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Early manipulation of inflammatory responses could be useful in modifying subsequent late effect [ 14].
By testing whether manipulation of inflammatory pathways changes the pathologic course, we would identify new targets for disease intervention.
Given their critical role in orchestrating cytokine networks, identifying driver nodes such as IL-12 (p40), IL-13 and MCP-1 may prove valuable in the exogenous manipulation of inflammatory networks.
Since persistent accumulation and activation of immune cells is a hallmark of chronic inflammation, early manipulation of inflammatory responses could be useful for modification of the subsequent late effects [ 8, 9].
Further elucidation of the mechanism of protection may lead to improved outcomes not only in the diabetic patients but also in the nondiabetic, nonobese population through pharmacologic manipulation of inflammatory regulation.
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These latter types of data have served to focus potential therapeutic manipulation of autoimmune inflammatory responses solely on the peripheral immune system.
In addition, evidence for significantly improved outcomes with normalisation of NLR after the first cycle is promising for possible manipulation of the systemic inflammatory response through targeted anti-inflammatory mediators such as IL-6 blocking antibodies.
Therefore, whether the manipulations of these inflammatory proteins in patients with certain genotypes would be able to alter the course of VKH disease remain to be seen.
TRPV1 channels presented a novel target for pharmacologic manipulation for inflammatory pain conditions (1, 2).
Perhaps the next generation of therapy will be focused on the manipulation of the immune and inflammatory response that has innately existed for decades but whose potential is yet uncovered within this complex field.
We propose that the manipulation of both these pro-inflammatory cytokines, IFN- γ and TNF- α, which seem to contribute to dopaminergic neuronal degeneration, could well be relevant for PD therapy in the near future.
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