Highlights d Peripheral CD4 + T cells control stress-induced anxiety-like behavior d Mitochondrial fission in peripheral CD4 + T cell causes severe anxiety symptoms d T cell-derived xanthine acts on the oligodendrocytes in the left amygdala d IRF-1 controls purine synthesis in CD4 + T cells and triggers the onset of anxiety

The response of immune cells in cardiac injury is divided into three continuous phases: inflammation, proliferation and maturation. The kinetics of the inflammatory and proliferation phases directly influence the tissue repair. In cardiac homeostasis, cardiac tissue resident macrophages (cTMs) phagocytose bacteria and apoptotic cells. Meanwhile, NK cells prevent the maturation and transport of inflammatory cells. After cardiac injury, cTMs phagocytose the dead cardiomyocytes (CMs), regulate the proliferation and angiogenesis of cardiac progenitor cells. NK cells prevent the cardiac fibrosis, and promote vascularization and angiogenesis. Type 1 macrophages trigger the cardioprotective responses and promote tissue fibrosis in the early stage. Reversely, type 2 macrophages promote cardiac remodeling and angiogenesis in the late stage. Circulating macrophages and neutrophils firstly lead to chronic inflammation by secreting proinflammatory cytokines, and then release anti-inflammatory cytokines and growth factors, which regulate cardiac remodeling. In this process, dendritic cells (DCs) mediate the regulation of monocyte and macrophage recruitment. Recruited eosinophils and Mast cells (MCs) release some mediators which contribute to coronary vasoconstriction, leukocyte recruitment, formation of new blood vessels, scar formation. In adaptive immunity, effector T cells, especially Th17 cells, lead to the pathogenesis of cardiac fibrosis, including the distal fibrosis and scar formation. CMs protectors, Treg cells, inhibit reduce the inflammatory response, then directly trigger the regeneration of local progenitor cell via IL-10. B cells reduce myocardial injury by preserving cardiac function during the resolution of inflammation.

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The nuclear factor κB (NF-κB) transcription factors exert central hub functions in multiple physiologicalprocesses including immune response, cell survival, proliferation and cytokine production, which hasnaturally become the core of research almost in all aspects of biomedical science over 30 years. Sinceboth the activation and termination of NF-κB pathway are tightly regulated, little alteration can lead toexcessive inflammatory responses and even result in tissue damage and severe diseases. The inhibitor ofnuclear factor kappa-B (IκB) kinase (IKK) complex is the main regulator of the NF-κB signaling pathway,they mediate and deliver signals through phosphorylating certain substrates. In recent years, increasedproteins have been identified to be targeted by IKK members and the particular modification mechanismbecomes clear with the development of detecting techniques and structural biology. In this review, wesummarize the known substrates of IKK family members either relevant or irrelevant to NF-κB signaling,their structures and phosphorylation patterns, and the related physiologic and/or pathologic responses.Understanding the regulation of IKKs on their substrates may be helpful to connect IKKs with specificsignaling pathways or physiological phenomena, and is essential for targeting IKKs in clinical research.