Figure 8.

Molecule signaling of Ly6C MC to MΦ subset differentiation and to lymphocyte subset functional adaptation. We established two models for molecule signaling of MC differentiation based on their preferential expression of lineage signature TF, surface marker and cytokine using information extracted from Figures 3 , 5 , and 7 . (A) Ly6C^high MC favors to MΦ subset differentiation and associated molecule signaling. Ly6C^high MC preferentially expressed lineage signature TF genes of MΦ/DC subsets, suggesting their potential differentiation to MΦ. The indicated immunological and inflammatory pathways lead to various changes of cytokines production, and effector function including T/NK cell proliferation, inflammatory response and calcification. Cbs ^-/- Ly6C^high MC exhibited inflammatory cytokine production. (B) Ly6C^low MC shares function with lymphocyte subset (molecule signaling). Ly6C^low MC preferentially expressed lineage signature TF genes of B/T cell subsets, suggesting their potential functional adaptation to lymphocyte subsets. The indicated immunological and inflammatory pathways lead to various changes of cytokines attributed to increased T/B cell activation, host defend, wound healing and anti-inflammatory responds. Cbs ^-/- Ly6C^low MC exhibited enhance T/B cell activation potential. Expression change and function implication of SDE cytokine genes in Ly6C MC were presented in Supplementary Table 7 . MC, monocyte; DC, dendritic cell; MΦ, macrophage; TREM1, the triggering receptor expressed on myeloid cells; NK, natural killer, TC, T cell; Th1, T helper 1 cell; Tfh, T follicular helper; BC, B cell, NFAT, Ca²⁺, Calcium; SLE, systemic lupus erythematosus, IL-7, Interleukin 7; NFAT, nuclear factor of activated T-cells; nNOS, neuronal nitric oxide synthase.