Dr France Debaugnies, from the team of Dr Patricia Borde in the Departement de Biologie Medicale, has just published a report in Arthritis & Rheumatology (doi.org/10.1002/ART.41763). This work was coordinated by Dr. rer. nat. Christoph Kessel from the Klinik für Pädiatrische Rheumatologie und Immunologie, Universitätsklinikum Münster in Germany.

This report  shows that significant immunological differences exist between the COVID-19 infection on the one hand, and  well-known, classical, inflammation-induced cytokine storm syndromes, such as those observed in the context of secondary hemophagocytic lymphohistiocytosis (sHLH)  or macrophage activation syndrome (MAS), on the other hand.

Very high activation of the IL18 – IFNg axis is observed in the latter syndromes, but not in COVID-19. Very high levels of IL1 receptor antagonist (IL1-Ra), intracellular adhesion molecule 1 (ICAM-1), and IL8 and very reduced levels of soluble Fas ligand (sFasL), are characteristic of the COVID-19 infection, but not the previously mentioned classical cytokine storm syndromes. These results were obtained by immunoenzymatic assays, using serum samples from different groups of patients. Furthermore, the publication  showed that different patterns of correlation between these cytokines and ferritin or thrombocyte counts (two of the hallmarks of COVID-19) are observed in COVID-19 and in classical inflammation-induced cytokine storm syndromes.

These results are important for the further translation of immunology research in COVID-19 towards evidence-based clinical trial and therapeutic targets. Indeed, it would appear that specifically blocking IL8 signaling and/or bypassing the low sFasL expression may represent promising routes for specific COVID-19 therapy.