Abstract
Cytokine release syndrome (CRS) is an acute systemic inflammatory syndrome characterized by fever and multiple organ dysfunction associated with (i) chimeric antigen receptor (CAR)-T cell therapy, (ii) therapeutic antibodies, and (iii) haploidentical allogeneic stem cell transplantation (haplo-allo-HSCT). Severe CRS can be life-threatening in some cases and requires prompt management of those toxicities and is still a great challenge for physicians. The pathophysiology of CRS is still not fully understood, which also applies to the identifications of predictive biomarkers that can forecast these features in advance. However, a broad range of cytokines are involved in the dynamics of CRS. Treatment approaches include both broad spectrum of immunosuppressant, such as corticosteroids, as well as more specific inhibition of cytokine release. In the present manuscript we will try to review an update regarding pathophysiology, etiology, diagnostics, and therapeutic options for this serious complication.
Highlights
Cytokine release syndrome (CRS) was first described in the late 1980s as a systemic inflammatory response following treatment with anti-CD3 monoclonal antibody for graft rejection after solid organ transplants [1]
Used interchangeably with cytokine storm, a much broader term describing hyperinflammation caused by a large variety of disorders [2], CRS refers to the immunological phenomenon triggered by immunotherapy such as, chimeric antigen receptor (CAR)-T cells [3], bi-specific T cell engagers (BiTEs) [4], or haploidentical allogeneic hematopoietic stem cell transplantation
The risk of CRS varies between different disorders and patients’ characteristics; with a significant higher incidence of CRS observed in patients with acute lymphoblastic leukemia (ALL) compared with MM, and higher incidence of severe CRS in elderly patients compared with younger patients
Summary
Cytokine release syndrome (CRS) was first described in the late 1980s as a systemic inflammatory response following treatment with anti-CD3 monoclonal antibody for graft rejection after solid organ transplants [1]. Used interchangeably with cytokine storm, a much broader term describing hyperinflammation caused by a large variety of disorders [2], CRS refers to the immunological phenomenon triggered by immunotherapy such as, chimeric antigen receptor (CAR)-T cells [3], bi-specific T cell engagers (BiTEs) [4], or haploidentical allogeneic hematopoietic stem cell transplantation (haplo-allo-HSCT). As discussed in detail in a recent review there are many similarities between. We discuss etiology, pathophysiology, clinical manifestation, diagnostic approaches, and treatment modalities regarding CRS
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