Immune compounds start cycle of destruction
Autoimmune disease rates are on the rise, and as such it is becoming increasingly important to analyze and understand the mechanisms behind such illnesses.
Autoimmune diseases arise when the body's defenses attack one's own cells and tissues, instead of just the harmful, foreign invaders that they are supposed to target. This leads to inflammation of and damage to the besieged tissue.
According to estimates by the National Institutes of Health, more than seven percent of Americans suffer from some type of autoimmune disease. Although nearly 100 such diseases have been identified, researchers suspect that nearly 40 more have an autoimmune basis.
Compiling a wide range of information about such diseases can be especially useful, and this is where scientists like John Hall and Antony Rosen of the Department of Rheumatology at the Hopkins School of Medicine come in.
Hall and Rosen have summarized much of the work on autoimmune responses, specifically the studies relating to the activity of certain immune factors, called interferons.
Interferons come in three types, but Hall and Rosen have specifically looked at type I interferons, which seem to be implicated in certain autoimmune disorders such as systemic lupus erythematosus, myositis, Sjögren's syndrome, systemic sclerosis and rheumatoid arthritis.
In these disorders, initial immune responses against invading pathogens naturally leads to cell death and tissue destruction as a consequence of the body's inclination to rid itself of potentially harmful particles. However, this inevitable step in the immune response is exacerbated by interferon signaling.
Interferons are proteins released by dying cells to warn their neighbors of the presence of pathogens. When the nearby cells receive the interferon message, they amplify their immune responses.
Interferons can facilitate the maturation of immune cells that can go on to fight infectious agents, and can increase cells' susceptibility to apoptosis, or planned cell death, which is especially helpful for eliminating virus-infected cells.
Autoimmune diseases arise when the body's defenses attack one's own cells and tissues, instead of just the harmful, foreign invaders that they are supposed to target. This leads to inflammation of and damage to the besieged tissue.
According to estimates by the National Institutes of Health, more than seven percent of Americans suffer from some type of autoimmune disease. Although nearly 100 such diseases have been identified, researchers suspect that nearly 40 more have an autoimmune basis.
Compiling a wide range of information about such diseases can be especially useful, and this is where scientists like John Hall and Antony Rosen of the Department of Rheumatology at the Hopkins School of Medicine come in.
Hall and Rosen have summarized much of the work on autoimmune responses, specifically the studies relating to the activity of certain immune factors, called interferons.
Interferons come in three types, but Hall and Rosen have specifically looked at type I interferons, which seem to be implicated in certain autoimmune disorders such as systemic lupus erythematosus, myositis, Sjögren's syndrome, systemic sclerosis and rheumatoid arthritis.
In these disorders, initial immune responses against invading pathogens naturally leads to cell death and tissue destruction as a consequence of the body's inclination to rid itself of potentially harmful particles. However, this inevitable step in the immune response is exacerbated by interferon signaling.
Interferons are proteins released by dying cells to warn their neighbors of the presence of pathogens. When the nearby cells receive the interferon message, they amplify their immune responses.
Interferons can facilitate the maturation of immune cells that can go on to fight infectious agents, and can increase cells' susceptibility to apoptosis, or planned cell death, which is especially helpful for eliminating virus-infected cells.
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