• BMB Reports
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• v.38 no.3
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• pp.334-342
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• 2005

Recently, the existence of T cells with dual T cell receptor (TCR) in the immune system is generally accepted, while it has been controversial whether signals through one TCR would affect the functions of the other. In this study T cells expressing two different TCR were obtained from cross-hybrids of LCMV and AND TCR transgenic mice specific for the gp33 and peptide fragment of PCC (fPCC), respectively. Peptide stimulation demonstrated that the dual TCR T cells functioned independently in an antigen-specific manner. To examine whether the tolerance targeted for the one TCR affects the responsiveness of the other, the cross-hybrids were treated with gp33. Although T cells from F1 mice were rendered anergenic to gp33, no functional changes to fPCC were observed in terms of cellular proliferation and IL-2 secretion, suggesting that the dual TCR T cells remained reactive to fPCC. We therefore propose that signaling through the TCR is receptor-specific and 'negative dominance' of one TCR by tolerance induction is not applicable in this dual TCR system.

• Korean Journal of Materials Research
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• v.26 no.6
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• pp.293-297
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• 2016

Ni-C composite films were prepared by co-deposition using a combined technique of plasma CVD and ion beam sputtering deposition. Depending on the deposition conditions, Ni-C thin films manifested three kinds of microstructure: (1) nanocrystallites of non-equilibrium carbide of nickel, (2) amorphous Ni-C film, and (3) granular Ni-C film. The electrical resistivity was also found to vary from about $10^2{\mu}{\Omega}cm$ for the carbide films to about $10^4{\mu}{\Omega}cm$ for the amorphous Ni-C films. The Ni-C films deposited at ambient temperatures showed very low TCR values compared with that of metallic nickel film, and all the films showed ohmic characterization, even those in the amorphous state with very high resistivity. The TCR value decreased slightly with increasing of the flow rate of $CH_4$. For the films deposited at $200^{\circ}C$, TCR decreased with increasing $CH_4$ flow rate; especially, it changed sign from positive to negative at a $CH_4$ flow rate of 0.35 sccm. By increasing the $CH_4$ flow rate, the amorphous component in the film increased; thus, the portion of $Ni_3C$ grains separated from each other became larger, and the contribution to electrical conductivity due to thermally activated tunneling became dominant. This also accounts for the sign change of TCR when the filme was deposited at higher flow rate of $CH_4$. The microstructures of the Ni-C films deposited in these ways range from amorphous Ni-C alloy to granular structures with $Ni_3C$ nanocrystallites. These films are characterized by high resistivity and low TCR values; the electrical properties can be adjusted over a wide range by controlling the microstructures and compositions of the films.

• IMMUNE NETWORK
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• v.23 no.2
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• pp.12.1-12.17
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• 2023

Ssu72, a dual-specificity protein phosphatase, not only participates in transcription biogenesis, but also affects pathophysiological functions in a tissue-specific manner. Recently, it has been shown that Ssu72 is required for T cell differentiation and function by controlling multiple immune receptor-mediated signals, including TCR and several cytokine receptor signaling pathways. Ssu72 deficiency in T cells is associated with impaired fine-tuning of receptor-mediated signaling and a defect in CD4⁺ T cell homeostasis, resulting in immune-mediated diseases. However, the mechanism by which Ssu72 in T cells integrates the pathophysiology of multiple immune-mediated diseases is still poorly elucidated. In this review, we will focus on the immunoregulatory mechanism of Ssu72 phosphatase in CD4⁺ T cell differentiation, activation, and phenotypic function. We will also discuss the current understanding of the correlation between Ssu72 in T cells and pathological functions which suggests that Ssu72 might be a therapeutic target in autoimmune disorders and other diseases.

• IMMUNE NETWORK
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• v.20 no.1
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• pp.5.1-5.15
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• 2020

The γδ T cells are unconventional lymphocytes that function in both innate and adaptive immune responses against various intracellular and infectious stresses. The γδ T cells can be exploited as cancer-killing effector cells since γδ TCRs recognize MHC-like molecules and growth factor receptors that are upregulated in cancer cells, and γδ T cells can differentiate into cytotoxic effector cells. However, γδ T cells may also promote tumor progression by secreting IL-17 or other cytokines. Therefore, it is essential to understand how the differentiation and homeostasis of γδ T cells are regulated and whether distinct γδ T cell subsets have different functions. Human γδ T cells are classified into Vδ2 and non-Vδ2 γδ T cells. The majority of Vδ2 γδ T cells are Vγ9δ2 T cells that recognize pyrophosphorylated isoprenoids generated by the dysregulated mevalonate pathway. In contrast, Vδ1 T cells expand from initially diverse TCR repertoire in patients with infectious diseases and cancers. The ligands of Vδ1 T cells are diverse and include the growth factor receptors such as endothelial protein C receptor. Both Vδ1 and Vδ2 γδ T cells are implicated to have immunotherapeutic potentials for cancers, but the detailed elucidation of the distinct characteristics of 2 populations will be required to enhance the immunotherapeutic potential of γδ T cells. Here, we summarize recent progress regarding cancer immunology of human γδ T cells, including their development, heterogeneity, and plasticity, the putative mechanisms underlying ligand recognition and activation, and their dual effects on tumor progression in the tumor microenvironment.