Abstract
The destruction of vascular smooth muscle cells (VSMC) in autoimmune arteritis is a poorly understood phenomenon. To approach this problem, VSMC cultures were established. The interaction of these cells (from normal or autoimmune mice) with lymphocytes was then evaluated. Specifically, splenocytes from MRL/1pr or C3H mice were co-cultivated with MRL/1pr or C3H VSMCs. Massive mononuclear inflammatory cell clusters enveloped MRL/1pr VSMCs which culminated in the detachment of MRL/1pr VSMCs from the culture plate. In contrast, the interaction of splenocytes from normal or autoimmune mice did not destroy normal VSMCs. Further investigation indicated that MRL/1pr VSMCs spontaneously expressed both Ia–k and Ia–d, as assessed by fluorescence microscopy and flow cytometry, and released interleukin-1-like factors–-characteristics of accessory cells to T-lymphocyte function. Evaluation of VSMCs accessory function in antigen presentation suggests that these cells may present antigen under specific experimental conditions. As a result of these studies, a novel mechanism of autoimmune vasculitis is proposed. Our hypothesis is that defective biological function of VSMCs from autoimmune mice stimulates a mononuclear inflammatory cell response which culminates in VSMC autodestruction.