Perturbation of experimental ultraviolet light-induced erythema by passive transfer of serum from subacute cutaneous lupus erythematosus patients.

Several lines of investigation have implicated anti-Ro/SS-A antibody in the pathogenesis of photosensitive forms of cutaneous lupus erythematosus such as neonatal lupus erythematosus and subacute cutaneous lupus erythematosus. To further explore this possibility, we have developed a quantitative, experimental system for examining the effect of passively transferring anti-Ro/SS-A antibody-containing and antibody-deficient subacute cutaneous lupus erythematosus patient sera on one aspect of cutaneous photoreactivity, UV-induced erythema. Laser-Doppler velocimetry was used to quantitate the microvascular flow rates in normal control, disease control (rheumatoid arthritis, discoid lupus erythematosus), and subacute cutaneous lupus erythematosus serum-injected guinea pig skin test sites before and after combined ultraviolet B and A radiation from a solar simulator. Results, expressed as change in milli-electron voltage (perturbed milli-electron volts after irradiation minus baseline milli-electron volts before irradiation), revealed that subacute cutaneous lupus erythematosus serum injections consistently resulted in greater UV-induced microvascular flow rates than those elicited by normal or disease control serum injections. Anti-Ro/SS-A containing subacute cutaneous lupus erythematosus sera produced the greatest flow rates observed in this study. Earlier studies have suggested that the pathogenesis of lupus photosensitivity is very likely multifactorial. Our current data suggest that anti-Ro/SS-A autoantibody or other closely related humoral elements should also be considered among the factors which might contribute to this clinical phenomenon.