T cell priming: let there be light

Jirmanova, Ludmila; Ashwell, Jonathan D.

doi:10.1038/cr.2010.72

Cited by 5 publications

(5 citation statements)

References 16 publications

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“…8). These intracellular signals induced T cell proliferation as it was demonstrated before (Jirmanova and Ashwell, 2010). Additionally, they also converge in the cell nucleus to induce the increment of TRα1 that in turn would lead to the genomic transcription of iNOS (Fig.…”

Section: Discussionsupporting

confidence: 72%

“…Physiological activation of T lymphocytes leading to proliferation and differentiation involves a complex cascade of intracellular signaling events that are initiated by protein tyrosine kinases activation and includes downstream an increased hydrolysis of inositol phospholipids, which gives rise to inositol triphosphate (IP3) and diaciylglicerol (DAG). From these intracellular messengers, IP3 triggers Ca 2+ flux and the activation of critical transcription factors and DAG up‐regulates the activity of PKC thus contributing to Ras and mitogen‐activated protein kinase (MAPK) cascade activation (Jirmanova and Ashwell, 2010). In BW cells, however proliferation was demonstrated to be independent of Ca 2+ , but dependent on both atypical PKCζ and NOS activities (Gorelik et al, 2002; Barreiro Arcos et al, 2003).…”

Section: Resultsmentioning

confidence: 99%

“…As sensitive factors of the endocrine system, THs exert regulatory activities on immune cells, being important their action on T lymphocytes that are crucial cells for immune system function. T lymphocytes respond to antigen and other stimuli through the activation of a complex network of signals that involves several protein kinases and transcription factors (Jirmanova and Ashwell, 2010). Recently, we demonstrated an important role for THs in promoting normal and tumor T lymphocyte cell division via the genomic increment and activation of individual PKC and NOS isoenzymes (Barreiro Arcos et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

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Cooperative nongenomic and genomic actions on thyroid hormone mediated-modulation of T cell proliferation involve up-regulation of thyroid hormone receptor and inducible nitric oxide synthase expression

et al. 2011

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Thyroid hormones (THs) exert a broad range of actions on development, growth, and cell differentiation by both genomic and nongenomic mechanisms. THs regulate lymphocyte function, but the participation of nongenomic actions is still unknown. Here the contribution of both genomic and nongenomic effects on TH-induced division of T cells was studied by using free and noncell permeable THs coupled to agarose (TH-ag). THs-ag led to cell division, but to a lesser extent than free hormones. THs induced nongenomically the rapid translocation of protein kinase C (PKC) ζ isoform to cell membranes, extracellular-signal-regulated kinases (ERK1/2) phosphorylation and nuclear factor-κB (NF-κB) activation. The signaling cascade include sphingomyelinases acting up-stream the activation of PKCζ isoform, while ERK and NF-κB are activated downstream this PKC isoenzyme. Both free and THs-ag increased the protein and mRNA levels of TH nuclear receptor TRα1, while only free hormones incremented the inducible NOS gene and protein levels as well as a calcium independent NOS activity. Both effects were blunted by PKCζ inhibition. These results indicate that THs, by triggering a nongenomic signaling cascade that involves Smases-mediated activation of PKCζ, lead to ERK 1/2 and NF-κB activation and to the genomic increase of TRs and the inducible nitric oxide synthase protein and mRNA levels, improving T lymphocyte proliferation. These finding not only contribute to the understanding of the mechanisms involved in TH modulation of lymphocyte physiology, but would also point out for the first time the interplay between genomic and nongenomic TH actions in T cells.

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Section: Discussionsupporting

confidence: 72%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Cooperative nongenomic and genomic actions on thyroid hormone mediated-modulation of T cell proliferation involve up-regulation of thyroid hormone receptor and inducible nitric oxide synthase expression

et al. 2011

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“…Since Th1 cells producing IFN-γ are main effector cells in autoimmune diabetes (36,48), reduced Th1 skewing by IRT5 is likely to contribute to the reduced incidence of autoimmune diabetes by IRT5. Significant changes of the proportion of Th1 cells in PLNs without alteration of diabetogenic T cell priming by IRT5 treatment could be due to differences in signal transduction and proliferative response between naïve cells and primed T cells (49,50). Recirculation of effector T cells back and forth between target tissues and draining lymph nodes (51,52) might also contribute to the reduced Th1 cells in PLNs because CCR9 + Treg cells are likely to act on effector T cells in pancreatic islets after homing to target tissues and such effector T cells may move back to PLNs.…”

Section: Discussionmentioning

confidence: 99%

Amelioration of Autoimmune Diabetes of NOD Mice by Immunomodulating Probiotics

Kim

Lee²,

et al. 2020

Front. Immunol.

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Type 1 autoimmune diabetes is an autoimmune disease characterized by specific destruction of pancreatic β-cells producing insulin. Recent studies have shown that gut microbiota and immunity are closely linked to systemic immunity, affecting the balance between pro-inflammatory and regulatory immune responses. Altered gut microbiota may be causally related to the development of immune-mediated diseases, and probiotics have been suggested to have modulatory effects on inflammatory diseases and immune disorders. We studied whether a probiotic combination that has immunomodulatory effects on several inflammatory diseases can reduce the incidence of diabetes in non-obese diabetic (NOD) mice, a classical animal model of human T1D. When Immune Regulation and Tolerance 5 (IRT5), a probiotic combination comprising Lactobacillus acidophilus, Lactobacillus casei, Lactobacillus reuteri, Bifidobacterium bifidium, and Streptococcus thermophiles, was administered 6 times a week for 36 weeks to NOD mice, beginning at 4 weeks of age, the incidence of diabetes was significantly reduced. Insulitis score was also significantly reduced, and β-cell mass was conversely increased by IRT5 administration. IRT5 administration significantly reduced gut permeability in NOD mice. The proportion of total regulatory T cells was not changed by IRT5 administration; however, the proportion of CCR9 + regulatory T (Treg) cells expressing gut-homing receptor was significantly increased in pancreatic lymph nodes (PLNs) and lamina propria of the small intestine (SI-LP). Type 1 T helper (Th1) skewing was reduced in PLNs by IRT5 administration. IRT5 could be a candidate for an effective probiotic combination, which can be safely administered to inhibit or prevent type 1 diabetes (T1D).

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“…The first type involves the cell-specific [14,188] and other hydrolysis reactions by exposing bound PIP 2 or PIP 3 . An increase in intracellular calcium is well documented to stimulate the catalytic activity of PKCa [189].…”

Section: Cross-talkmentioning

confidence: 99%