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CAR T cell–derived TNF is an early determinant of cytokine release syndrome severity

Science Immunology

Cytokine release syndrome (CRS) is a common and potentially life-threatening complication of chimeric antigen receptor (CAR) T cell therapy and other immunotherapies. Although pro-inflammatory cytokines produced by host myeloid cells such as interleukin-6 (IL-6) are known to drive CRS, the upstream signals that initiate these responses remain incompletely understood. By selectively disrupting tumor necrosis factor (TNF) signaling in a mouse model of CRS, we show that CAR T cell–derived TNF promotes the accumulation of pro-inflammatory monocyte-derived macrophages at the tumor site and the induction of host-derived cytokines including IL-6 and IL-1β. We further show that TNF is a determinant of CRS severity in humanized xenochimeras, governing the overall disease course including eventual lethality. Our findings thus identify TNF as an upstream regulator of CRS acting at least in part via the host macrophage compartment.

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CAR T cell–derived TNF is an early determinant of cytokine release syndrome severity