FIGURE 4 | Induction of tertiary follicles and prion replication competence in non-lymphoid tissue.

a | A hypothetical hierarchical cascade resulting in the generation of tertiary follicles in non-lymphoid tissue, with the possible induction of ectopic prion replication competence. Autoimmune diseases and chronic lymphocytic inflammations have been demonstrated to induce prion replication competence in non-lymphoid tissue, whereas other conditions have not been investigated in this regard yet (indicated by the question marks). b | A model of the events that induce the generation of tertiary follicles and prion replication competence in the context of inflammatory conditions. Activation of B- and T lymphocytes induced by inflammatory stimuli upregulates lymphotoxin (LT) expression on lymphocytes (for example, on B lymphocytes). LT secreted by (LT₃), or expressed on the extracellular membrane (LT₁₂) of B lymphocytes, binds to LTR (or TNFR1) of stromal precursor cells, inducing the upregulation of adhesion molecules, chemokines and/or cytokines. The effect of these events is the induction of tertiary lymphoid follicles and prion replication competence. A HE section of an inflamed kidney is shown (lower panel). Small arrows indicate follicular inflammation. Section image reproduced with permission from Ref. 18. © (2005) American Association for the Advancement of Science.

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