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Cytokine release syndrome (CRS) is a systemic inflammatory response triggered by the activation of T-cells and is commonly seen in patients receiving immune effector cell therapies such as chimeric antigen receptor (CAR) T-cell therapy and bispecific antibodies (BsAbs) which target varying tumor antigens such as CD19, CD20, B-cell maturation antigen (BCMA), or GPRC5D depending on the type of malignancy. CRS characteristics include fever, hypotension, and dyspnea due to increases in inflammatory mediators such as interleukin-6, interferon-γ, and tumor necrosis factor, which can be life-threatening if left untreated 1 . Although the grading of CRS associated with BsAbs is well established, management of CRS associated with BsAbs may vary depending on disease type, product, and institutional protocol and generally includes the use of antipyretics, hydration, oxygen, tocilizumab, and/or corticosteroids 2 , 3 .
Davis et al. (Tue,) studied this question.
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