Difference between revisions of "Team:Oxford/Description"

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             <h2>Global Burden of IBD</h2>
 
             <h2>Global Burden of IBD</h2>
 
             <p class="lead">Inflammatory Bowel Disease (IBD) is a heterogeneous group of autoimmune disorders encompassing Crohn’s disease and Ulcerative Colitis. It is estimated to affect 0.3% of the population in industrialised nations, including over 5 million adults in the UK, and 1.6 million in USA.
 
             <p class="lead">Inflammatory Bowel Disease (IBD) is a heterogeneous group of autoimmune disorders encompassing Crohn’s disease and Ulcerative Colitis. It is estimated to affect 0.3% of the population in industrialised nations, including over 5 million adults in the UK, and 1.6 million in USA.
 
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The global prevalence of IBD is increasing rapidly as countries become more developed. In addition, instances of IBD in developing countries are thought to be accelerated by the presence of bacteria, such as segmented filamentous bacteria (SFB), in water sources influencing the gut microbiome and host immune response. Gram positive SFB have recently been implicated in promoting the development of lymphocytes and the growth of Th17 populations.  
 
The global prevalence of IBD is increasing rapidly as countries become more developed. In addition, instances of IBD in developing countries are thought to be accelerated by the presence of bacteria, such as segmented filamentous bacteria (SFB), in water sources influencing the gut microbiome and host immune response. Gram positive SFB have recently been implicated in promoting the development of lymphocytes and the growth of Th17 populations.  
 
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</div>
 
An additional effect of the signals required for Th17 differentiation is the inhibition of the production of Treg cells. Once fully differentiated, Th17 cells produce interleukin 17a (IL-17a) a proinflammatory cytokine. Elevated levels of IL-17a are associated with MS and the development of epilepsy and other autoimmune diseases.
 
An additional effect of the signals required for Th17 differentiation is the inhibition of the production of Treg cells. Once fully differentiated, Th17 cells produce interleukin 17a (IL-17a) a proinflammatory cytokine. Elevated levels of IL-17a are associated with MS and the development of epilepsy and other autoimmune diseases.
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</div>
 
Most diagnoses occur between the ages of 20 and 30; the disease presents a significant burden to patients, societies, and healthcare systems. Current treatment is focused on symptom management, frequently resulting in sub-optimal control despite the burden of long-term treatment. Common therapeutics, such as corticosteroids, require regular administration, have many side-effects, and are less accessible in the developing world. The aim of our project is to address these problems and meet the notable, yet currently unmet, need for curative treatments for autoimmune diseases. This will be achieved via regulation of Treg and T helper cell populations to ensure immune responses of the correct magnitude. The specific control mechanism is discussed below.
 
Most diagnoses occur between the ages of 20 and 30; the disease presents a significant burden to patients, societies, and healthcare systems. Current treatment is focused on symptom management, frequently resulting in sub-optimal control despite the burden of long-term treatment. Common therapeutics, such as corticosteroids, require regular administration, have many side-effects, and are less accessible in the developing world. The aim of our project is to address these problems and meet the notable, yet currently unmet, need for curative treatments for autoimmune diseases. This will be achieved via regulation of Treg and T helper cell populations to ensure immune responses of the correct magnitude. The specific control mechanism is discussed below.
 
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Revision as of 12:44, 13 October 2018

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Description

Autoimmune Disease

Autoimmune diseases encompass a range of disorders that result from attack of self-tissues by a dysregulated immune system. More than 80 autoimmune diseases have been characterised, each with long-term effects on health, quality of life and cost to healthcare services. These include Crohn’s disease, Coeliac disease, type 1 diabetes, multiple sclerosis, systemic lupus erythematosus and rheumatic disease.

Global Burden of IBD

Inflammatory Bowel Disease (IBD) is a heterogeneous group of autoimmune disorders encompassing Crohn’s disease and Ulcerative Colitis. It is estimated to affect 0.3% of the population in industrialised nations, including over 5 million adults in the UK, and 1.6 million in USA.

The global prevalence of IBD is increasing rapidly as countries become more developed. In addition, instances of IBD in developing countries are thought to be accelerated by the presence of bacteria, such as segmented filamentous bacteria (SFB), in water sources influencing the gut microbiome and host immune response. Gram positive SFB have recently been implicated in promoting the development of lymphocytes and the growth of Th17 populations.
An additional effect of the signals required for Th17 differentiation is the inhibition of the production of Treg cells. Once fully differentiated, Th17 cells produce interleukin 17a (IL-17a) a proinflammatory cytokine. Elevated levels of IL-17a are associated with MS and the development of epilepsy and other autoimmune diseases.
Most diagnoses occur between the ages of 20 and 30; the disease presents a significant burden to patients, societies, and healthcare systems. Current treatment is focused on symptom management, frequently resulting in sub-optimal control despite the burden of long-term treatment. Common therapeutics, such as corticosteroids, require regular administration, have many side-effects, and are less accessible in the developing world. The aim of our project is to address these problems and meet the notable, yet currently unmet, need for curative treatments for autoimmune diseases. This will be achieved via regulation of Treg and T helper cell populations to ensure immune responses of the correct magnitude. The specific control mechanism is discussed below. .

Section 3

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