Furthermore, complementary experiments in BMDM, which expressed the GLP-1R, found that exendin-4 differentially modulated basal levels of both resident and secreted macrophage response genes, which are known to contribute to tissue remodelling and repair [ 52, 53].
To the best of our knowledge, this is the first evidence of persistence and survival of M. celatum inside human macrophages inducing a cell response which is different from that of M. tuberculosis, the typical pathogenic slow-growing bacillus.
TBET promotes Th1 lineage commitment [ 24] and maintains the Th1 mediated immune response, which fosters macrophage activation, infiltration, and the resulting ACS [ 25].
Current data indicate that apoE4 macrophages have an altered inflammatory response, which may contribute to the higher CVD risk observed in apoE4 carriers.
It remains to be tested if the LdMAcP enzyme also plays a role in the modulation of secretion of the macrophage's cytokines in the inflammatory response, which could affect the pathophysiology of the potentially lethal visceral leishmaniasis.
M2 macrophages exhibit anti-inflammatory activities and Th2 response, which promote tissue repair and remodeling (Vernon et al., 2010; Wynn and Vannella, 2016).
Moreover, IL-10−/− macrophages might enhance the M1 macrophage mediated proinflammatory response, which accelerates the RA inflammation response.
Additionally, lamina propria macrophages also suppress intestinal DC induced Th17 response, which could inadvertently prime iTreg differentiation[ 90].
MCP-1 recruits macrophages to adipose tissue and induces an inflammatory response, which was observed in this nSREBP1c lipodystrophy model.
These macrophages secrete cytokines and, in this way, initiate an inflammatory response, which results in more cells of the immune system at the place of infection [11].
