FIG. 3.
Biological effects of inhibition of LTα1β2/LIGHT-LTβR interaction in autoimmune and infectious diseases. Soluble LTβRIgG fusion protein blocks LTβR-mediated signaling. Three biological mechanisms (circles) have been described: loss of CXCL13 gradient in follicular dendritic cell networks, loss of adhesion molecule expression, and loss of proper and timely positioning of T cells in lymphoid organs. These mechanisms contribute to changes in secondary lymphoid organ formation and microarchitecture, as indicated by the four boxes. The altered lymphoid organs are associated with changes in the courses of autoimmune and infectious inflammatory diseases. Animal models in which LTβRIgG has been used in adult mice, a situation comparable to potential human treatment, are indicated by italic font and underlining. Disease models which are not altered in mice with blocked LTβR have not been depicted. ind., induced.