This study investigated the effects of betamethasone on lung maturation and growth in the presence of inflammation by treating sheep with both maternal intramuscular betamethasone and intra-amniotic endotoxin injections.
Immature DC express a range of receptors for the inflammatory chemokines including CCR1, CCR2, CCR5, CCR6 and CXCR1 which guide the cell to sites of inflammation however maturation results in a down-regulation of many of these receptors and an up-regulation of receptors for constitutive chemokines such as CCR7 and CXCR4 [ 44, 45].
However, at sites of chronic T cell-mediated inflammation, maturation of DCs appears to involve antigen-specific effector T cells and the cells remain locally [ 10, 11], thus focusing the inflammatory response.
The outcomes that were studied included the rates of fetal death and the features of inflammation and lung maturation in survivors.
They slowly process through the normal healing cycle of inflammation, proliferation, and maturation, while the keloid scar does not [ 9].
Normal wound healing involves a sequence of inflammation, proliferation, and maturation or remodelling [12] and local IGF-I production increases as wound healing progresses [35].
Upon receiving appropriate stimuli and in the context of inflammation, DCs undergo maturation process characterized by increased surface expression of antigen presenting HLA molecules and co-stimulatory molecules such as CD80 and CD86 and secrete several pro-inflammatory cytokines [ 20].
ESX-1-related effects on host immunity include modulation of inflammation, apoptosis, necrosis, phagosomal maturation, phagosomal escape, membrane/cell lysis, tissue invasion, cell-to-cell spread and virulence.
These data suggest that presence of citrullinated proteins in the RA synovium causes antigen-driven maturation of B cells at the site of inflammation.
Perhaps most relevant in autoimmune disease is the role of type I interferons, as they are also able to activate monocytes - stimulating dendritic cell differentiation in vitro and, in a model of chronic inflammation, blocking maturation of Ly6Chi monocytes into Ly6Clo resident monocytes typically recruited to non-inflamed tissues [ 13].
