Expression of CD45 isoforms correlates with differential proliferative responses of peripheral CD4+ and CD8+ T cells

Seki, Iwao; Suzuki, Mihoko; Miyasaka, Nobuyuki; Kohsaka, Hitoshi

doi:10.1016/j.imlet.2009.12.020

Cited by 9 publications

(8 citation statements)

References 42 publications

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“…The transitions of CD45R isoforms are rapidly induced upon TCR activation [11,12]. In the present study, the CD45RB mRNA expression coincided most consistently with CTLA4 mRNA levels, but with wide inter-individual variations.…”

Section: Discussionsupporting

confidence: 64%

“…CD28/T-cell receptor/CTLA4 complex controls T-cell homeostasis, tolerance, and autoimmunity in Hashimoto's thyroiditis [9,10]. In addition, many other molecules, such as CD45 protein tyrosine phosphatase (PTPase) [11,12] and vitamin D receptor (VDR) [13,14], cooperatively interact with the TCR complex to affect Th1/Th17/Treg processes central to the pathogenesis of HT. Nevertheless, their role has been comparatively less well established.…”

Section: Introductionmentioning

confidence: 99%

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Zmiana ekspresji mRNA dla CTLA-4, CD28, VDR i CD45 w limfocytach T u osób z chorobą Hashimoto — badanie pilotowe

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Karner

et al. 2017

Endokrynologia Polska

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Section: Discussionsupporting

confidence: 64%

Section: Introductionmentioning

confidence: 99%

Zmiana ekspresji mRNA dla CTLA-4, CD28, VDR i CD45 w limfocytach T u osób z chorobą Hashimoto — badanie pilotowe

Tokić

Štefanić

Karner

et al. 2017

Endokrynologia Polska

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“…Finally, in in vitro studies using mouse T cells, Seki et al. 49 showed that CD45 expressed on CD8 + T cells was less active than CD45 expressed on CD4 + T cells and correlated this difference to the distinctive expression pattern of CD45 isoforms between CD8 + (primarily expressing CD45RBC) and CD4 + (primarily expressing the RO and RB isoforms) T cells.…”

Section: Class I Enzymesmentioning

confidence: 99%

Regulation of TCR signalling by tyrosine phosphatases: from immune homeostasis to autoimmunity

2012

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Activation of T cells is largely mediated through signal transduction downstream from the T-cell receptor (TCR) expressed on the cell surface. The TCR is a transmembrane receptor complex comprised of a and b chains, which bind ligands, and CD3 (e, c and d) and f chains containing motifs that are phosphorylated on tyrosine, called immunoreceptor tyrosine-based activation motifs. Signal transduction through the TCR is initiated when the receptor binds to a peptide-MHC complex presented by an antigen-presenting cell. This interaction initiates a cascade of signalling events, which induces the proliferation, mobilization and differentiation of T cells. For an updated and comprehensive review of signalling through the TCR the reader is referred to recent authoritative publications. [1][2][3][4] A dynamic wave of tyrosine phosphorylation phenomena is critical for ignition of intracellular signalling in T cells. Engagement of the TCR leads to the activation of the Src family protein tyrosine kinases (PTKs) LCK and FYN, which phosphorylate the immunoreceptor tyrosinebased activation motifs of the TCR. This provides docking sites for the SH2 domains of ZAP-70, a Syk family PTK, allowing ZAP-70 to be phosphorylated and activated by LCK. Once activated, ZAP-70 phosphorylates the adaptor proteins SLP-76 and LAT, which nucleate signalling complexes, leading to the phosphorylation and activation of multiple downstream effectors. This results in calcium mobilization, activation of mitogen-activated protein kinases (MAPKs), transcriptional regulation and cytoskeletal rearrangements.Protein tyrosine phosphatases (PTPs) are the natural counterpart of PTKs. Much like PTKs, depending upon the phosphorylation site and the signalling context, they can enhance or reduce the function of their protein target(s). The modern view of phosphorylation networks is one of dynamic 'always-on' grids where the stoichiometry of each phosphorylation site is continuously controlled by the changing balance between the activities of kinases and phosphatases. For example, the activation state of the Src family kinases (SFKs) is balanced between the activities of CSK and CD45, which respectively phosphorylate and dephosphorylate the inhibitory C-terminal site (Y505 of LCK), and the negative regulators LYP and SHP-1, which dephosphorylate an activating tyrosine in the catalytic domain (Y394 of LCK). Acute changes in PTP activity/ expression are in principle sufficient to alter the network status and even trigger true signalling waves. The recent 'kinetic-segregation' model postulates that PTPs are responsible for the very initiation of signalling after engagement of the TCR. SummaryMore than half of the known protein tyrosine phosphatases (PTPs) in the human genome are expressed in T cells, and significant progress has been made in elucidating the biology of these enzymes in T-cell development and function. Here we provide a systematic review of the current understanding of the roles of PTPs in T-cell activation, providing insight into their mechanisms ...

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“…In order to determine whether or not the lymphocytes infiltrating SCC lesions presented a memory phenotype, we analyzed percentages of T cells expressing CD45RA and CD45RB [31] – [32] . CD4 + CD45RB + T cells were detected in lower frequency from tumors samples of mice with inflammasome loss of function at 12 th and 20 th week ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Inflammasome Activation Is Critical to the Protective Immune Response during Chemically Induced Squamous Cell Carcinoma

et al. 2014

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Chronic inflammation affects most stages of tumorigenesis, including initiation, promotion, malignant differentiation, invasion and metastasis. Inflammasomes have been described as involved with persistent inflammation and are known to exert both pro and antitumour effects. We evaluated the influence of apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) and caspase (CASP)-1 in the antitumor immune response using a multistage model of squamous cell carcinoma (SCC) development. Absence of ASC and CASP-1 resulted in an earlier incidence and increased number of papilloma. Loss of inflammassome function in mice resulted in decreased presence of natural killer (NK), dendritic (DC), CD4+, CD8+ and CD45RB+ T cells in the tumor lesions as well as in lymph nodes (LN) compared with WT mice. Increased percentage of CD4+CD25+Foxp3+ T cells was associated with association with inflammasome loss of function. Moreover, significant differences were also found with neutrophils and macrophage infiltrating the lesions. Myeloperoxidase (MPO), but not elastase (ELA), activity oscillated among the groups during the SCC development. Levels of proinflammatory cytokines IL-1β, IL-18, Tumor Necrosis Factor (TNF)-α and Interferon (IFN)-γ were decreased in the tumor microenvironment in the absence of inflammasome proteins. These observations suggest a link between inflammasome function and SCC tumorigenesis, indicating an important role for inflammasome activation in the control of SCC development.

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Expression of CD45 isoforms correlates with differential proliferative responses of peripheral CD4+ and CD8+ T cells

Cited by 9 publications

References 42 publications

Zmiana ekspresji mRNA dla CTLA-4, CD28, VDR i CD45 w limfocytach T u osób z chorobą Hashimoto — badanie pilotowe

Zmiana ekspresji mRNA dla CTLA-4, CD28, VDR i CD45 w limfocytach T u osób z chorobą Hashimoto — badanie pilotowe

Regulation of TCR signalling by tyrosine phosphatases: from immune homeostasis to autoimmunity

Inflammasome Activation Is Critical to the Protective Immune Response during Chemically Induced Squamous Cell Carcinoma

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