Systemic Lupus Erythematosus (SLE) is associated with which type of hypersensitivity?

In Systemic Lupus Erythematosus (SLE), the underlying pathophysiology primarily involves immune complex formation, which aligns with Type III hypersensitivity reactions. This type of hypersensitivity is characterized by the deposition of antigen-antibody complexes in various tissues, leading to subsequent inflammation and damage. In SLE, the body produces antibodies against its own nuclear components and other tissue antigens, resulting in the formation of these immune complexes. When these complexes accumulate in tissues such as the kidneys, skin, and joints, they trigger an inflammatory response that can cause a range of symptoms, including rash, arthritis, and nephritis.

The other types of hypersensitivity have distinct mechanisms that do not apply to SLE. Type I hypersensitivity involves immediate allergic reactions mediated by IgE and mast cells, commonly associated with asthma or anaphylaxis. Type II hypersensitivity is primarily mediated by IgG or IgM antibodies binding to cell surface antigens, leading to cell destruction, such as in autoimmune hemolytic anemia. Type IV hypersensitivity, also known as delayed-type hypersensitivity, is mediated by T lymphocytes and is involved in responses such as contact dermatitis but does not play a central role in the pathogenesis of SLE. Thus,