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. 2021 Aug 24;8:708453. doi: 10.3389/fmed.2021.708453

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Copyright © 2021 Li, Ma, Han, Chi, Sai, Zhu, Ding, Song and Liu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Immunomodulatory activity of heme oxygenase 1 (HO-1) in immune cells. HO-1 is stress-inducible by macrophages and promotes the phenotypic shift to M2 macrophages, associated anti-inflammatory activities. HO-1 also modulates the production of interferon (IFN)-β in macrophages through direct HO-1 binding to interferon regulatory factor 3 (IRF3) in response to pro-inflammatory stimuli. HO-1 induction in dendritic cells (DCs) inhibits their maturation, secretion of pro-inflammatory cytokines, and induction of ROS. Mast cells (MCs) can sense local stressor insults to induce HO-1, thereby suppressing their degranulation and production of inflammatory cytokines. Moreover, inhibiting MCs' degranulation can also inhibit DCs' maturation. These effects all result in the promotion of DCs into a tolerogenic phenotype, thus promoting regulatory T cell (Treg cell) differentiation. HO-1 expression by T cells can additionally inhibit T helper 17 cells (TH17 cells) differentiation, Th2-related cytokines secretion, as well as limit proliferation. Activated Treg cells can initiate HO-1 expression in neutrophils shifting them to a suppressive phenotype, which inhibits their infiltration, basophil activation as well as migration of eosinophils. HO-1 expression by B cells can additionally promote their development and growth. HO-1 induction can also inhibit NK cells effector functions and activity.