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In its more severe forms, COVID-19 progresses towards an excessive immuneresponse, leading to the systemic overexpression of proinflammatory cytokineslike IL6, mostly from the infected lungs. This cytokine storm can causemultiple organ damage and death. Consequently, there is a pressing need toidentify therapies to treat and prevent severe symptoms during COVID-19. Basedon previous clinical evidence, we hypothesized that inhibiting T cellco-stimulation by blocking CD80/86 could be an effective therapeutic strategyagainst progression to severe proinflammatory states. To support thishypothesis, we performed an analysis integrating blood transcriptional data wegenerated from rheumatoid arthritis patients treated with abatacept -- aCD80/86 co-stimulation inhibitor -- with the pathological features associatedwith COVID-19, particularly in its more severe forms. We have found that manyof the biological processes that have been consistently associated withCOVID-19 pathology are reversed by CD80/86 co-stimulation inhibition, includingthe downregulation of IL6 production. Also, analysis of previoustranscriptional data from blood of SARS-CoV-infected patients showed that theresponse to abatacept has a very high level of antagonism to that elicited byCOVID-19. Finally, analyzing a recent single cell RNA-seq dataset frombronchoalveolar lavage fluid cells from COVID-19 patients, we found asignificant correlation along the main elements of the C80/86 axis: CD86+/80+antigen presenting cells, activated CD4+ T cells and IL6 production. Ourin-silico study provides additional support to the hypothesis that blocking ofthe CD80/CD86 signaling axis may be protective of the excessive proinflammatorystate associated with COVID-19 in the lungs.

Blocking of the CD80/86 axis as a therapeutic approach to prevent progression to more severe forms of COVID-19