ASPEK IMUNOLOGI SLE

Abstract

Systemic Lupus Erythematosus (SLE) is autoimmune disease characterised by the production of
autoantibodies to component of the cell nucleus in association with a diverse array of clinical manifestations.
The patho-aetiology of systemic Lupus Erythematosus probably involves multifactorial interaction among
various genetic and environmental factors. Multiple genes contribute to disease susceptibility, including genes
encoding complement and other components of the immune response. The interaction of sex, hormonal millieu
and the hypothalamus-pituitary-adrenal axis modifies this susceptibility and the clinical expression of the
disease. Defective immune regulatory mechanism, such as the clearance of apoptotic cells and immune
complexes, are important contributors to the development of SLE. The loss of immune tolerance, increase
antigenic load, excess T cells helper, defective B cell suppression, and the shifting of T helper 1 (Th1) to Th2
immune responses leads to the B cell hyperactivity and the production of pathogenic autoantibodies. ANAs are
antibodies against both functional and structural in the cell nucleus. ANA is early detection of autoantibodies for
the patient with clinical features that suggest SLE. Positive test for antinuclear antibodies may support the
diagnosis, especially if more spesific autoantibodies are present, such as anti-double-stranded DNA, anti-Sm,
anti-RNP or anti-Ro. Understanding the value of autoantibody testing in patient care requires clinical judgment
and experience.