Systemic lupus erythematosus (SLE) is a rheumatic disease attributed to autoimmune mechanisms.
Systemic lupus erythematosus (SLE, lupus) is characterized by a global loss of self-tolerance with activation of autoreactive T and B cells, leading to the production of pathogen autoantibodies and tissue damage.
Innate immune mechanisms are required for aberrant adaptive immune responses in SLE. Recent advances in basic and clinical biology have shed new light on the disease mechanisms of lupus. This review article describes recent studies that provide valuable insights into disease-specific therapeutic targets.
Systemic lupus erythematosus (SLE or lupus) is a systemic autoimmune disease with inflammation of multiple organs. SLE is characterized by the production of pathogenic autoantibodies against nucleic acids and their binding proteins, reflecting a global loss of self-tolerance.
Loss of tolerance with subsequent immune dysregulation is the result of genetic factors in the context of environmental triggers and stochastic events, with recent studies implicating more than 30 genetic loci in disease pathogenesis.
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Heat stroke
The adult has a body temperature higher than 104° and they are showing symptoms of a heat stroke.
Social media, home delivered meals, cell phones
Answer:
Eating the proper foods.
Explanation:
Like veggies, fruits, grains and ect.
Answer: Certain pathogens enter and multiply within the human body.
Explanation:
Infection or invasion of a pathogen inside the body of the human host does not necessary causes the disease. Instead the multiplication and colonization of these pathogens inside the body of the human host is responsible for disease. This is because of the fact that the pathogen's cells multiply and invade the healthy cells of the human host. This process weaken up the host immune system. This process leads to the occurrence of signs and symptoms of the disease.
