Abstract
Lupus erythematosus (LE) is a systemic autoimmune disorder associated with polyclonal B-cell activation, resulting in diverse patterns of autoantibody production and a heterogeneous clinical expression constituting a spectrum extending from limited cutaneous disease (cutaneous lupus LE) to a life-threatening systemic disease process (systemic LE). While the clinical characteristics of cutaneous LE are well defined in terms of morphology, and for the classification of systemic LE (SLE), clinical and laboratory criteria are available, recent advances in basic and clinical research have contributed to a better understanding of the cellular and molecular events that lead to LE. The importance of genetic susceptibility, environmental factors, and hormonal elements are well appreciated, although we as clinicians are faced with relatively late-term manifestations of the immunologic events that lead to the clinical manifestations of disease. Nevertheless, combining our knowledge of the clinical patterns of LE with the advances in our understanding of the underlying immunology, has led to the concept of "subsets" of disease, where a correlation between immune genetic markers, autoantibody profiles, distinctive cutaneous morphology, and ...Continue Reading
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