Dendritic Cells under Hypoxia: How Oxygen Shortage Affects the Linkage between Innate and Adaptive Immunity

Figure 1

Features of dendritic cells in the presence or absence of active HIF-1α. Dendritic cells expressing HIF-1α have been shown to induce costimulatory molecules (CD80, CD86, and MHCII/HLA class II) under inflammatory hypoxic conditions. Transcripts of nod2, cxcr4, cxcr1, ccr3, ccr2, trem-1, il-8, and mif are upregulated. Induced expression of CCR7 favors migration of DC towards secondary lymph nodes. These DCs are potent inducers of Tregs via TGF-β, IL-10, RA, and IL-22 although they are able to induce a robust early T cell activation by secretion of type I interferons. Via TSLP, DCs in the gut may be shifted towards a tolerogenic phenotype (: TSLPR expression is limited to gut DCs). Dendritic cells lacking HIF-1α under inflammatory conditions secrete steady high levels of IL-12 and thereby induce a robust activation of proinflammatory T cell populations. They upregulate transcripts of chemokines to attract more immune cells.