Mouse studies have helped us to uncover the underlying inflammatory mechanisms (mediated by multiple immune cell types that produce Th1, Th2 or Th17 cytokines) and non-inflammatory pathways, in addition to shedding light on asthma that is associated with obesity or steroid unresponsiveness.
Together, these results argue that Btk inhibition suppresses inflammation, bone erosion, and autoimmunity in vivo by affecting the function of multiple immune cells involved in both the propagation and effector phases of CIA.
The first line of defence is the physical barrier carried out by the intestinal mucosa, in which multiple immune cells (macrophages, polymorphonuclear neutrophils, mast cells reside, and innate lymphoid cells) implicated in the immediate unspecific reactions to antigens shared by a plethora of pathogens.
CXCL10 is secreted by immune cells as well as resident cells of tissues and organs (23) and recruits multiple immune cells, including T-cells, NK cells, macrophages and DCs through engagement of CXCR3.
This is achieved by promoting the differentiation of multiple immune cell lineages that contribute to cell-mediated immunity and by suppressing the function of counterregulatory lineages.
Specific miRNAs, such as miR-155 and miR-146a, were initially linked with the inflammatory response by virtue of their potent up-regulation in multiple immune cell lineages by Toll-like receptor ligands, inflammatory cytokines, and specific antigens [ 15- 17].
Taken together, these observations indicate that the exacerbated TPA response in EPI−/− skin involves multiple immune cell types and cannot be normalized by inhibiting one specific leukocyte subset.
TGF-β regulates immune responses and maintains immune homeostasis through its impact on multiple immune cell lineages.
