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Loss of filaggrin function seems to play a role both in the pathogenesis of eczema and the subsequent progression of atopy.
Cytokines and procalcitonin (PCT) have been shown to play a crucial role both in the pathogenesis of sepsis and as diagnostic tools for the inflammatory process.
It is well known that platelets play an important role in CAD both in the pathogenesis of atherosclerosis and in the development of acute thrombotic events.
Interleukin 6 is secreted by macrophages and also by T cells (in the context of chronic inflammation) and has been clearly implicated both in the pathogenesis of COPD and in lung cancer.
These are being intensively investigated for their pivotal role both in the pathogenesis and development of DVLC.
Thus, there may be a possible role for SIC, DRS or both in the pathogenesis of PSGN.
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It enhances the differentiation of naïve T cells into Th1 cells but suppresses naïve T cells from differentiating into Th17 cells, resulting in mutual antagonism of Th1 and Th17 cells which are both involved in the pathogenesis of uveitis [[75],[76]].
A significantly decreased expression of CD18 and AKNA suggests a role for both proteins in the pathogenesis of this syndrome.
In general, Foxp3 + Treg and Th17 cells are both involved in the pathogenesis of CHB.
Together, these results suggest that THP and OPN are both involved in the pathogenesis and response to oxalate exposure.
Oxidative stress and release of pro-inflammatory cytokines are both implicated in the pathogenesis of LPS-induced acute liver injury.
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