizes the relationship between immune cells and atherosclerotic calcification, and it will be beneficial to understand the relationship of immune cells and atherosclerotic calcification.

scholarly journals Critical Involvement of CD44 in T Helper Type 2 Cell-Mediated Eosinophilic Airway Inflammation in a Mouse Model of Acute Asthma

2022 ◽  
Vol 12 ◽  
Author(s):  
Shigeki Katoh
Keyword(s):  
Monoclonal Antibodies ◽  
Airway Inflammation ◽  
Th17 Cells ◽  
Acute Asthma ◽  
Mite Allergen ◽  
Th2 Cells ◽  
T Helper ◽  
Th2 Cell ◽  
Helper Type

Interactions between CD44 and hyaluronan (HA) are crucial for recruiting leukocytes to inflamed tissues. This review summarizes findings from our studies of the roles of CD44-HA interactions in leukocyte trafficking, with a particular focus on airway T helper type 2 (Th2) cells in mouse models of acute asthma. In a mite allergen-induced model of acute asthma, intraperitoneal injection of anti-CD44 monoclonal antibodies blocked lymphocytes and eosinophils from accumulating in the lung, and suppressed both the antigen-induced increase in Th2 cytokines in the bronchoalveolar lavage fluid (BALF) and airway hyperresponsiveness (AHR). CD44 deficiency was associated with decreased mite allergen-induced Th2 cell-mediated airway inflammation and AHR in sensitized mice. Asthmatic responses to antigen-sensitized splenic CD4+ T cells transferred from CD44-deficient mice were weaker than in wild-type mice. Administration of anti-CD44 monoclonal antibodies preferentially suppressed the airway accumulation of antigen-specific Th2 cells induced by antigen challenge, without affecting Th1 and Th17 cells. Increased HA-binding ability of CD44 and expression of Neu1 sialidase were observed on antigen-specific Th2 cells compared with antigen-specific Th1 and Th17 cells. Finally, in a mouse model of acute asthma, neuraminidase 1-deficient SM/J mice exhibited a lower Th2 cytokine concentration and a lower absolute Th2 cell number in the BALF, as well as an attenuated AHR. Our findings indicate that CD44 critically contributes to the antigen challenge-induced airway accumulation of antigen-specific Th2 cells, without affecting Th1 and Th17 cells, in mice. Furthermore, neuraminidase 1 activity is necessary for the interaction between HA and CD44, and Th2 cell-mediated airway inflammation.

scholarly journals Cc Chemokine Receptor (Ccr)3/Eotaxin Is Followed by Ccr4/Monocyte-Derived Chemokine in Mediating Pulmonary T Helper Lymphocyte Type 2 Recruitment after Serial Antigen Challenge in Vivo

2000 ◽  
Vol 191 (2) ◽  
pp. 265-274 ◽  
Author(s):  
Clare M. Lloyd ◽  
Tracy Delaney ◽  
Trang Nguyen ◽  
Jane Tian ◽  
Carlos Martinez-A ◽  
...  
Keyword(s):  
Chemokine Receptor ◽  
Progressive Increase ◽  
Allergic Airway Disease ◽  
Antigen Challenge ◽  
Th2 Cells ◽  
T Helper ◽  
Cc Chemokine

Isolated peripheral blood CD4 cells from allergic individuals express CC chemokine receptor (CCR)3 and CCR4 after expansion in vitro. In addition, human T helper type 2 (Th2) cells polarized in vitro selectively express CCR3 and CCR4 at certain stages of activation/differentiation and respond preferentially to the ligands eotaxin and monocyte-derived chemokine (MDC). However, controversy arises when the in vivo significance of this distinct expression is discussed. To address the functional role of CCR3/eotaxin and CCR4/MDC during the in vivo recruitment of Th2 cells, we have transferred effector Th cells into naive mice to induce allergic airway disease. Tracking of these cells after repeated antigen challenge has established that both CCR3/eotaxin and CCR4/MDC axes contribute to the recruitment of Th2 cells to the lung, demonstrating the in vivo relevance of the expression of these receptors on Th2 cells. We have shown that involvement of the CCR3/eotaxin pathway is confined to early stages of the response in vivo, whereas repeated antigen stimulation results in the predominant use of the CCR4/MDC pathway. We propose that effector Th2 cells respond to both CCR3/eotaxin and CCR4/MDC pathways initially, but that a progressive increase in CCR4-positive cells results in the predominance of the CCR4/MDC axis in the long-term recruitment of Th2 cells in vivo.

scholarly journals Prostaglandin D2 Selectively Induces Chemotaxis in T Helper Type 2 Cells, Eosinophils, and Basophils via Seven-Transmembrane Receptor Crth2

2001 ◽  
Vol 193 (2) ◽  
pp. 255-262 ◽  
Author(s):  
Hiroyuki Hirai ◽  
Kazuya Tanaka ◽  
Osamu Yoshie ◽  
Kazuyuki Ogawa ◽  
Kazumi Kenmotsu ◽  
...  
Keyword(s):  
Allergic Inflammation ◽  
Allergic Diseases ◽  
Th2 Cells ◽  
Prostaglandin D2 ◽  
Dependent Manner ◽  
T Helper ◽  
Dependent Cell ◽  
Blood Eosinophils ◽  
Helper Type

Prostaglandin (PG)D2, which has long been implicated in allergic diseases, is currently considered to elicit its biological actions through the DP receptor (DP). Involvement of DP in the formation of allergic asthma was recently demonstrated with DP-deficient mice. However, proinflammatory functions of PGD2 cannot be explained by DP alone. We show here that a seven-transmembrane receptor, CRTH2, which is preferentially expressed in T helper type 2 (Th2) cells, eosinophils, and basophils in humans, serves as the novel receptor for PGD2. In response to PGD2, CRTH2 induces intracellular Ca2+ mobilization and chemotaxis in Th2 cells in a Gαi-dependent manner. In addition, CRTH2, but not DP, mediates PGD2-dependent cell migration of blood eosinophils and basophils. Thus, PGD2 is likely involved in multiple aspects of allergic inflammation through its dual receptor systems, DP and CRTH2.

Interleukin-4-dependent induction of preproenkephalin in antigen-specific T helper-type 2 (Th2) cells

2000 ◽  
Vol 105 (2) ◽  
pp. 103-108 ◽  
Author(s):  
Takashi Yahata ◽  
Chie Yahata ◽  
Akio Ohta ◽  
Masashi Sekimoto ◽  
Hidemitsu Kitamura ◽  
...  
Keyword(s):  
Interleukin 4 ◽  
Th2 Cells ◽  
T Helper ◽  
Helper Type

scholarly journals Early Growth Response Protein-1 (Egr-1) Is Preferentially Expressed in T Helper Type 2 (Th2) Cells and Is Involved in Acute Transcription of the Th2 Cytokine Interleukin-4

2009 ◽  
Vol 285 (3) ◽  
pp. 1643-1652 ◽  
Author(s):  
Michael Lohoff ◽  
Marco Giaisi ◽  
Rebecca Köhler ◽  
Bärbel Casper ◽  
Peter H. Krammer ◽  
...  
Keyword(s):  
Growth Response ◽  
Early Growth ◽  
Interleukin 4 ◽  
Th2 Cells ◽  
T Helper ◽  
Early Growth Response ◽  
Th2 Cytokine ◽  
Helper Type

scholarly journals STAT6-mediated displacement of polycomb by trithorax complex establishes long-term maintenance of GATA3 expression in T helper type 2 cells

2010 ◽  
Vol 207 (11) ◽  
pp. 2493-2506 ◽  
Author(s):  
Atsushi Onodera ◽  
Masakatsu Yamashita ◽  
Yusuke Endo ◽  
Makoto Kuwahara ◽  
Soichi Tofukuji ◽  
...  
Keyword(s):  
Hox Genes ◽  
Polycomb Group ◽  
Th2 Cells ◽  
Upstream Region ◽  
T Helper ◽  
Gata3 Expression ◽  
Term Maintenance ◽  
Helper Type

Polycomb group (PcG) and trithorax group (TrxG) complexes exert opposing effects on the maintenance of the transcriptional status of the developmentally regulated Hox genes. In this study, we show that activation of STAT6 induces displacement of the PcG complex by the TrxG complex at the upstream region of the gene encoding GATA3, a transcription factor essential for T helper type 2 (Th2) cell differentiation. Once Th2 cells differentiate, TrxG complex associated with the TrxG component Menin binds to the whole GATA3 gene locus, and this binding is required for the long-term maintenance of expression of GATA3 and Th2 cytokine. Thus, STAT6-mediated displacement of PcG by the TrxG complex establishes subsequent STAT6-independent maintenance of GATA3 expression in Th2 cells via the recruitment of the Menin–TrxG complex.

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