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      Follistatin‐like protein 1 contributes to dendritic cell and T‐lymphocyte activation in nasopharyngeal carcinoma patients by altering nuclear factor κb and Jun N‐terminal kinase expression

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          Abstract

          Follistatin‐like protein 1 (FSTL1) is a newly characterized protein that can regulate the immune response in various ways. Dendritic cells (DCs) are central to immune regulation. In this study, we explored the impact of FSTL1 on DC activity in nasopharyngeal carcinoma (NPC) patients. The surface expression of CD40, CD86, and HLA‐DR on DCs was analyzed and showed significantly elevated expression levels, indicating DC maturity. After FSTL1 was added to DCs collected from NPC patients (n = 50), controls (n = 47), and healthy donors (n = 10), interferon γ secretion and T‐cell receptor expression in cytotoxic T lymphocytes were also investigated. In the experimental groups, the expression of the critical immune protein nuclear factor (NF)‐κb was upregulated, whereas Jun N‐terminal kinase (JNK) was downregulated. Our findings demonstrate that FSTL1 plays a critical role in immune regulation, enhancing the antigen presentation ability of DCs by up‐regulating NF‐κb expression and down‐regulating JNK expression.

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          Endoplasmic reticulum stress in liver disease.

          Harmeet Malhi, Randal Kaufman (2011)
          The unfolded protein response (UPR) is activated upon the accumulation of misfolded proteins in the endoplasmic reticulum (ER) that are sensed by the binding immunoglobulin protein (BiP)/glucose-regulated protein 78 (GRP78). The accumulation of unfolded proteins sequesters BiP so it dissociates from three ER-transmembrane transducers leading to their activation. These transducers are inositol requiring (IRE) 1α, PKR-like ER kinase (PERK), and activating transcription factor (ATF) 6α. PERK phosphorylates eukaryotic initiation factor 2 alpha (eIF2α) resulting in global mRNA translation attenuation, and concurrently selectively increases the translation of several mRNAs, including the transcription factor ATF4, and its downstream target CHOP. IRE1α has kinase and endoribonuclease (RNase) activities. IRE1α autophosphorylation activates the RNase activity to splice XBP1 mRNA, to produce the active transcription factor sXBP1. IRE1α activation also recruits and activates the stress kinase JNK. ATF6α transits to the Golgi compartment where it is cleaved by intramembrane proteolysis to generate a soluble active transcription factor. These UPR pathways act in concert to increase ER content, expand the ER protein folding capacity, degrade misfolded proteins, and reduce the load of new proteins entering the ER. All of these are geared toward adaptation to resolve the protein folding defect. Faced with persistent ER stress, adaptation starts to fail and apoptosis occurs, possibly mediated through calcium perturbations, reactive oxygen species, and the proapoptotic transcription factor CHOP. The UPR is activated in several liver diseases; including obesity associated fatty liver disease, viral hepatitis, and alcohol-induced liver injury, all of which are associated with steatosis, raising the possibility that ER stress-dependent alteration in lipid homeostasis is the mechanism that underlies the steatosis. Hepatocyte apoptosis is a pathogenic event in several liver diseases, and may be linked to unresolved ER stress. If this is true, restoration of ER homeostasis prior to ER stress-induced cell death may provide a therapeutic rationale in these diseases. Herein we discuss each branch of the UPR and how they may impact hepatocyte function in different pathologic states. Copyright © 2010 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
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            Lethal graft-versus-host disease in mouse models of T cell receptor gene therapy.

            Gavin M Bendle, Carsten Linnemann, Anna I Hooijkaas … (2010)
            The transfer of T cell receptor (TCR) genes can be used to induce immune reactivity toward defined antigens to which endogenous T cells are insufficiently reactive. This approach, which is called TCR gene therapy, is being developed to target tumors and pathogens, and its clinical testing has commenced in patients with cancer. In this study we show that lethal cytokine-driven autoimmune pathology can occur in mouse models of TCR gene therapy under conditions that closely mimic the clinical setting. We show that the pairing of introduced and endogenous TCR chains in TCR gene-modified T cells leads to the formation of self-reactive TCRs that are responsible for the observed autoimmunity. Furthermore, we demonstrate that adjustments in the design of gene therapy vectors and target T cell populations can be used to reduce the risk of TCR gene therapy-induced autoimmune pathology.
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              Mixed T cell receptor dimers harbor potentially harmful neoreactivity.

              Kimberly R. Boer, Moaath A. Amir, Gerdien Volbeda … (2010)
              Adoptive transfer of T cell receptor (TCR)-transduced T cells may be an attractive strategy to target both hematological malignancies and solid tumors. By introducing a TCR, large numbers of T cells with defined antigen (Ag) specificity can be obtained. However, by introduction of a TCR, mixed TCR dimers can be formed. Besides the decrease in TCR expression of the introduced and endogenous TCR, these mixed TCR dimers could harbor potentially harmful specificities. In this study, we demonstrate that introduction of TCRs resulted in formation of neoreactive mixed TCR dimers, composed of the introduced TCR chains pairing with either the endogenous TCR alpha or beta chain. Neoreactivities observed were HLA class I or class II restricted. Most neoreactive mixed TCR dimers were allo-HLA reactive; however, neoreactive mixed TCR dimers with autoreactive activity were also observed. We demonstrate that inclusion of an extra disulfide bond between the constant domains of the introduced TCR markedly reduced neoreactivity, whereas enhanced effectiveness of the introduced TCR was observed. In conclusion, TCR transfer results in the formation of neoreactive mixed TCR dimers with the potential to generate off-target effects, underlining the importance of searching for techniques to facilitate preferential pairing.
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                Author and article information

                Contributors
                Anzhou Tang: anzhoutang@126.com
                Wensheng Wen: wenwensheng2000@126.com
                Journal
                Journal ID (nlm-ta): Cell Biochem Funct
                Journal ID (iso-abbrev): Cell Biochem. Funct
                Journal ID (doi): 10.1002/(ISSN)1099-0844
                Journal ID (publisher-id): CBF
                Title: Cell Biochemistry and Function
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 0263-6484
                ISSN (Electronic): 1099-0844
                Publication date (Electronic): 16 November 2016
                Publication date (Print): December 2016
                Volume: 34
                Issue: 8 ( doiID: 10.1002/cbf.v34.8 )
                Pages: 554-562
                Affiliations
                [ 1 ] Department of Otorhinolaryngology Head and Neck SurgeryFirst Affiliated Hospital of Guangxi Medical University Nanning GuangxiChina
                [ 2 ] Department of Otorhinolaryngology Head and Neck SurgeryThe People's Hospital Guigang GuangxiChina
                [ 3 ] Department of OtolaryngologyThe Cooperation of Chinese and Western Medicine Hospital in Guangzhou GuangzhouChina
                [ 4 ] Department of OtolaryngologyThe People's Hospital of Hezhou GuangxiChina
                Author notes
                [*] [* ] Correspondence

                Anzhou Tang and Wensheng Wen, Department of Otorhinolaryngology Head and Neck Surgery, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, China.

                Email: wenwensheng2000@ 123456126.com ; anzhoutang@ 123456126.com

                [†]

                Anzhou Tang and Wensheng Wen contributed equally to this work.

                Article
                Publisher ID: CBF3227 Other ID: CBF-16-0133.R1
                DOI: 10.1002/cbf.3227
                PMC ID: 5215428
                PubMed ID: 27859422
                SO-VID: 4b1fe119-b204-4791-b878-33714528665a
                Copyright © Copyright © 2016 The Authors Cell Biochemistry and Function published by John Wiley & Sons Ltd.
                License:

                This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                Date received : 06 July 2016
                Date revision received : 01 September 2016
                Date accepted : 14 September 2016
                Page count
                Figures: 4, Tables: 1, Pages: 9, Words: 4034
                Funding
                Funded by: Nature Science Foundation of Guangxi
                Award ID: Grant/Award Number: [2015]139
                Categories
                Subject: Research Article
                Subject: Research Articles
                Custom metadata
                source-schema-version-number 2.0
                component-id cbf3227
                cover-date December 2016
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:5.0.0 mode:remove_FC converted:05.01.2017

                Keywords: dendritic cell,follistatin‐like protein 1,jun n‐terminal kinase,nasopharyngeal carcinoma,nuclear factor κb,t lymphocyte
                Data availability:
                Keywords: dendritic cell, follistatin‐like protein 1, jun n‐terminal kinase, nasopharyngeal carcinoma, nuclear factor κb, t lymphocyte

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