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These subjects had originally been considered as separate fields of research. Inflammation is due to inflammatory mediators such as lymphotoxin (LT) and its close relative, tumor necrosis factor (TNF). The two fields converged with the realization that LT is also crucial for secondary lymphoid organ (SLO) development and that it induces chronic lymphoid infiltrates, called tertiary lymphoid organs (TLOs) or tertiary lymphoid structures (TLSs) that are remarkably like SLOs. TLSs, which were initially described in mice transgenic for the rat insulin promoter driving LT (RIPLT mice), occur in chronic inflammation in autoimmune diseases, atherosclerosis, graft rejection, microbial infection, aging, and cancer. The thesis presented here is that understanding SLO development, structure, and function is key to understanding TLSs. Key discoveries are presented which include the observations that LT's two forms, LT\u03b13 and LT\u03b11\u03b22, signal through different receptors that induce both SLOs and TLSs. Similarities and differences between TLSs and SLOs are presented. Prospects for their inhibition in autoimmune diseases where they are detrimental, and induction in cancer, where they are beneficial, are presented. 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