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We studied the autoimmune serologic features and histocompatibility antigen associations of 27 patients who had a widespread, nonscarring and often photosensitive form of histologically specific cutaneous lupus erythematosus. We designated this disorder as subacute cutaneous lupus erythematosus. Skin lesions from this disorder can be distinguished from scarring discoid lupus erythematosus lesions both on a morphologic and histopathologic basis. Antinuclear and anticytoplasmic antibodies (Ro or Ro and La) and circulating immune complexes were frequently present in patients with subacute cutaneous lupus erythematosus, whereas rheumatoid factor and anti-lymphocyte, anti-DNA, anti-nRNP, and anti-Sm antibodies were found less frequently. Patients having annular skin lesions represented a particularly homogeneous subgroup in which there was a striking concordance of anti-Ro antibodies and the HLA-DR3 phenotype. These studies clearly establish that the presence of these lesions can serve as a cutaneous marker for a distinct subset of patients with lupus erythematosus who share similar clinical, serologic, and genetic features.

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In 50 to 60 percent of patients with systemic lupus erythematosus (SLE), a band of immunoglobulins beneath the epidermis of visibly normal skin. This highly specific finding has been used as a diagnostic test (Lupus Band Test) for SLE. Similar immunoglobulin deposits are found in an inbred strain of New Zealand mice which spontaneously develop an autoimmune disease with many features of SLE. Subepidermal immunoglobulin deposits are found most frequently in SLE patients with proliferative glomerulonephritis, hypocomplementemia, and serum antibodies to native DNA (anti-nDNA). When anti-nDNA levels are suppressed by cyclophosphamide, these deposits disappear. The subepidermal accumulation of immunoglobulin in SLE patients and in the mouse model apparently depends on the presence of antibody to native DNA. It is proposed that serum anti-nDNA precipitates with nDNA which is released locally from epidermal nuclear breakdown.

Epidermal Langerhans cells have been implicated in the process by which animals skin painted with highly reactive haptens, such as DNFB, develop contact hypersensitivity. Compared to normal body wall skin, murine tail skin contains relatively few, unevenly distributed Langerhans cells; ultraviolet light exposure depletes the epidermis transiently of normal numbers of morphologically identifiable Langerhans cells. When mice are painted with DNFB on skin naturally or artificially depleted of Langerhans cells, contact hypersensitivity is not induced. More importantly, these animals become specifically unresponsive to the chemical contact, and are unable to mount effective hypersensitivity reactions if presented subsequently with an immunogenic regimen. It is concluded that Langerhans cells provide the skin with an intricate dendritic network just beneath the keratinized layer, the function of which is to receive, process and present cutaneously applied antigens in an immunogenic form. When this barrier network is breached, the host responds to antigenic exposure by becoming profoundly and specifically unresponsive. Implications of this hypothesis for epidermal virus infections and cutaneous malignancy are discussed.

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