Research Topics
Species | Angelica S I LoskogSummaryAffiliation: Uppsala University Country: Sweden Publications
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Detail Information
Publications
Human bladder carcinoma is dominated by T-regulatory cells and Th1 inhibitory cytokinesAngelica Loskog
Clinical Immunology Division, Rudbeck Laboratory C11 Uppsala University, Uppsala, Sweden
J Urol 177:353-8. 2007..We are developing immunostimulating gene therapy for treating bladder cancer. In this study we constructed an immunological profile of patients with bladder carcinoma to understand which obstacles must be circumvented...
Dendritic cells engineered to express CD40L continuously produce IL12 and resist negative signals from Tr1/Th3 dominated tumorsAngelica Loskog
Clinical Immunology Division, Rudbeck Laboratory, Uppsala University, Dag Hammarskjoldsvag, 20 751 85, Uppsala, Sweden
Cancer Immunol Immunother 55:588-97. 2006..Thus, CD40L-engineered DCs are robust Th1-promoting ones that are resistant to Tr1/Th3-signaling via IL10 and TGFbeta...
CD40L - a multipotent molecule for tumor therapyAngelica Loskog
Clinical Immunology Division, Uppsala University, 751 85 Uppsala, Sweden
Endocr Metab Immune Disord Drug Targets 7:23-8. 2007..In this survey, different types and mechanisms of CD40L-based therapy will be discussed from bench to bedside...
Addition of the CD28 signaling domain to chimeric T-cell receptors enhances chimeric T-cell resistance to T regulatory cellsA Loskog
Center for Cell and Gene Therapy, Baylor College of Medicine, Houston, TX, USA
Leukemia 20:1819-28. 2006..These effects are seen whether the chimeric T cells are derived from normal donors or from patients with B-cell chronic lymphocytic leukemia, indicating the potential for clinical application in B cell malignancies...
AdCD40L gene therapy counteracts T regulatory cells and cures aggressive tumors in an orthotopic bladder cancer modelAngelica S I Loskog
Rudbeck Laboratory, Clinical Immunology Division, Uppsala University, Uppsala, Sweden
Clin Cancer Res 11:8816-21. 2005..CD40L stimulation of dendritic cells induces interleukin-12 expression that drives Th1 type of immune responses with activation of cytotoxic T cells...
Optimization of the MB49 mouse bladder cancer model for adenoviral gene therapyA Loskog
Clinical Immunology Division, Rudbeck Laboratory, Uppsala University, Sweden
Lab Anim 39:384-93. 2005..Given the possibility for efficient genetic modification of the bladder and the presence of known tumour antigens, the MB49 models can be used in innovative ways to explore immunogene therapy...
AdCD40L immunogene therapy for bladder carcinoma--the first phase I/IIa trialPer Uno Malmstrom
Division of Urology, Uppsala University, Uppsala, Sweden
Clin Cancer Res 16:3279-87. 2010..Immunostimulating gene therapy with adenoviral vectors expressing CD40 ligand (AdCD40L) has shown efficacy in tumor models. CD40 ligand stimulates systemic immunity and may be effective in local and invasive human disease...
AdCD40L--crossing the valley of death?Gustav Ullenhag
Department of Radiology, Oncology and Radiation Science, Uppsala University, Uppsala, Sweden
Int Rev Immunol 31:289-98. 2012..This review discusses the currently unfolding mechanisms of action of AdCD40L gene therapy and its possibilities to reach clinical care...
Both CD4+ FoxP3+ and CD4+ FoxP3- T cells from patients with B-cell malignancy express cytolytic markers and kill autologous leukaemic B cells in vitroCamilla A Lindqvist
Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, Sweden
Immunology 133:296-306. 2011..In conclusion, cytotoxic populations of CD4(+) T cells, including Tregs, are present in patients with B-cell malignancy and may be an important factor in immune-related disease control...
CAR/FoxP3-engineered T regulatory cells target the CNS and suppress EAE upon intranasal deliveryMoa Fransson
Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden
J Neuroinflammation 9:112. 2012..Here, we propose gene engineering to achieve CNS-targeting Tregs from naïve CD4 cells and demonstrate their efficacy in the EAE model...
Increased level of myeloid-derived suppressor cells, programmed death receptor ligand 1/programmed death receptor 1, and soluble CD25 in Sokal high risk chronic myeloid leukemiaLisa Christiansson
Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, Uppsala, Sweden
PLoS ONE 8:e55818. 2013..These escape mechanisms should be monitored in trials to understand their importance and how to overcome the immune suppression...
T regulatory cells in B-cell malignancy - tumour support or kiss of death?Camilla A Lindqvist
Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, Uppsala, Sweden
Immunology 135:255-60. 2012..In this review, we discuss the origin and function of Treg cells and their role in patients with B-cell tumours...
T regulatory cells control T-cell proliferation partly by the release of soluble CD25 in patients with B-cell malignanciesCamilla A Lindqvist
Division of Clinical Immunology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden
Immunology 131:371-6. 2010..Recombinant sCD25 could suppress T-cell proliferation in vitro. In conclusion, the release of sCD25 by Treg cells may be a mechanism to deprive IL-2 and thereby inhibit anti-tumour T-cell responses...
The T-cell pool is anergized in patients with multiple sclerosis in remissionMoa E Fransson
Clinical Immunology Division, Uppsala University, Uppsala, Sweden
Immunology 126:92-101. 2009..In conclusion, patients in relapse/remission demonstrate in vitro T-cell responses that are both Th1 and Th17 that, while in remission, appear to be controlled by tolerogenic mechanisms yet to be investigated...
The Janus faces of CD40 in cancerAngelica S I Loskog
Rudbeck Laboratory, Clinical Immunology Division, Uppsala University, Uppsala, Sweden
Semin Immunol 21:301-7. 2009..Here, we provide an overview of the multifaceted functions of the CD40 pathway in cancer and its emerging role in the treatment of malignancy...
