The Draining Lymph Node in Rheumatoid Arthritis: Current Concepts and Research Perspectives

Figure 1

Potential pathophysiologic changes of and interactions between the joint and draining LN in course of inflammatory arthritis. (a) Schematic representation of the main anatomic compartments within a noninflamed joint and a resting LN. (b) Hypothetical spectrum of interactive relationships between the joint and the draining LN in course of arthritis. Joint inflammation promotes local accumulation of immune cells, synovial tissue hypertrophy and structural damage through the differentiation/activation of osteoclasts. These changes can promote increased fluid and cell drainage to adjoining LN through the afferent lymphatic system. An efficient drainage activity (left diagram, blue-filled arrow) may exert a compensatory effect on joint pathology by promoting fluid and cell exit. As an additional (nonmutually exclusive) effect, it might also contribute to disease immune-pathology by favouring neoantigen delivery, local immune-reactivity and (auto)antibody production. In the left LN diagram of (b), these mechanisms, together with putative structural changes (hypertrophy, cell accumulation, follicular hyperplasia, and increased vascularity) characterizing the challenged LN are shown. On the other side, a defective or insufficient drainage activity to the node (right diagram, blue-dashed arrow) may directly contribute to accumulation of inflammatory cells in the joint, promoting local cell activation and enhancing local disease (right hand side diagram of the joint).

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