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. 2020 Sep 30:11:2061.
doi: 10.3389/fimmu.2020.02061. eCollection 2020.

Immune Tolerance as the Physiologic Counterpart of Chronic Inflammation

Vladimir Rogovskii  1   2
Affiliations

Immune Tolerance as the Physiologic Counterpart of Chronic Inflammation

Vladimir Rogovskii. Front Immunol. .
No abstract available

Keywords: chronic inflammation; cytokines; immune privilege; immune tolerance; inflammation in aging; oral tolerance; tumor immunity.

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Figures

Figure 1
Figure 1
Low-grade constitutive inflammation might be the mechanism of immune tolerance. Various mechanisms of the transition to immune suppression during chronic inflammation exist. The figure depicts some of them. Inflammatory factors induce anti-inflammatory factors, which cause immune suppression (7). In the case of acute inflammation, the resolution of inflammation proceeds without suppressing immunity. It is necessary to stop an acute inflammation in time to prevent its transition to the chronic form. In the treatment of diseases linked to chronic inflammation, there may be two methods to utilize—anti-inflammatory and pro-inflammatory therapy. Both of these therapies are aimed at overcoming the vicious cycle of chronic inflammation. Pro-inflammatory therapy can cause a subsequent anti-inflammatory response, resulting in the resolution of chronic inflammation. For instance, this can be the case in hyperthermia therapy (8). Chronic inflammation, which can occur for various reasons (chronic contact with infection or irritants, chronic stress, and the presence of cells that continuously secrete inflammatory mediators), lacks a complete resolution phase—it never ends. Anti-inflammatory cytokines are released continuously—along with pro-inflammatory cytokines. So, when the inflammatory stimulus becomes permanent, immunosuppression begins. This property can be used to achieve immune tolerance. Chronic low-grade inflammation might be localized—either in immune-privileged organs or tumors. It can lead to immunological tolerance (unresponsiveness to antigens) in the areas of chronic inflammation.
See this image and copyright information in PMC

References

    1. Medzhitov R. Origin and physiological roles of inflammation. Nature. (2008) 454:428–35. 10.1038/nature07201 - DOI - PubMed
    1. Kany S, Vollrath JT, Relja B. Cytokines in inflammatory disease. Int J Mol Sci. (2019) 20:6008. 10.3390/ijms20236008 - DOI - PMC - PubMed
    1. Schett G, Neurath MF. Resolution of chronic inflammatory disease: universal and tissue-specific concepts. Nat Commun. (2018) 9:3261. 10.1038/s41467-018-05800-6 - DOI - PMC - PubMed
    1. Gudernatsch V, Stefanczyk SA, Mirakaj V. Novel resolution mediators of severe systemic inflammation. Immunotargets Ther. (2020) 9:31–41. 10.2147/ITT.S243238 - DOI - PMC - PubMed
    1. Rogovskii VS. Modulation of inflammation-induced tolerance in cancer. Front Immunol. (2020) 11:1180. 10.3389/fimmu.2020.01180 - DOI - PMC - PubMed