Cytokine release syndrome commonly complicates first infusions of certain therapeutic monoclonal antibodies which have lymphocyte mitogenic properties in vitro. Agents with which CRS has been described include OKT3 (anti-CD3), CAMPATH (anti-CD52), and rituximab (anti-CD20). CRS is characterized clinically by hypothermia or fever, rigors, hypotension, rash, dyspnea and occasionally bronchospasm, rash, nausea and diarrhea. These side effects develop soon after the administration of the agent and can last for several hours. Typically discontinuing the drug and employing supportive measures leads to recovery. However, severe and even fatal reactions associated with pulmonary edema and hepatitis have been described. The clinical syndrome is caused by a sudden increase in TNF-α, IFN-γ, and IL-6 release. The CRS potential of biological agents can be predicted by the presence of mitogenicity and induction of TNF-α and IFN-γ release in whole blood cultures exposed to...