Abstract
The abstract encapsulates the complex landscape of systemic lupus erythematosus (SLE), an autoimmune disease impacting multiple organ systems, characterized by immunosuppression and immunomodulation. SLE is recognized as a quintessential connective tissue disorder arising from immune system dysfunction and an overabundance of diverse autoantibodies. Clinical manifestations of SLE encompass nonspecific constitutional symptoms, including fever, exhaustion, anorexia, weight loss, and arthralgias. Additionally, signs of generalized inflammation like hepatosplenomegaly and lymphadenopathy may manifest at disease onset or during flare-ups. The adaptive immune response in SLE is underpinned by the critical role of B lymphocytes in generating autoantibodies, presenting autoantigens, and activating autoreactive T cells. Treatment strategies for SLE primarily involve biologics and therapeutic options approved by the FDA for refractory cutaneous, articular, and renal disease. Belimumab, infliximab, rituximab, abatacept, and tocilizumab represent some of these approved medications. The management of SLE during remission emphasizes the cautious use of prednisone to mitigate flare-ups, considering potential adverse psychiatric effects associated with steroid medication.[14]
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