Altered pattern recognition receptor expression
In response to a primary challenge, macrophages acquire an immune memory
phenotype and upregulate PRR expression to promote the recognition of
diverse foreign antigen-derived pathogen-associated molecular patterns
(PAMPs) and self-derived danger-associated molecular patterns (DAMPs),
and subsequently produce an altered immune memory response23-25. Following stimulation by different PRR ligands
such as the dectin-1 ligand β-glucan, Toll like receptor 2 (TLR2) ligand
lipoteichoic acid, TLR4 ligand LPS, and nucleotide-binding
oligomerization domain-containing protein 2 (NOD2) ligand muramyl
dipeptide, monocytes/macrophages modify the secretion of
pro-inflammatory cytokines tumor necrosis factor-ɑ (TNF-α) and
interleukin (IL)-6, and initiate an altered immune response on secondary
encounter 26. In addition, the macrophage memory
induced by cell surface receptors may be retained following cell
differentiation. The findings of a recent study have revealed that
macrophages derived from mice or human hematopoietic stem and progenitor
cell subsets that are exposed to a TLR2 agonist prior to or during
macrophages differentiation, develop immune tolerance during the
secondary response and produce lower levels of the inflammatory
cytokines TNF-α, IL-6, and IL-1β 27.