scholarly journals The role of ICAM‐1/LFA‐1 and VCAM‐1/VLA‐4 interactions on T helper 2 cytokine production by lung T cells ofToxocara canis‐infected mice

Immunology ◽  
1998 ◽  
Vol 95 (3) ◽  
pp. 419-426 ◽  
Author(s):  
TAKAMOTO ◽  
ISOBE ◽  
SUGANE
Keyword(s):  
T Cells ◽  
Cytokine Production ◽  
T Helper ◽  
T Helper 2

Tregs in fibrosis: To know your enemy, you must become your enemy

2019 ◽  
Vol 4 (39) ◽  
pp. eaay1160 ◽  
Author(s):  
Suzanne M. Bal ◽  
Ralph Stadhouders
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Cytokine Production ◽  
T Helper ◽  
Related Research ◽  
T Helper 2 ◽  
Link Type ◽  
Research Article

T helper 2–skewed regulatory T cells in the skin use GATA3 to suppress local profibrotic type 2 cytokine production. See the related Research Article by Kalekar et al.

scholarly journals Critical role of CD28/B7 costimulation in the development of human Th2 cytokine-producing cells

Blood ◽  
1995 ◽  
Vol 86 (9) ◽  
pp. 3479-3486 ◽  
Author(s):  
LM Webb ◽  
M Feldmann
Keyword(s):  
T Cells ◽  
Cytokine Production ◽  
Critical Role ◽  
Th2 Cytokines ◽  
T Helper ◽  
Cd4 Cells ◽  
Th2 Cytokine ◽  
Cd28 Costimulation ◽  
Costimulatory Pathway

CD28 is a major costimulatory signal receptor for T cells. We have used human naive CD4+ cells from cord blood to analyze the effect of the CD28/B7 costimulatory pathway on development of T helper (Th) subsets. We show that CD28 costimulation is critical for development of the Th2 cytokine-producing cells and that in the absence of CD28 costimulation, cells are not primed to produce Th2 cytokines and consequently “default” to the Th1 subset, independent of the presence of exogenous cytokines. After CD28 costimulation, cells differentiate into a subset that produces Th2 cytokines. However, further CD28 costimulation is not required to maintain Th2 cytokine production. We conclude that D28 costimulation is critical for the development of Th0 and Th2 subsets, but not for the maintenance of cytokine production.

scholarly journals Development of chronic allergic responses by dampening Bcl6-mediated suppressor activity in memory T helper 2 cells

2017 ◽  
Vol 114 (5) ◽  
pp. E741-E750 ◽  
Author(s):  
Takashi Ogasawara ◽  
Masahiko Hatano ◽  
Hisae Satake ◽  
Jun Ikari ◽  
Toshibumi Taniguchi ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Cytokine Production ◽  
Allergic Diseases ◽  
Cytokine Gene ◽  
T Helper ◽  
Suppressor Activity ◽  
T Helper 2 ◽  
Asthma Model ◽  
Murine Asthma Model

Mice deficient in the transcriptional repressor B-cell CLL/lymphoma 6 (Bcl6) exhibit similar T helper 2 (TH2) immune responses as patients with allergic diseases. However, the molecular mechanisms underlying Bcl6-directed regulation of TH2 cytokine genes remain unclear. We identified multiple Bcl6/STAT binding sites (BSs) in TH2 cytokine gene loci. We found that Bcl6 is modestly associated with the BSs, and it had no significant effect on cytokine production in newly differentiated TH2 cells. Contrarily, in memory TH2 (mTH2) cells derived from adaptively transferred TH2 effectors, Bcl6 outcompeted STAT5 for binding to TH2 cytokine gene loci, particularlyInterleukin4(Il4) loci, and attenuated GATA binding protein 3 (GATA3) binding to highly conserved intron enhancer regions in mTH2 cells. Bcl6 suppressed cytokine production epigenetically in mTH2 cells to negatively tune histone acetylation at TH2 cytokine gene loci, includingIl4loci. In addition, IL-33, a pro-TH2 cytokine, diminished Bcl6’s association with loci to which GATA3 recruitment was inversely augmented, resulting in altered IL-4, but not IL-5 and IL-13, production in mTH2 cells but no altered production in newly differentiated TH2 cells. Use of a murine asthma model that generates high levels of pro-TH2 cytokines, such as IL-33, suggested that the suppressive function of Bcl6 in mTH2 cells is abolished in severe asthma. These findings indicate a role of the interaction between TH2-promoting factors and Bcl6 in promoting appropriate IL-4 production in mTH2 cells and suggest that chronic allergic diseases involve the TH2-promoting factor-mediated functional breakdown of Bcl6, resulting in allergy exacerbation.

scholarly journals Evaluation of Serum Cytokines Levels and the Role of Cannabidiol Treatment in Animal Model of Asthma

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Francieli Vuolo ◽  
Fabricia Petronilho ◽  
Beatriz Sonai ◽  
Cristiane Ritter ◽  
Jaime E. C. Hallak ◽  
...  
Keyword(s):  
Cytokine Production ◽  
Inflammatory Diseases ◽  
Bronchial Hyperresponsiveness ◽  
Public Health Problem ◽  
Serum Levels ◽  
Atopic Disease ◽  
Cell Interaction ◽  
T Helper ◽  
T Helper 2

Asthma represents a public health problem and traditionally is classified as an atopic disease, where the allergen can induce clinical airway inflammation, bronchial hyperresponsiveness, and reversible obstruction of airways. Studies have demonstrated the presence of T-helper 2 lymphocytes in the lung of patients with asthma. These cells are involved in cytokine production that regulates immunoglobulin synthesis. Recognizing that T cell interaction with antigens/allergens is key to the development of inflammatory diseases, the aim of this study is to evaluate the anti-inflammatory potential of cannabidiol (CBD) in this setting. Asthma was induced in 8-week-old Wistar rats by ovalbumin (OVA). In the last 2 days of OVA challenge animals received CBD (5 mg/kg, i.p.) and were killed 24 hours after. The levels of IL-4, IL-5, IL-13, IL-6, IL-10, and TNF-αwere determinate in the serum. CBD treatment was able to decrease the serum levels of all analyzed cytokines except for IL-10 levels. CBD seems to be a potential new drug to modulate inflammatory response in asthma.

Role of CD4+CD25+Regulatory T Cells in T Helper 2 Cell-mediated Allergic Inflammation in the Airways

2001 ◽  
Vol 164 (4) ◽  
pp. 680-687 ◽  
Author(s):  
AKIRA SUTO ◽  
HIROSHI NAKAJIMA ◽  
SHIN-ICHIRO KAGAMI ◽  
KOTARO SUZUKI ◽  
YASUSHI SAITO ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Allergic Inflammation ◽  
T Helper ◽  
T Helper 2

scholarly journals Double Positive CD4+CD8+ T Cells Are Enriched in Urological Cancers and Favor T Helper-2 Polarization

2019 ◽  
Vol 10 ◽  
Author(s):  
Perrine Bohner ◽  
Mathieu F. Chevalier ◽  
Valérie Cesson ◽  
Sonia-Christina Rodrigues-Dias ◽  
Florence Dartiguenave ◽  
...  
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
T Helper ◽  
Double Positive ◽  
T Helper 2 ◽  
Urological Cancers

scholarly journals OX40L–OX40 Signaling in Atopic Dermatitis

2021 ◽  
Vol 10 (12) ◽  
pp. 2578
Author(s):  
Masutaka Furue ◽  
Mihoko Furue
Keyword(s):  
T Cells ◽  
Atopic Dermatitis ◽  
Memory T Cells ◽  
Effector Memory ◽  
T Helper ◽  
T Helper 1 ◽  
Therapeutic Success ◽  
T Helper 2 ◽  
Promising Target ◽  
Antigen Presenting

OX40 is one of the co-stimulatory molecules expressed on T cells, and it is engaged by OX40L, primarily expressed on professional antigen-presenting cells such as dendritic cells. The OX40L–OX40 axis is involved in the sustained activation and expansion of effector T and effector memory T cells, but it is not active in naïve and resting memory T cells. Ligation of OX40 by OX40L accelerates both T helper 1 (Th1) and T helper 2 (Th2) effector cell differentiation. Recent therapeutic success in clinical trials highlights the importance of the OX40L–OX40 axis as a promising target for the treatment of atopic dermatitis.

scholarly journals Gastric Hyperplasia and Increased Proliferative Responses of Lymphocytes in Mice Lacking the COOH-terminal Ankyrin Domain of NF-κB2

1997 ◽  
Vol 186 (7) ◽  
pp. 999-1014 ◽  
Author(s):  
Hideaki Ishikawa ◽  
Daniel Carrasco ◽  
Estefania Claudio ◽  
Rolf-Peter Ryseck ◽  
Rodrigo Bravo
Keyword(s):  
T Cells ◽  
Lymphocyte Proliferation ◽  
Cytokine Production ◽  
Cell Types ◽  
Homozygous Deletion ◽  
Binding Activity ◽  
Activated T Cells ◽  
Physiological Relevance

The nfkb2 gene encodes the p100 precursor which produces the p52 protein after proteolytic cleavage of its COOH-terminal domain. Although the p52 product can act as an alternative subunit of NF-κB, the p100 precursor is believed to function as an inhibitor of Rel/NF-κB activity by cytoplasmic retention of Rel/NF-κB complexes, like other members of the IκB family. However, the physiological relevance of the p100 precursor as an IκB molecule has not been understood. To assess the role of the precursor in vivo, we generated, by gene targeting, mice lacking p100 but still containing a functional p52 protein. Mice with a homozygous deletion of the COOH-terminal ankyrin repeats of NF-κB2 (p100−/−) had marked gastric hyperplasia, resulting in early postnatal death. p100−/− animals also presented histopathological alterations of hematopoietic tissues, enlarged lymph nodes, increased lymphocyte proliferation in response to several stimuli, and enhanced cytokine production in activated T cells. Dramatic induction of nuclear κB–binding activity composed of p52-containing complexes was found in all tissues examined and also in stimulated lymphocytes. Thus, the p100 precursor is essential for the proper regulation of p52-containing Rel/NF-κB complexes in various cell types and its absence cannot be efficiently compensated for by other IκB proteins.

IL-36R ligands are potent regulators of dendritic and T cells

Blood ◽  
2011 ◽  
Vol 118 (22) ◽  
pp. 5813-5823 ◽  
Author(s):  
Solenne Vigne ◽  
Gaby Palmer ◽  
Céline Lamacchia ◽  
Praxedis Martin ◽  
Dominique Talabot-Ayer ◽  
...  
Keyword(s):  
T Cells ◽  
Mhc Class Ii ◽  
Critical Role ◽  
T Helper ◽  
Innate And Adaptive Immunity ◽  
Murine Bone Marrow ◽  
Intracellular Signals ◽  
Tnf Α ◽  
Ifn Γ

Abstract IL-36α (IL-1F6), IL-36β (IL-1F8), and IL-36γ (IL-1F9) are members of the IL-1 family of cytokines. These cytokines bind to IL-36R (IL-1Rrp2) and IL-1RAcP, activating similar intracellular signals as IL-1, whereas IL-36Ra (IL-1F5) acts as an IL-36R antagonist (IL-36Ra). In this study, we show that both murine bone marrow-derived dendritic cells (BMDCs) and CD4+ T lymphocytes constitutively express IL-36R and respond to IL-36α, IL-36β, and IL-36γ. IL-36 induced the production of proinflammatory cytokines, including IL-12, IL-1β, IL-6, TNF-α, and IL-23 by BMDCs with a more potent stimulatory effect than that of other IL-1 cytokines. In addition, IL-36β enhanced the expression of CD80, CD86, and MHC class II by BMDCs. IL-36 also induced the production of IFN-γ, IL-4, and IL-17 by CD4+ T cells and cultured splenocytes. These stimulatory effects were antagonized by IL-36Ra when used in 100- to 1000-fold molar excess. The immunization of mice with IL-36β significantly and specifically promoted Th1 responses. Our data thus indicate a critical role of IL-36R ligands in the interface between innate and adaptive immunity, leading to the stimulation of T helper responses.

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