Ultraviolet-radiation-induced keratinocyte apoptosis in C1q-deficient mice

Exposure to ultraviolet B radiation is an important trigger of both systemi c and cutaneous disease flares in individuals with systemic lupus erythemat osus, More than 90% of individuals with homozygous C1q deficiency develop a systemic-lupus-erythematosus-like illness, which is typically associated w ith a severe photosensitive rash, Apoptotic, human keratinocytes have been shown in vitro to bind C1q, in the absence of antibody, These observations, together with the hypothesis that a major source of the autoantigens drivi ng the immune response in systemic lupus erythematosus comes from apoptotic cells, led us to investigate the effects of murine C1q deficiency on ultra violet-radiation-induced keratinocyte apoptosis in vivo. In this work, we d emonstrated C1q binding to apoptotic murine keratinocytes in vitro and show ed for the first time that C1q is also present on sunburn cells in vivo. In addition to C1q, we detected C3 deposition on sunburn cells in both wild-t ype and C1q-deficient mice, suggesting activation of the alternative pathwa y, Following acute ultraviolet exposure in vivo, no difference in the rate of clearance of sunburn cells was found ill C1q-deficient mice from three d ifferent genetic backgrounds, compared with strain-matched wild-type contro ls, Furthermore, chronic ultraviolet exposure did not result in the product ion of autoantibodies or the development of glomerulonephritis. Our finding s suggest that C1q does not play a critical role in the physiologic clearan ce of apoptotic murine keratinocytes in vivo.