Study found that Gnaq −/− DCs were unable to migrate to inflammatory sites and LNs in vivo, which indicated the role of G αq in the chemokine receptor signaling.
Given the strong predilection to migrate to inflammatory tissues coupled with their effector phenotype, TCRζdim T cells should now be considered a valid cellular target for treating a wide range of chronic inflammatory diseases.
Our results suggest that exposure of PB lymphocytes to a cocktail of proinflammatory cytokines induces the outgrowth of an activated effector memory lymphocyte population with the capacity to migrate to inflammatory sites.
Recent studies reported that VEGF-C is also expressed by CD11b+ myeloid cells that have migrated to inflammatory sites in several animal models of inflammation [ 14- 17], such as corneal transplantation and bacterial lung infection.
The B1 cell subset of B lymphocytes, which are mainly present in the pleural and peritoneal cavities, can migrate to inflammatory sites and differentiate into mononuclear phagocytes with macrophage-like phenotypes [ 3].
After migrating to the inflammatory microenvironment, Th17 cells acquire pathological effector functions by expressing specific cytokines including GM-CSF [ 56, 57].
Neutrophils, as the first immune cells migrating to a tumor inflammatory site, promote inflammation and activate macrophages and DCs [ 88].
In early RA, pro-inflammatory T cells migrate to inflammatory sites and contribute to disease progression [ 27– 29].
We can observe in in vitro chemotaxis that if HT29 cells prevent DC from migrating to MIP3α mimicking an inflammatory focus then fewer DC reach the location to stimulate T cells and the immune response is accordingly less intense.
In response to a variety of agents, they migrate to the inflammatory site where they release proteases, bactericidal peptides and large quantities of ROS, a process known as the respiratory burst [9].
