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. Author manuscript; available in PMC: 2010 Oct 27.
Published in final edited form as: Expert Rev Endocrinol Metab. 2010 Jul 1;5(4):603–614. doi: 10.1586/eem.10.3

Figure 5.

Figure 5

Brx/NFAT5-mediated adaptive response to osmotic stress in a putative inflammatory site and in pathologic conditions associated with extracellular hyperosmolarity.

Inflammation activates lymphocytes and macrophages accumulated in an inflammatory site not only through injurious agents and cytokines but also through osmotic stress. The Brx/NFAT5-mediated intracellular signaling system stimulates further expression of cytokines to modulate local and systemic inflammatory reactions, while it induces hyperosmolarity-responsive genes to protect immune and immune accessory cells from the local hyperosmolar environment. Pathologic conditions associated with extracellular hyperosmolarity may alter the various functions of white cells through activation of Brx/NFAT5-mediated signaling system.

BAFF: B-cell activating factor, IL: interleukin, LTβ: lymphotoxin β, NFAT5: nuclear factor of activated T-cells 5, TNFα: tumor necrosis factor α