Figure 1: Hypothetical relationship between nonimmune (preinflammatory) phase and immune reaction (acquired immunity). Female B/WF1 mice, a model for SLE and sSjS, develop several autoantibodies (e.g., anti-dsDNA and antinuclear antibodies: ANA) from younger ages (approximately 12 weeks of age) and thereafter immune-complexes- (ICs-) mediated glomerulonephritis (GN) develops with age, leading to overt disease (renal failure). On the other hand, production of anti-Ro/SS-A antibodies begin at the age of 20 weeks of age and dacryoadenitis and sialoadenitis (SA/DA) may develop in salivary and lacrimal glands. During the nonimmune phase, abnormal function and morphology of these tissues such endothelial cells (Ec) may permit leak of cytokines produced systemically. Dotted line shows hypothetical functional defect. Green lines may indicate clinical manifestation (self-reported symptoms) in human patients with sSjS. In this figure, the regenerative changes of acini components are not shown. T cell (T), B cell (B), and plasma cell (P).