While the exact cellular determinants and pathogenic molecular mediators remain elusive, the clinical picture and cytokine profile of PFAPA outline a very complex, heterogeneous, but nevertheless autoinflammatory, disease [ 55].
While these molecules may contribute to the malaria-induced pathogenesis, it is clear that other P. falciparum-derived inflammatory mediators remain unknown [6].
To date, targeted therapies against mediators remain experimental.
However, the consistency of this association in normal-birth-weight children and its potential mediators remain unknown.
Although many zebrafish counterparts of mammalian immune mediators remain to be identified, recent studies have revealed zebrafish homologs of factors controlling macrophage behavior (Zakrzewska et al., 2010).
Our preliminary studies identify oxygen-dependent changes in the protein content of CT exosomes; however, effects on miRNA mediators remain to be established.
While it has been established that lymph serves as a conduit for the pathogenesis of T/HS-induced multiple organ failure, the specific mediators remain to be fully described.
To date, clinical success with therapies against key profibrotic mediators such as CTGF and TGF-β has not been demonstrated, although studies are ongoing and these mediators remain logical targets.
Although there is evidence from this model to suggest that Tsk fibrillin regulates gene expression through altered interactions with other matrix proteins, the identities of these mediators remain to be elucidated.
Cells were first incubated with TGF-β (TGF-β 5 ng/ml), in some experiments Ang-1 (250 ng/ml) was added after a period of 2 hours, both mediators remained in the culture medium for one more hour.
