Modifying Immunity

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Suppression/Tolerization (0)
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(Journal Article): The Role of Regulatory T Cell Defects in Type I Diabetes and the Potential of these Cells for Therapy
 
Thomas D, Zaccone P, Cooke A (Department of Pathology, Immunology Division, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QP, United Kingdom, ac(at)mole.bio.cam.ac.uk )
 
IN: Rev Diabetic Stud 2005; 2(1):9-18
Impact Factor(s) of Rev Diabetic Stud: 0.125 (2006)

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ABSTRACT: Type I diabetes is increasing in incidence in developed countries [1]. Diabetes arises from a breakdown of tolerance to islet antigens, resulting in T cell-driven destruction of the islet cells and concomitant hyperglycemia. In this review, we explore whether this loss of tolerance results in part from a defect in the action of regulatory T cells. We draw on both human data and that obtained from NOD mice, the murine model of autoimmune diabetes. Although insulin-based therapies have been highly successful in treating diabetes, the complications of long-term hyperglycemia are still major causes of morbidity and mortality. Accordingly, we also discuss whether treatment with regulatory T cells is a viable method for restoring long-term tolerance to self-antigens in recently diagnosed or pre-diabetic individuals. Regulatory T cell therapy offers many potential advantages, including a specific and lasting dampening of inflammation. However, some significant hurdles would have to be overcome before it could become an established treatment.

TYPE OF PUBLICATION: Review

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Hint: Your Response should directly apply to The Role of Regulatory T Cell Defects in Type I Diabetes and the Potential of these Cells for Therapy. Please check, if this context applies best to your contribution. Otherwise click HERE to change to the appropriate subject area. The actual subject area is Modifying Immunity.

 

(Journal Article): The concept of space and competition in immune regulation.
 
Stockinger B, Barthlott T, Kassiotis G (Division of Molecular Immunology, The National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1 AA, UK.)
 
IN: Immunology 2004; 111(3):241-247
Impact Factor(s) of Immunology: 2.965 (2004), 2.853 (2003), 2.729 (2002), 2.656 (2001)

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ABSTRACT: Not availabe

TYPE OF PUBLICATION: Original article

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(Journal Article): Cancer immunotherapy: a treatment for the masses.
 
Blattman JN, Greenberg PD (Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, WA 98109, USA.)
 
IN: Science 2004; 305(5681):200-205
Impact Factor(s) of Science: 30.927 (2005), 31.853 (2004), 29.162 (2003), 26.682 (2002), 23.329 (2001)

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ABSTRACT: Cancer immunotherapy attempts to harness the exquisite power and specificity of the immune system for the treatment of malignancy. Although cancer cells are less immunogenic than pathogens, the immune system is clearly capable of recognizing and eliminating tumor cells. However, tumors frequently interfere with the development and function of immune responses. Thus, the challenge for immunotherapy is to use advances in cellular and molecular immunology to develop strategies that effectively and safely augment antitumor responses.

TYPE OF PUBLICATION: Original article

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(Journal Article): Imbalance in Th Cell Polarization and its Relevance in Type 1 Diabetes Mellitus
 
Sia C (Department of Immunology, United Biomedical Inc., 25 Davids Drive, Hauppage, New York 11788, USA, csia(at)unitedbiomedical.com )
 
IN: Rev Diabetic Stud 2005; 2(4):182-186
Impact Factor(s) of Rev Diabetic Stud: 0.125 (2006)

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ABSTRACT: Functional polarization of T helper (Th) subsets of lymphocytes has been implicated in promoting or conferring risk to Type 1 diabetes mellitus (T1DM) development in human and diabetic animal models. It is assumed that an immoderate preponderance of type 1 immunity establishes the prerequisite for this development. Over the past years, various immune-intervention strategies have been tested to protect diabetic animals from developing overt diabetes. These protocols implicate a protective mechanism that is attributed to a change in the set of autoreactive Th cells from their Th1 to the Th2 phenotype. The studies were aimed at improving the effectiveness of Th2 cells to secrete the principal cytokines, IL-4 and IL-10, in order to mediate protection from diabetes in NOD mice. In contrast, some immune-modulation protocols utilizing non-specific reagents report that diabetes protection is apparently attributed to preferential survival of both Th1 and Th2 cells, rather than via a shift from their Th1 to Th2 phenotypes. Even though we know that excessive immune responses against self antigens are also controlled and terminated by regulatory T cells, this article focuses on the polarization of Th effector cells and discusses the controversial findings regarding the Th1/Th2 hypothesis to draw a conclusion on its relevance in T1DM from the existing knowledge.

TYPE OF PUBLICATION: Review

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