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Kim, Young H.,Choi, Beom K.,Kang, Woo J.,Kim, Kwang H.,Kang, Sang W.,Mellor, Andrew L.,Munn, David H.,Kwon, Byoung S. Wiley (John WileySons) 2009 Journal of leukocyte biology Vol.85 No.5
<P>It has been reported that 4-1BB triggering in vivo selectively suppressed the recall response of staphylococcal enterotoxin A (SEA)-specific CD4(+) T cells, in which CD8(+) T-derived TGF-beta was involved. Here, we have examined an alternative mechanism for the 4-1BB-mediated CD4(+) T suppression, as the neutralization of TGF-beta is only effective in rescuing the SEA-specific recall response at high cellular concentrations. We show that this selective suppression of CD4(+) T cells by 4-1BB triggering in vivo is mediated mainly by induction of indoleamine 2,3-dioxygenase (IDO) in an IFN-gamma-dependent manner. SEA-specific CD4(+) T responses were suppressed partly by TGF-beta-expressing CD8(+) T cells, particularly CD11c(+)CD8(+) T cells, but strongly inhibited by dendritic cells (DCs) expressing IDO. IFN-gamma that increased IDO in DCs was produced primarily from CD11c(+)CD8(+) T cells, which were expanded selectively by 4-1BB stimulation. CD4(+), CD8(+), and plasmacytoid DCs exerted a similar suppressive activity toward the SEA-specific CD4(+) T cells. Neutralization of IFN-gamma or IDO activity in vivo largely reversed the 4-1BB-mediated CD4(+) T suppression. Collectively, these data indicate that 4-1BB-dependent suppression of SEA-specific CD4(+) T responses was mediated mainly by IFN-gamma-dependent IDO induction and partially by TGF-beta.</P>
Influence of Ionic Strength on the Deposition of Metal–Phenolic Networks
Guo, Junling,Richardson, Joseph J.,Besford, Quinn A.,Christofferson, Andrew J.,Dai, Yunlu,Ong, Chien W.,Tardy, Blaise L.,Liang, Kang,Choi, Gwan H.,Cui, Jiwei,Yoo, Pil J.,Yarovsky, Irene,Caruso, Frank American Chemical Society 2017 Langmuir Vol.33 No.40
<P>Metal–phenolic networks (MPNs) are a versatile class of self-assembled materials that are able to form functional thin films on various substrates with potential applications in areas including drug delivery and catalysis. Different metal ions (e.g., Fe<SUP>III</SUP>, Cu<SUP>II</SUP>) and phenols (e.g., tannic acid, gallic acid) have been investigated for MPN film assembly; however, a mechanistic understanding of the thermodynamics governing MPN formation remains largely unexplored. To date, MPNs have been deposited at low ionic strengths (<5 mM), resulting in films with typical thicknesses of ∼10 nm, and it is still unclear how a bulk complexation reaction results in homogeneous thin films when a substrate is present. Herein we explore the influence of ionic strength (0–2 M NaCl) on the conformation of MPN precursors in solution and how this determines the final thickness and morphology of MPN films. Specifically, the film thickness increases from 10 nm in 0 M NaCl to 12 nm in 0.5 M NaCl and 15 nm in 1 M NaCl, after which the films grow rougher rather than thicker. For example, the root-mean-square roughness values of the films are constant below 1 M NaCl at 1.5 nm; in contrast, the roughness is 3 nm at 1 M NaCl and increases to 5 nm at 2 M NaCl. Small-angle X-ray scattering and molecular dynamics simulations allow for comparisons to be made with chelated metals and polyelectrolyte thin films. For example, at a higher ionic strength (2 M NaCl), sodium ions shield the galloyl groups of tannic acid, allowing them to extend away from the Fe<SUP>III</SUP> center and interact with other MPN complexes in solution to form thicker and rougher films. As the properties of films determine their final performance and application, the ability to tune both thickness and roughness using salts may allow for new applications of MPNs.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/langd5/2017/langd5.2017.33.issue-40/acs.langmuir.7b02692/production/images/medium/la-2017-026926_0007.gif'></P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/la7b02692'>ACS Electronic Supporting Info</A></P>
( Xiao Wen He ),( John M. Stuart ),( Linda K. Myers ),( Andrew H. Kang ) 대한류마티스학회 2002 대한류마티스학회지 Vol.9 No.1
Collagen induced arthritis (CIA) is an animal model that in many ways resembles rheumatoid arthritis (RA). CIA can be induced in susceptible animals by immunization with type II collagen (CII). Like RA, CIA is characterized by intense joint inflammation and destruction. On histological examination, there is synovitis accompanied by erosion of cartilage and subchondral bone. Autoantibodies to CII initiate joint inflammation by binding to articular cartilage, forming antigen-antibody complexes locally and activating hemolytic complement. Susceptibility to CIA in mice is linked to the expression of specific class II MHC molecules, which dictate the T cell determinants on CII, and therefore, the subsets of T cells that can be activated by CII. In addition to activation of B cells reactive to CII, the T cells stimulate monocytes/macrophages. These cells amplify the inflammatory cascade by secretion of proinflammatory monokines, including TNF-α and IL-1, leading to the production of other proinflammatory proteins, including matrix metalloproteinases (MMPs). The importance of CIA lies in its possible relationship to arthritis in humans. Progress in understanding CIA has contributed to the development of new therapies for RA. In addition, it has been found that mice with human HLA-DR1, DR4 and HLA-DQ8 transgenes, which have been demonstrated to be the susceptibility markers for RA, confer susceptibility to CIA. These observations coupled with the finding of T cells and B cells reactive with CII in the inflamed joints of RA patients establish the potential role of CII autoimmunity in the pathogenesis of RA.
The Somatic Genomic Landscape of Chromophobe Renal Cell Carcinoma
The Cancer Genome Atlas Research Network,Davis, Caleb F.,Ricketts, C.J.,Wang, M.,Yang, L.,Cherniack, Andrew D.,Shen, H.,Buhay, C.,Kang, H.,Kim, S.,Fahey, Catherine C.,Hacker, Kathryn E.,Bhanot, G.,Gor Cell Press 2014 Cancer Cell Vol.26 No.3
We describe the landscape of somatic genomic alterations of 66 chromophobe renal cell carcinomas (ChRCCs) on the basis of multidimensional and comprehensive characterization, including mtDNA and whole-genome sequencing. The result is consistent that ChRCC originates from the distal nephron compared with other kidney cancers with more proximal origins. Combined mtDNA and gene expression analysis implicates changes in mitochondrial function as a component of the disease biology, while suggesting alternative roles for mtDNA mutations in cancers relying on oxidative phosphorylation. Genomic rearrangements lead to recurrent structural breakpoints within TERT promoter region, which correlates with highly elevated TERT expression and manifestation of kataegis, representing a mechanism of TERT upregulation in cancer distinct from previously observed amplifications and point mutations.