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  • 1.
    Barathan, Muttiah
    et al.
    University of Malaya, Malaysia.
    Mohamed, Rosmawati
    University of Malaya, Malaysia.
    Vadivelu, Jamuna
    University of Malaya, Malaysia.
    Yen Chang, Li
    University of Malaya, Malaysia.
    Vignesh, Ramachandran
    University of Kuala Lumpur, Malaysia.
    Krishnan, Jayalakshmi
    CUTN, India.
    Sigamani, Panneer
    CUTN, India.
    Saeidi, Alireza
    University of Malaya, Malaysia.
    Ravishankar Ram, M.
    University of Malaya, Malaysia.
    Velu, Vijayakumar
    Emory Vaccine Centre, GA 30329 USA.
    Larsson, Marie
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Medicine and Health Sciences.
    Shankar, Esaki M.
    University of Malaya, Malaysia; CUTN, India; University of Malaya, Malaysia.
    CD8+T cells of chronic HCV-infected patients express multiple negative immune checkpoints following stimulation with HCV peptides2017In: Cellular Immunology, ISSN 0008-8749, E-ISSN 1090-2163, Vol. 313Article in journal (Refereed)
    Abstract [en]

    Hepatitis C virus (HCV)-specific CD4+ and CD8+ T cells are key to successful viral clearance in HCV disease. Accumulation of exhausted HCV-specific T cells during chronic infection results in considerable loss of protective functional immune responses. The role of T-cell exhaustion in chronic HCV disease remains poorly understood. Here, we studied the frequency of HCV peptide-stimulated T cells expressing negative immune checkpoints (PD-1, CTLA-4, TRAIL, TIM-3 and BTLA) by flow cytometry, and measured the levels of Th1/Th2/Th17 cytokines secreted by T cells by a commercial Multi-Analyte ELISArray (TM) following in vitro stimulation of T cells using HCV peptides and phytohemagglutinin (PHA). HCV peptide stimulated CD4+ and CD8+ T cells of chronic HCV (CHC) patients showed significant increase of CTLA-4. Furthermore, HCV peptide-stimulated CD4+ T cells of CHC patients also displayed relatively higher levels of PD-1 and TRAIL, whereas TIM-3 was up-regulated on HCV peptide-stimulated CD8+ T cells. Whereas the levels of IL-10 and TGF-beta 1 were significantly increased, the levels of pro-inflammatory cytokines IL-2, TNF-alpha, IL-17A and IL-6 were markedly decreased in the T cell cultures of CHC patients. Chronic HCV infection results in functional exhaustion of CD4+ and CD8+ T cells likely contributing to viral persistence. (C) 2016 Elsevier Inc. All rights reserved.

  • 2.
    Johansson, Susanne E
    et al.
    Karolinska Institutet.
    Bauner, Hanna
    Karolinska Institutet.
    Hinkula, Jorma
    Linköping University, Department of Clinical and Experimental Medicine, Molecular Virology. Linköping University, Faculty of Health Sciences.
    Wahren, Britta
    Karolinska Institutet.
    Berg, Louise
    Karolinska Institutet.
    Johansson, Maria H
    Karolinska Institutet.
    Accumulation and activation of natural killer cells in local intraperitoneal HIV-1/MuLV infection results in early control of virus infected cells2011In: Cellular Immunology, ISSN 0008-8749, E-ISSN 1090-2163, Vol. 272, no 1, p. 71-78Article in journal (Refereed)
    Abstract [en]

    Natural killer (NK) cells are important effectors in resistance to viral infections. The role of NK cells in the acute response to human immunodeficiency virus 1 (HIV-1) infected cells was investigated in a mouse model based on a HIV-1/murine leukemia virus (MuLV) pseudovirus. Splenocytes infected with HIV-1/MuLV were injected intraperitoneally and local immunologic responses and persistence of infected cells were investigated. In vivo depletion with an anti-NK1.1 antibody showed that NK cells are important in resistance to virus infected cells. Moreover, NK cell frequency in the peritoneal cavity increased in response to infected cells and these NK cells had a more mature phenotype, as determined by CD27 and Mac-1 expression. Interestingly, after injection of HIV-1/MuLV infected cells, but not MuLV infected cells, peritoneal NK cells had an increased cytotoxic activity.

  • 3.
    Saeidi, Alireza
    et al.
    University of Malaya, Malaysia.
    Buggert, Marcus
    University of Penn, PA 19104 USA.
    Che, Karlhans F.
    Karolinska Institute, Sweden.
    Kong, Yong Y.
    University of Malaya, Malaysia.
    Velu, Vijayakumar
    Emory University, GA 30322 USA.
    Larsson, Marie
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Medicine and Health Sciences.
    Shankar, Esaki M.
    University of Malaya, Malaysia; University of Malaya, Malaysia.
    Regulation of CD8+T-cell cytotoxicity in HIV-1 infection2015In: Cellular Immunology, ISSN 0008-8749, E-ISSN 1090-2163, Vol. 298, no 1-2, p. 126-133Article, review/survey (Refereed)
    Abstract [en]

    Understanding the mechanisms involved in cellular immune responses against control of human immunodeficiency virus (HIV) infection is key to development of effective immunotherapeutic strategies against viral proliferation. Clear insights into the regulation of cytotoxic CD8+ T cells is crucial to development of effective immunotherapeutic strategies due to their unique ability to eliminate virus-infected cells during the course of infection. Here, we reviewed the roles of transcription factors, co-inhibitory molecules and regulatory cytokines following HIV infection and their potential significance in regulating the cytotoxic potentials of CD8+ T cells. (C) 2015 Elsevier Inc. All rights reserved.

  • 4.
    Saeidi, Alireza
    et al.
    University of Malaya, Malaysia.
    Chong, Yee K.
    University of Malaya, Malaysia.
    Yong, Yean K.
    University of Malaya, Malaysia.
    Tan, Hong Y.
    University of Malaya, Malaysia.
    Barathan, Muttiah
    University of Malaya, Malaysia.
    Rajarajeswaran, Jayakumar
    University of Malaya, Malaysia.
    Sabet, Negar S.
    SEGi University, Malaysia.
    Sekaran, Shamala D.
    University of Malaya, Malaysia.
    Ponnampalavanar, Sasheela
    University of Malaya, Malaysia.
    Che, Karlhans F.
    Karolinska Institute, Sweden.
    Velu, Vijayakumar
    Emory Vaccine Centre, GA 30329 USA.
    Kamarulzaman, Adeeba
    University of Malaya, Malaysia.
    Larsson, Marie
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Medicine and Health Sciences.
    Shankar, Esaki M.
    University of Malaya, Malaysia; University of Malaya, Malaysia; University of Malaya, Malaysia.
    Concurrent loss of co-stimulatory molecules and functional cytokine secretion attributes leads to proliferative senescence of CD8(+) T cells in HIV/TB co-infection2015In: Cellular Immunology, ISSN 0008-8749, E-ISSN 1090-2163, Vol. 297, no 1, p. 19-32Article in journal (Refereed)
    Abstract [en]

    The role of T-cell immunosenescence and functional CD8(+) T-cell responses in HIV/TB co-infection is unclear. We examined and correlated surrogate markers of HIV disease progression with immune activation, immunosenescence and differentiation using T-cell pools of HIV/TB co-infected, HIV-infected and healthy controls. Our investigations showed increased plasma viremia and reduced CD4/CD8 T-cell ratio in HIV/TB co-infected subjects relative to HIV-infected, and also a closer association with changes in the expression of CD38, a cyclic ADP ribose hydrolase and CD57, which were consistently expressed on late-senescent CD8(+) T cells. Up-regulation of CD57 and CD38 were directly proportional to lack of co-stimulatory markers on CD8(+) T cells, besides diminished expression of CD127 (IL-7R alpha) on CD57(+)CD4(+) T cells. Notably, intracellular IFN-gamma, perforin and granzyme B levels in HIV-specific CD8(+) T cells of HIV/TB co-infected subjects were diminished. Intracellular CD57 levels in HIV gag p24-specific CD8(+) T cells were significantly increased in HIV/TB co-infection. We suggest that HIV-TB co-infection contributes to senescence associated with chronic immune activation, which could be due to functional insufficiency of CD8(+) T cells. (C) 2015 Elsevier Inc. All rights reserved.

  • 5.
    Tegnér, Jesper
    et al.
    Linköping University, The Institute of Technology. Linköping University, Department of Physics, Chemistry and Biology, Computational Biology .
    Nilsson, Roland
    Linköping University, The Institute of Technology. Linköping University, Department of Physics, Chemistry and Biology, Computational Biology .
    Bajic, V.B.
    University of Western Cape, SANBI, Bellville, 7535, South Africa.
    Bjorkegren, J.
    Björkegren, J., Unit of Computational Medicine, King Gustaf V Research Institute, Department of Medicine, SE-171 76 Stockholm, Sweden.
    Ravasi, T.
    Genome Exploration Research Group (Genome Network Project Core Group), RIKEN Genomic Sciences Center (GSC), RIKEN Yokohama Institute, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa, Japan, Scripps NeuroAIDS Preclinical Studies Centre, Jacobs School of Engineering, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, United States, Department of Bioengineering, Jacobs School of Engineering, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, United States.
    Systems biology of innate immunity2006In: Cellular Immunology, ISSN 0008-8749, E-ISSN 1090-2163, Vol. 244, no 2, p. 105-109Article in journal (Refereed)
    Abstract [en]

    Systems Biology has emerged as an exciting research approach in molecular biology and functional genomics that involves a systematic use of genomic, proteomic, and metabolomic technologies for the construction of network-based models of biological processes. These endeavors, collectively referred to as systems biology establish a paradigm by which to systematically interrogate, model, and iteratively refine our knowledge of the regulatory events within a cell. Here, we present a new systems approach, integrating DNA and transcript expression information, specifically designed to identify transcriptional networks governing the macrophage immune response to lipopolysaccharide (LPS). Using this approach, we are not only able to infer a global macrophage transcriptional network, but also time-specific sub-networks that are dynamically active across the LPS response. We believe that our system biological approach could be useful for identifying other complex networks mediating immunological responses. © 2007 Elsevier Inc. All rights reserved.

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