COVID-19: risk for cytokine targeting in chronic inflammatory diseases?

Abstract

COVID-19, caused by the SARS-CoV-2 virus, has become pandemic. With sharply rising infection rates, patient groups characterized by an enhanced infection risk will be challenged by the virus. In this context, patients with chronic immune-mediated inflammatory diseases are of particular interest, as these diseases are characterized by an intrinsic immune dysfunction leading to inflammation that may enhance risk for severe infection.

Fig. 1. Cytokines in IMIDs and in COVID-19.

a | A ‘cytokine tree’ of immune-mediated inflammatory diseases (IMIDs) showing their individual responsiveness to cytokine inhibitor therapy. The risk for viral, bacterial and fungal infections and effects on blood immune cells of the respective cytokine inhibition strategies are indicated below (red equals risk and green equals no risk). b | Cytokine pathogenesis of coronavirus disease 2019 (COVID-19). AC, alveolar cell; ACE2, angiotensin-converting enzyme 2; AD, atopic dermatitis; CD, Crohn’s disease; JAK, Janus kinase; NK, natural killer; PMN, polymorphonuclear granulocyte; PsO, psoriasis; RA, rheumatoid arthritis; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; SpA, spondyloarthritis; T_EFF cell, T effector cell; T_reg cell, regulatory T cell; UC, ulcerative colitis.