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Article ; Online: Exemplifying complexity of immune suppression by a "canonical" speech: A glimpse into TNFRSF-activated signaling pathways in Treg cells.

Ayroldi, Emira / Grohmann, Ursula

2020 Volume 50, Issue 7, Page(s) 944–948

Abstract: Regulatory T (Treg) cells are crucial mediators of immune tolerance suppressing self-reactive T cells and preventing autoimmune diseases. Besides activation of the T cell receptor (TCR), empowerment of Treg cell functions requires co-accessory signals, ... ...

Abstract	Regulatory T (Treg) cells are crucial mediators of immune tolerance suppressing self-reactive T cells and preventing autoimmune diseases. Besides activation of the T cell receptor (TCR), empowerment of Treg cell functions requires co-accessory signals, such as those released by the TNF receptor superfamily (TNFRSF) that, however, can also promote immunostimulatory responses when engaged by effector T cells. In this issue of European Journal of Immunology, Lubrano di Ricco et al. [Eur. J. Immunol. 2020. 50: 972-985] have taken a closer look at the important question of the functional meaning of TNFRSF-activated signaling pathways in Treg cells. They have demonstrated that costimulation by TNFR2, 4-1BB, GITR, DR3, but not OX40 in mouse Foxp3
MeSH term(s)	Animals ; Humans ; Immune Tolerance ; Mice ; Receptors, Tumor Necrosis Factor/immunology ; Signal Transduction/immunology ; T-Lymphocytes, Regulatory/cytology ; T-Lymphocytes, Regulatory/immunology
Chemical Substances	Receptors, Tumor Necrosis Factor
Language	English
Publishing date	2020-06-24
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.202048711
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Article ; Online: Biological effects of bergamot and its potential therapeutic use as an anti-inflammatory, antioxidant, and anticancer agent.

Adorisio, Sabrina / Muscari, Isabella / Fierabracci, Alessandra / Thi Thuy, Trinh / Marchetti, Maria Cristina / Ayroldi, Emira / Delfino, Domenico Vittorio

Pharmaceutical biology

2023 Volume 61, Issue 1, Page(s) 639–646

Abstract: Context: ...

Abstract	Context:
MeSH term(s)	Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; Apoptosis ; Biological Products/pharmacology ; Biological Products/therapeutic use ; Cell Proliferation ; Citrus ; Fruit and Vegetable Juices ; Humans
Chemical Substances	Anti-Inflammatory Agents ; Antineoplastic Agents ; Antioxidants ; bergamot oil (39W1PKE3JI) ; Biological Products
Language	English
Publishing date	2023-04-17
Publishing country	England
Document type	Review ; Journal Article
ZDB-ID	1440131-9
ISSN	1744-5116 ; 1388-0209
ISSN (online)	1744-5116
ISSN	1388-0209
DOI	10.1080/13880209.2023.2197010
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Article ; Online: Glucocorticoid and PD-1 Cross-Talk: Does the Immune System Become Confused?

Adorisio, Sabrina / Cannarile, Lorenza / Delfino, Domenico V / Ayroldi, Emira

Cells

2021 Volume 10, Issue 9

Abstract: Programmed cell death protein 1 (PD-1) and its ligands, PD-L1/2, control T cell activation and tolerance. While PD-1 expression is induced upon T cell receptor (TCR) activation or cytokine signaling, PD-L1 is expressed on B cells, antigen presenting ... ...

Abstract	Programmed cell death protein 1 (PD-1) and its ligands, PD-L1/2, control T cell activation and tolerance. While PD-1 expression is induced upon T cell receptor (TCR) activation or cytokine signaling, PD-L1 is expressed on B cells, antigen presenting cells, and on non-immune tissues, including cancer cells. Importantly, PD-L1 binding inhibits T cell activation. Therefore, the modulation of PD-1/PD-L1 expression on immune cells, both circulating or in a tumor microenvironment and/or on the tumor cell surface, is one mechanism of cancer immune evasion. Therapies that target PD-1/PD-L1, blocking the T cell-cancer cell interaction, have been successful in patients with various types of cancer. Glucocorticoids (GCs) are often administered to manage the side effects of chemo- or immuno-therapy, exerting a wide range of immunosuppressive and anti-inflammatory effects. However, GCs may also have tumor-promoting effects, interfering with therapy. In this review, we examine GC signaling and how it intersects with PD-1/PD-L1 pathways, including a discussion on the potential for GC- and PD-1/PD-L1-targeted therapies to "confuse" the immune system, leading to a cancer cell advantage that counteracts anti-cancer immunotherapy. Therefore, combination therapies should be utilized with an awareness of the potential for opposing effects on the immune system.
MeSH term(s)	Animals ; Glucocorticoids/immunology ; Glucocorticoids/metabolism ; Humans ; Immune System/metabolism ; Immunotherapy/methods ; Programmed Cell Death 1 Receptor/immunology ; Programmed Cell Death 1 Receptor/metabolism ; Signal Transduction/immunology ; Tumor Microenvironment/immunology
Chemical Substances	Glucocorticoids ; Programmed Cell Death 1 Receptor
Language	English
Publishing date	2021-09-06
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10092333
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Article ; Online: Glucocorticoid and PD-1 Cross-Talk

Sabrina Adorisio / Lorenza Cannarile / Domenico V. Delfino / Emira Ayroldi

Cells, Vol 10, Iss 2333, p

Does the Immune System Become Confused?

2021 Volume 2333

Abstract	Programmed cell death protein 1 (PD-1) and its ligands, PD-L1/2, control T cell activation and tolerance. While PD-1 expression is induced upon T cell receptor (TCR) activation or cytokine signaling, PD-L1 is expressed on B cells, antigen presenting cells, and on non-immune tissues, including cancer cells. Importantly, PD-L1 binding inhibits T cell activation. Therefore, the modulation of PD-1/PD-L1 expression on immune cells, both circulating or in a tumor microenvironment and/or on the tumor cell surface, is one mechanism of cancer immune evasion. Therapies that target PD-1/PD-L1, blocking the T cell-cancer cell interaction, have been successful in patients with various types of cancer. Glucocorticoids (GCs) are often administered to manage the side effects of chemo- or immuno-therapy, exerting a wide range of immunosuppressive and anti-inflammatory effects. However, GCs may also have tumor-promoting effects, interfering with therapy. In this review, we examine GC signaling and how it intersects with PD-1/PD-L1 pathways, including a discussion on the potential for GC- and PD-1/PD-L1-targeted therapies to “confuse” the immune system, leading to a cancer cell advantage that counteracts anti-cancer immunotherapy. Therefore, combination therapies should be utilized with an awareness of the potential for opposing effects on the immune system.
Keywords	PD-1/PD-L1 ; glucocorticoids ; cancer ; immune response ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2021-09-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: A Glance at the Use of Glucocorticoids in Rare Inflammatory and Autoimmune Diseases: Still an Indispensable Pharmacological Tool?

Ronchetti, Simona / Ayroldi, Emira / Ricci, Erika / Gentili, Marco / Migliorati, Graziella / Riccardi, Carlo

Frontiers in immunology

2021 Volume 11, Page(s) 613435

Abstract: Since their discovery, glucocorticoids (GCs) have been used to treat almost all autoimmune and chronic inflammatory diseases, as well as allergies and some forms of malignancies, because of their immunosuppressive and anti-inflammatory effects. Although ... ...

Abstract	Since their discovery, glucocorticoids (GCs) have been used to treat almost all autoimmune and chronic inflammatory diseases, as well as allergies and some forms of malignancies, because of their immunosuppressive and anti-inflammatory effects. Although GCs provide only symptomatic relief and do not eliminate the cause of the pathology, in the majority of treatments, GCs frequently cannot be replaced by other classes of drugs. Consequently, long-term treatments cause adverse effects that may, in turn, lead to new pathologies that sometimes require the withdrawal of GC therapy. Therefore, thus far, researchers have focused their efforts on molecules that have the same efficacy as that of GCs but cause fewer adverse effects. To this end, some GC-induced proteins, such as glucocorticoid-induced leucine zipper (GILZ), have been used as drugs in mouse models of inflammatory pathologies. In this review, we focus on some important but rare autoimmune and chronic inflammatory diseases for which the biomedical research investment in new therapies is less likely. Additionally, we critically evaluate the possibility of treating such diseases with other drugs, either GC-related or unrelated.
MeSH term(s)	Animals ; Autoimmune Diseases/drug therapy ; Glucocorticoids/pharmacology ; Humans ; Inflammation/drug therapy ; Leucine Zippers/drug effects
Chemical Substances	Glucocorticoids
Language	English
Publishing date	2021-01-21
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.613435
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Article ; Online: Glucocorticoids and natural killer cells: A suppressive relationship.

Muscari, Isabella / Fierabracci, Alessandra / Adorisio, Sabrina / Moretti, Marina / Cannarile, Lorenza / Thi Minh Hong, Vu / Ayroldi, Emira / Delfino, Domenico V

Biochemical pharmacology

2022 Volume 198, Page(s) 114930

Abstract: Glucocorticoids exert their pharmacological actions by mimicking and amplifying the function of the endogenous glucocorticoid system's canonical physiological stress response. They affect the immune system at the levels of inflammation and adaptive and ... ...

Abstract	Glucocorticoids exert their pharmacological actions by mimicking and amplifying the function of the endogenous glucocorticoid system's canonical physiological stress response. They affect the immune system at the levels of inflammation and adaptive and innate immunity. These effects are the basis for therapeutic use of glucocorticoids. Innate immunity is the body's first line of defense against disease conditions. It is relatively nonspecific and, among its mediators, natural killer (NK) cells link innate and acquired immunity. NK cell numbers are altered in patients with auto immune diseases, and research suggests that interactions between glucocorticoids and natural killer cells are critical for successful glucocorticoid therapy. The aim of this review is to summarize these interactions while highlighting the latest and most important developments in this field. Production and release in the blood of endogenous glucocorticoids are strictly regulated by the hypothalamus-pituitary adrenal axis. A self-regulatory mechanism prevents excessive plasma levels of these hormones. However, exogenous stimuli such as stress, inflammation, infections, cancer, and autoimmune disease can trigger the hypothalamus-pituitary-adrenal axis response and lead to excessive systemic release of glucocorticoids. Thus, stress stimuli, such as sleep deprivation, intense exercise, depression, viral infections, and cancer, can result in release of glucocorticoids and associated immunosuppressant effects. Among these effects are decreases in the numbers and activities of NK cells in inflammatory and autoimmune diseases (e.g., giant cell arteritis, polymyalgia rheumatica, and familial hypogammaglobulinemia).
MeSH term(s)	Autoimmune Diseases ; Glucocorticoids/pharmacology ; Glucocorticoids/therapeutic use ; Humans ; Hypothalamo-Hypophyseal System ; Inflammation ; Killer Cells, Natural ; Pituitary-Adrenal System
Chemical Substances	Glucocorticoids
Language	English
Publishing date	2022-02-09
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2022.114930
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Article: Cyclooxygenase-2 Upregulated by Temozolomide in Glioblastoma Cells Is Shuttled In Extracellular Vesicles Modifying Recipient Cell Phenotype.

Lombardi, Francesca / Augello, Francesca Rosaria / Artone, Serena / Ayroldi, Emira / Giusti, Ilaria / Dolo, Vincenza / Cifone, Maria Grazia / Cinque, Benedetta / Palumbo, Paola

Frontiers in oncology

2022 Volume 12, Page(s) 933746

Abstract: Temozolomide (TMZ) resistance is frequent in patients with glioblastoma (GBM), a tumor characterized by a marked inflammatory microenvironment. Recently, we reported that cyclooxygenase-2 (COX-2) is upregulated in TMZ-resistant GBM cells treated with ... ...

Abstract	Temozolomide (TMZ) resistance is frequent in patients with glioblastoma (GBM), a tumor characterized by a marked inflammatory microenvironment. Recently, we reported that cyclooxygenase-2 (COX-2) is upregulated in TMZ-resistant GBM cells treated with high TMZ concentrations. Moreover, COX-2 activity inhibition significantly counteracted TMZ-resistance of GBM cells. Extracellular vesicles (EV) are considered crucial mediators in orchestrating GBM drug resistance by modulating the tumor microenvironment (TME) and affecting the surrounding recipient cell phenotype and behavior. This work aimed to verify whether TMZ, at low and clinically relevant doses (5-20 µM), could induce COX-2 overexpression in GBM cells (T98G and U87MG) and explore if secreted EV shuttled COX-2 to recipient cells. The effect of COX-2 inhibitors (COXIB), Celecoxib (CXB), or NS398, alone or TMZ-combined, was also investigated. Our results indicated that TMZ at clinically relevant doses upregulated COX-2 in GBM cells. COXIB treatment significantly counteracted TMZ-induced COX-2 expression, confirming the crucial role of the COX-2/PGE2 system in TMZ-resistance. The COXIB specificity was verified on U251MG, COX-2 null GBM cells. Western blotting of GBM-EV cells showed the COX-2 presence, with the same intracellular trend, increasing in EV derived from TMZ-treated cells and decreasing in those derived from COXIB+TMZ-treated cells. We then evaluated the effect of EV secreted by TMZ-treated cells on U937 and U251MG, used as recipient cells. In human macrophage cell line U937, the internalization of EV derived by TMZ-T98G cells led to a shift versus a pro-tumor M2-like phenotype. On the other hand, EV from TMZ-T98G induced a significant decrease in TMZ sensitivity in U251MG cells. Overall, our results, in confirming the crucial role played by COX-2 in TMZ-resistance, provide the first evidence of the presence and effective functional transfer of this enzyme through EV derived from GBM cells, with multiple potential consequences at the level of TME.
Language	English
Publishing date	2022-07-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2022.933746
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Article ; Online: L-GILZ binds and inhibits nuclear factor κB nuclear translocation in undifferentiated thyroid cancer cells.

Marchetti, Maria Cristina / Cannarile, Lorenza / Ronchetti, Simona / Delfino, Domenico V / Riccardi, Carlo / Ayroldi, Emira

Journal of chemotherapy (Florence, Italy)

2020 Volume 32, Issue 5, Page(s) 263–267

Abstract: Proto-oncogene mutations and abnormal activation of mitogen-activated protein kinase (MAPK) signalling are recurrently found in thyroid cancers. Some thyroid neoplasms respond to drugs that inhibit MAPK pathway activation. Previously, we showed that ... ...

Abstract	Proto-oncogene mutations and abnormal activation of mitogen-activated protein kinase (MAPK) signalling are recurrently found in thyroid cancers. Some thyroid neoplasms respond to drugs that inhibit MAPK pathway activation. Previously, we showed that pharmacological inhibition of MAPK in thyroid cancer cells inhibits cell proliferation and upregulates L-GILZ (long glucocorticoid-induced leucine zipper), a protein with anti-oncogenic and antiproliferative activity, and that L-GILZ is partially responsible for the antiproliferative activity of MAPK inhibitors. Here, we demonstrate that pharmacological inhibition of MAPK in the anaplastic thyroid cancer cell line CAL-62 upregulated L-GILZ, which bound nuclear factor κB (NF-κB) and inhibited its nuclear translocation. These data demonstrate a unique L-GILZ-mediated molecular mechanism that, by trapping NF-κB in the cytoplasm, contributes to the inhibition of proliferation induced by drugs targeting the MAPK transduction cascade. Enhanced knowledge of the mechanism of action of MAPK pathway-inhibiting drugs may improve their clinical use.
Language	English
Publishing date	2020-02-18
Publishing country	England
Document type	Journal Article
ZDB-ID	1036294-0
ISSN	1973-9478 ; 1120-009X
ISSN (online)	1973-9478
ISSN	1120-009X
DOI	10.1080/1120009X.2020.1728862
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Article ; Online: A dual role for glucocorticoid-induced leucine zipper in glucocorticoid function: tumor growth promotion or suppression?

Ayroldi, Emira / Cannarile, Lorenza / Delfino, Domenico V / Riccardi, Carlo

Cell death & disease

2018 Volume 9, Issue 5, Page(s) 463

Abstract: Glucocorticoids (GCs), important therapeutic tools to treat inflammatory and immunosuppressive diseases, can also be used as part of cancer therapy. In oncology, GCs are used as anticancer drugs for lymphohematopoietic malignancies, while in solid ... ...

Abstract	Glucocorticoids (GCs), important therapeutic tools to treat inflammatory and immunosuppressive diseases, can also be used as part of cancer therapy. In oncology, GCs are used as anticancer drugs for lymphohematopoietic malignancies, while in solid neoplasms primarily to control the side effects of chemo/radiotherapy treatments. The molecular mechanisms underlying the effects of GCs are numerous and often overlapping, but not all have been elucidated. In normal, cancerous, and inflammatory tissues, the response to GCs differs based on the tissue type. The effects of GCs are dependent on several factors: the tumor type, the GC therapy being used, the expression level of the glucocorticoid receptor (GR), and the presence of any other stimuli such as signals from immune cells and the tumor microenvironment. Therefore, GCs may either promote or suppress tumor growth via different molecular mechanisms. Stress exposure results in dysregulation of the hypothalamic-pituitary-adrenal axis with increased levels of endogenous GCs that promote tumorigenesis, confirming the importance of GCs in tumor growth. Most of the effects of GCs are genomic and mediated by the modulation of GR gene transcription. Moreover, among the GR-induced genes, glucocorticoid-induced leucine zipper (GILZ), which was cloned and characterized primarily in our laboratory, mediates many GC anti-inflammatory effects. In this review, we analyzed the possible role for GILZ in the effects GCs have on tumors cells. We also suggest that GILZ, by affecting the immune system, tumor microenvironment, and directly cancer cell biology, has a tumor-promoting function. However, it may also induce apoptosis or decrease the proliferation of cancer cells, thus inhibiting tumor growth. The potential therapeutic implications of GILZ activity on tumor cells are discussed here.
MeSH term(s)	Animals ; Glucocorticoids/therapeutic use ; Hematologic Neoplasms/drug therapy ; Hematologic Neoplasms/immunology ; Hematologic Neoplasms/pathology ; Humans ; Leucine Zippers/immunology ; Neoplasm Proteins/immunology ; Receptors, Glucocorticoid/immunology ; Signal Transduction/drug effects ; Signal Transduction/immunology ; Transcription Factors/immunology ; Tumor Microenvironment/drug effects ; Tumor Microenvironment/immunology
Chemical Substances	Glucocorticoids ; Neoplasm Proteins ; Receptors, Glucocorticoid ; TSC22D3 protein, human ; Transcription Factors
Language	English
Publishing date	2018-05-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-018-0558-1
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Article ; Online: Implicating the Role of GILZ in Glucocorticoid Modulation of T-Cell Activation.

Cannarile, Lorenza / Delfino, Domenico V / Adorisio, Sabrina / Riccardi, Carlo / Ayroldi, Emira

Frontiers in immunology

2019 Volume 10, Page(s) 1823

Abstract: Glucocorticoid-induced leucine zipper (GILZ) is a protein with multiple biological roles that is upregulated by glucocorticoids (GCs) in both immune and non-immune cells. Importantly, GCs are immunosuppressive primarily due to their regulation of cell ... ...

Abstract	Glucocorticoid-induced leucine zipper (GILZ) is a protein with multiple biological roles that is upregulated by glucocorticoids (GCs) in both immune and non-immune cells. Importantly, GCs are immunosuppressive primarily due to their regulation of cell signaling pathways that are crucial for immune system activity. GILZ, which is transcriptionally induced by the glucocorticoid receptor (GR), mediates part of these immunosuppressive, and anti-inflammatory effects, thereby controlling immune cell proliferation, survival, and differentiation. The primary immune cells targeted by the immunosuppressive activity of GCs are T cells. Importantly, the effects of GCs on T cells are partially mediated by GILZ. In fact, GILZ regulates T-cell activation, and differentiation by binding and inhibiting factors essential for T-cell function. For example, GILZ associates with nuclear factor-κB (NF-κB), c-Fos, and c-Jun and inhibits NF-κB-, and AP-1-dependent transcription. GILZ also binds Raf and Ras, inhibits activation of Ras/Raf downstream targets, including mitogen-activated protein kinase 1 (MAPK1). In addition GILZ inhibits forkhead box O3 (FoxO3) without physical interaction. GILZ also promotes the activity of regulatory T cells (Tregs) by activating transforming growth factor-β (TGF-β) signaling. Ultimately, these actions inhibit T-cell activation and modulate the differentiation of T helper (Th)-1, Th-2, Th-17 cells, thereby mediating the immunosuppressive effects of GCs on T cells. In this mini-review, we discuss how GILZ mediates GC activity on T cells, focusing mainly on the therapeutic potential of this protein as a more targeted anti-inflammatory/immunosuppressive GC therapy.
MeSH term(s)	Animals ; Cell Differentiation/immunology ; Glucocorticoids/immunology ; Humans ; Immune Tolerance ; Lymphocyte Activation ; Receptors, Glucocorticoid/immunology ; Signal Transduction/immunology ; T-Lymphocytes/immunology ; Transcription Factors/immunology ; Transcription, Genetic/immunology
Chemical Substances	Glucocorticoids ; Receptors, Glucocorticoid ; TSC22D3 protein, human ; Transcription Factors
Language	English
Publishing date	2019-08-07
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2019.01823
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