The exact mechanisms leading to immune deposits along the DEJ in LE are still unknown. Despite numerous experimental attempts, the characterization of putative antigen(s) or specific antibodies within the lupus band have remained largely unsuccessful (Schreiner and Wolff 1970). It is likely that immunoglobulins and complement factors reacting with slowly released nuclear and cytoplasmic cell components from apoptotic keratinocytes are involved in the formation of such deposits (Casciola-Rosen and Rosen 1997). The polyanionic nature of some nuclear antigens such as native DNA may further induce or support a nonspecific binding to immunoglobulin aggregates and complement proteins such as C3 (Meurer and Gigli 1978). It is of interest that in SCLE or mixed connective tissue disease associated with high-titered serum autoantibodies to the nuclear U1RNP and La/SSB antigens or to the cytoplas-
Table 22.2. Diseases with immune deposits along the dermoepidermal junction (false-positive lupus band test result)
Dermatomyositis Systemic scleroderma Rheumatoid arthritis Porphyria cutanea tarda Lichen ruber planus Rosacea mic Ro/SSA antigen, DIF reveals nuclear or intracytoplasmatic fluorescence rather than the typical bandlike immune deposits seen in DLE where no antinuclear antibodies can be detected in the serum.
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