Explore chapters and articles related to this topic
Fenugreek in Management of Immunological, Infectious, and Malignant Disorders
Published in Dilip Ghosh, Prasad Thakurdesai, Fenugreek, 2022
Rohini Pujari, Prasad Thakurdesai
The initial evidence of the anti-allergic potential of ethanolic extract of fenugreek seed (250 mg/kg for 7 days) was reported against experimental allergy models in vivo (TMA-induced contact hypersensitivity in BALB/c mice) and ex vivo (OVA-induced lung hypersensitiveness) (Bae et al. 2012). In this study, oral treatment with ethanolic extract of fenugreek seeds showed a reduction of allergic parameters such as ear thickness, infiltration of eosinophils and mast cells, the production of interleukins (IL-4, IL-5, IL-13, and IL-1β). Researchers suggested the mechanism such as the suppression of the IL-4 secretion and mRNA expression of GATA-binding protein 3 (GATA-3, an IL-4 transcription factor), and promotion of Th1 differentiation (enhanced production of IFN- γ and by IFN-γ-producing CD4þ T-cells), which is dependent on the mRNA expression of T-box transcription factor 21 gene (T-bet, and IFN-γ transcription factor) (Bae et al. 2012).
Endocrine and Neuroendocrine Tumors
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
Natasha Shrikrishnapalasuriyar, P.N. Plowman, Márta Korbonits, Ashley B. Grossman
In 2017, the World Health Organisation (WHO) changed the classification of pituitary adenomas.4,5 The new classification describes pituitary adenomas according to their adenohypophyseal lineage and transcription factors, and their clinical and prognostic factors. There are three main pathways of adenohypophyseal cell differentiation and their consequent transcription factors. Corticotrophs are determined by the T-box transcription factor (T-Pit), while somatotrophs, lactotrophs, and thyrotroph are characterized by pituitary transcription factor-1 (Pit1).4,5 Gonadotrophs involve Steroidogenic Factor 1 (SF-1). The original distinction between “typical” and “atypical” tumors has been removed, and it is now suggested that the Ki-67 proliferation index alone be used to indicate the degree of aggressiveness. Immunostaining for p53 should not be routine but can be used in some circumstances, as can (rarely) electron microscopy. Thus, all such tumors are considered to have the propensity of an aggressive course, but metastases specifically define a pituitary carcinoma.
Familial Chordoma
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Alexandra Suttman, Sydney T. Grob, Jean M. Mulcahy Levy
The susceptibility to chordoma is multivariate and complex, and it involves multiple mechanisms of common and rare genetic variants [8]. Hereditary predisposition to chordoma can occur due to T-box transcription factor T (TBXT) gene duplication, single and compound single-nucleotide polymorphisms (SNPs), as well as in the context of tuberous sclerosis complex (TSC). Hereditary predisposition to chordoma should be considered in individuals with early-onset chordoma, features of TSC, and/or in families with >1 diagnosis of chordoma.
The immunomodulatory effects of all-trans retinoic acid and docosahexaenoic acid combination treatment on the expression of IL-2, IL-4, T-bet, and GATA3 genes in PBMCs of multiple sclerosis patients
Published in Neurological Research, 2023
Ateke Mousavi Nasl-Khameneh, Abbas Mirshafiey, Abdorreza Naser Moghadasi, Mir Saeed Yekaninejad, Karim Parastouei, Shima Nejati, Ali Akbar Saboor-Yaraghi
T cells play a major role in MS pathogenesis. Antigen-activated naive CD4+ T cells may differentiate into various lineages of effector T cells with pro- and anti-inflammatory outcomes [7]. T helper (Th)1 cells are responsible for cell-mediated responses against intracellular pathogens and Th2 cells mediate humoral immunity through secretion of interleukin (IL)-4, IL-5, IL-6, IL-10, and IL-13. Dysregulation of the Th1/Th2 balance is one of the mechanisms, which underlies experimental autoimmune encephalomyelitis (EAE) [8]. Th1 cells were thought to initiate the disease by passing the blood–brain barrier (BBB), whereas, Th2 cells are believed to diminish inflammatory progression [9]. Master transcription factors have been identified in each T cell subset. T-box expressed in T cells (T-bet) and signal transducer and activator of transcription (STAT) 4 are specific transcription factors that control the expression of the hallmark Th1 cytokines; whereas, GATA-binding protein 3 (GATA3) causes both an increase in the number of Th2 cells and their cytokine production [10]. The main effector cytokines of Th1 cells are interferon gamma (IFN-γ), IL-2, and tumor necrosis factor alpha (TNFα) with IL-12 being required for the differentiation of these cells [11].
Biologic therapies for chronic obstructive pulmonary disease
Published in Expert Opinion on Biological Therapy, 2023
Maria Gabriella Matera, Luigino Calzetta, Mario Cazzola, Josuel Ora, Paola Rogliani
The pattern of inflammation differs, with type (T)1 and T3 immunity being the most prevalent [3]. T1 immunity protects against microbial infections and is governed by type 1 T helper (Th1) cells, cytotoxic T cells, and type 1 innate lymphoid cells (ILC1s), as well as the T-box protein produced in T cells (T-bet or Tbx21) transcription factor, which regulates interferon-gamma (IFN-γ) production. It is linked to an increase in the activation of pro-inflammatory macrophages. Th17 cells and type 3 ILCs (ILC3s), which express retinoic-acid-receptor-related orphan nuclear receptor gamma t (RORγt), one of the master regulators in the development of Th17 cells and secrete interleukin (IL)-17 and IL-22, causing neutrophilic inflammation, orchestrate T3 immunity, a type of immunity that is specifically directed against fungi.
T helper cells in depression: central role of Th17 cells
Published in Critical Reviews in Clinical Laboratory Sciences, 2022
Raghumoy Ghosh, Prasenjit Mitra, P. V. S. N. Kiran Kumar, Taru Goyal, Praveen Sharma
Th1 differentiation is dependent on strong T cell receptor (TCR) stimulation along with IFN-γ/signal transducer and activator of transcription 1 (STAT1), IL-2/STAT5, or IL-12/STAT4 signaling. The lineage-specific transcription factor for the Th1 subset is the T box containing protein (T-bet). IFN-γ, a predominantly pro-inflammatory cytokine, is known to increase TLR expression in innate immune cells, induce phagocytosis, upregulate major histocompatibility complex (MHC) class I and II gene expression and antigen presentation, and favor immunoglobin (Ig) G class switching. It has also been associated with various autoimmune diseases like MS and type 1 diabetes [26]. Further evidence of involvement in autoimmune diseases was found in animal models of SLE and experimental autoimmune encephalomyelitis (EAE) [26].