Autoimmune Disease
The Lancet: "Despite its emergence only in the 1950s, autoimmune aetiology now applies to, or is suspected in, a long list of chronic diseases�multiple sclerosis, type I diabetes, and Crohn's disease being prominent examples.
The idea of disease as a self-destructive process has been a part of disease theory since the beginning of the 20th century. Possibly the first definition of autoimmune disease was provided by Paul Ehrlich in 1904 when he coined the term "horror autotoxicus". However, for many decades, Ehrlich's dictum was wrongly understood to mean that autoantibodies could not exist. It was only in the 1940s, and notably in the 1950s, that evidence accumulated on the existence of specific antibodies against specific bodily tissues. Germinal was the work of Ernst Witebsky and Noel Rose, which revealed the existence of antithyroid antibodies in rabbits. Shortly afterwards, in 1956, British scientists showed that these antibodies were indeed manifest in people with chronic thyroiditis. Within a few years, a whole series of diseases was shown to have similar autoimmunological components, thus giving birth to this new nosological category.
Also in the early 1950s, Peter Medawar, in London, UK, introduced the idea of self-tolerance�ie, a mechanism preventing the immune system from attacking its host tissues. He further argued that self-tolerance was not the result of inherently inborn genetic differences, but was an adaptive process taking place during embryonic development. In 1957, this idea was elaborated by the Australian immunologist, Macfarlane Burnet. His "clonal selection theory" contended that the immune system was made of numerous "immunologically competent" clones of cells (lymphocytes) circulating around the body in a constant surveillance for harmful invaders. Autoimmune disease must then be the result of the appearance of a “forbidden clone”. Burnet's theoretical framework served until the 1990s, when it was supplanted by an understanding that autoimmune processes were part of the normal physiology of an individual, and autoimmune components (antibodies, T cells) were permanent parts of the immune repertoire, even in the absence of a pathological condition. Answers now focus less on the autospecificity of immune components, than on the regulation mechanisms that seem able to control the pathogenicity of these components."
The idea of disease as a self-destructive process has been a part of disease theory since the beginning of the 20th century. Possibly the first definition of autoimmune disease was provided by Paul Ehrlich in 1904 when he coined the term "horror autotoxicus". However, for many decades, Ehrlich's dictum was wrongly understood to mean that autoantibodies could not exist. It was only in the 1940s, and notably in the 1950s, that evidence accumulated on the existence of specific antibodies against specific bodily tissues. Germinal was the work of Ernst Witebsky and Noel Rose, which revealed the existence of antithyroid antibodies in rabbits. Shortly afterwards, in 1956, British scientists showed that these antibodies were indeed manifest in people with chronic thyroiditis. Within a few years, a whole series of diseases was shown to have similar autoimmunological components, thus giving birth to this new nosological category.
Also in the early 1950s, Peter Medawar, in London, UK, introduced the idea of self-tolerance�ie, a mechanism preventing the immune system from attacking its host tissues. He further argued that self-tolerance was not the result of inherently inborn genetic differences, but was an adaptive process taking place during embryonic development. In 1957, this idea was elaborated by the Australian immunologist, Macfarlane Burnet. His "clonal selection theory" contended that the immune system was made of numerous "immunologically competent" clones of cells (lymphocytes) circulating around the body in a constant surveillance for harmful invaders. Autoimmune disease must then be the result of the appearance of a “forbidden clone”. Burnet's theoretical framework served until the 1990s, when it was supplanted by an understanding that autoimmune processes were part of the normal physiology of an individual, and autoimmune components (antibodies, T cells) were permanent parts of the immune repertoire, even in the absence of a pathological condition. Answers now focus less on the autospecificity of immune components, than on the regulation mechanisms that seem able to control the pathogenicity of these components."
posted by Aloyzio Achutti at 10:43 PM
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