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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The rounded mass of fatty tissue lying over the joint of the pubic bones, in women typically more prominent and also called the mons veneris<span>.</span>
secondary occurs among critically ill, older or hospitalized patients. it is reversible if the illness resolves
primary immunodeficiency are genetically determined they typically occur during infancy and childhood
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