Sökning: "CTLA-4"

Visar resultat 1 - 5 av 46 avhandlingar innehållade ordet CTLA-4.

  1. 1. Immunological Checkpoint Blockade and TLR Stimulation for Improved Cancer Therapy

    Detta är en avhandling från Uppsala : Acta Universitatis Upsaliensis

    Författare :Sara Mangsbo; Uppsala universitet.; [2009]
    Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; CpG ODNs; TLR-9; CTLA-4; PD-1; PD-L1; B7. H1; immunotherapy; checkpoint blockade; bladder cancer; cancer; complement; TLRs; Compstatin; properdin; C3; experimental animal model; whole blood loop system; combination therapies; MEDICINE Microbiology; immunology; infectious diseases Immunology Clinical immunology; MEDICIN Mikrobiologi; immunologi; infektionssjukdomar Immunologi Klinisk immunologi; MEDICINE Microbiology; immunology; infectious diseases Immunology Tumour immunology; MEDICIN Mikrobiologi; immunologi; infektionssjukdomar Immunologi Tumörimmunologi; immunologi; Immunology;

    Sammanfattning : This thesis concerns the investigation of novel immunotherapies for cancer eradication. CpG therapy was used in order to target antigen-presenting cells (APCs), facilitating antigen presentation and activation of T cells. LÄS MER

  2. 2. CTLA-4 expression, regulation and associations in autoimmune myasthenia gravis

    Detta är en avhandling från Stockholm : Karolinska Institutet, Department of Medicine

    Författare :XiongBiao Wang; Karolinska Institutet.; Karolinska Institutet.; [2003]
    Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Cytotoxic-T-lymphocyte-associated antigen 4 CTLA-4 ; Myasthenia gravis MG ; Immune inhibitory receptor; Autoimmune disease; Genetic polymorphism.;

    Sammanfattning : Myasthenia gravis (MG) is a neuromuscular disease with muscle weakness due to an autoimmune attack against the nicotinic acetylcholine receptor (nAChR) on the skeletal muscle endplate. Cytotoxic-T-lymphocyte-associated antigen 4 (CTLA-4) plays a global inhibitory role in the immune system and has a crucial role in autoimmunity. LÄS MER

  3. 3. FOXP3 and CTLA-4 : how isoforms regulate immunological tolerance

    Detta är en avhandling från Stockholm : Karolinska Institutet, Dept of Medicine, Solna

    Författare :Sang Liu; Karolinska Institutet.; Karolinska Institutet.; [2015]
    Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES;

    Sammanfattning : The maintenance of immunological tolerance is vital for preventing the immune system to damage normal tissues and physiological function of the body. CD4+FOXP3+ regulatory T (Treg) cells can suppress immune responses in a dominant manner and are essential for immunological tolerance. LÄS MER

  4. 4. The role of CTLA-4 in health and autoimmune disease

    Detta är en avhandling från Stockholm : Karolinska Institutet, Dept of Medical Biochemistry and Biophysics

    Författare :Katrin Klocke; Karolinska Institutet.; Karolinska Institutet.; [2017]
    Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES;

    Sammanfattning : FOXP3+ regulatory T (Treg) cells are powerful regulators of the immune system, as shown by the development of multi-organ autoimmunity in mice and men upon loss or dysfunction of these cells. Whilst Treg cells are vital to control normal immune responses, they are also involved in the development of autoimmunity and the failure to combat cancer. LÄS MER

  5. 5. Functional studies of candidate genes contributing to type 1 diabetes in the NOD mouse

    Detta är en avhandling från Umeå : Medicinsk biovetenskap

    Författare :Marie Lundholm; Umeå universitet.; Umeå universitet.; [2009]
    Nyckelord :Type 1 Diabetes; NOD mouse; CTLA-4; Ctex; CD3ζ; apoptosis; Idd6; Lrmp; medicinsk genetik; Medical Genetics;

    Sammanfattning : Type 1 Diabetes (T1D) is an autoimmune disorder caused by both genetic and environmental factors. The non-obese diabetic (NOD) mouse is one of the best and most commonly studied animal models for T1D. This mouse strain spontaneously develops diabetes through a process that closely resembles the human pathogenesis. LÄS MER