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COVID-19 vaccine-readiness for anti-CD20-depleting therapy in autoimmune diseases

Author

Clin Exp Immunol. 2020 Jul 16. doi: 10.1111/cei.13495. Online ahead of print.

David Baker 1, Charles Ak Roberts 1, Gareth Pryce 1, Angray S Kang 1 2, Monica Marta 1 3, Saul Reyes 1 3, Klaus Schmierer 1 3, Gavin Giovannoni 1 3, Sandra Amor 1 4

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Abstract

Although most autoimmune diseases are considered to be CD4 T-cell or antibody-mediated, many respond to CD20-depleting antibodies that have limited influence on CD4 and plasma cells. This includes rituximab, oblinutuzumab, ofatumumab that are used in cancer, rheumatoid arthritis and off-label in a large number of other autoimmunities, and ocrelizumab in multiple sclerosis. Recently, the COVID-19 pandemic created concerns about immunosuppression in autoimmunity, leading to cessation or a delay in immunotherapy treatments. However, based on the known and emerging biology of autoimmunity and COVID-19, it was hypothesised that whilst B-cell depletion should not necessarily expose people to severe SARS-CoV-2-related issues, it may inhibit protective immunity following infection and vaccination. As such, drug-induced B-cell subset inhibition that controls at least some autoimmunities, would not influence innate and CD8 T-cell responses, which are central to SARS-CoV-2 elimination, nor the hyper-coagulation and innate inflammation causing severe morbidity. This is supported clinically, as the majority of SARS-CoV-2 infected, CD20-depleted people with autoimmunity, have recovered. However, protective neutralising-antibody and vaccination responses are predicted to be blunted, until naïve B-cells repopulate, based on B-cell repopulation-kinetics and vaccination responses, from published rituximab and unpublished ocrelizumab (NCT00676715NCT02545868) trial data, shown here. This suggests that it may be possible to undertake dose-interruption to maintain inflammatory disease control, whilst allowing effective vaccination against SARS-CoV-29, if and when an effective vaccine is available.