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Infection by hepatitis C virus causes chronic disease in approximately 3% of the population of the earth, and results in chronic inflammation and cirrhosis of the liver. At present there is no effective treatment for all patients, and no vaccine has been developed. The immune response against hepatitis C virus is being investigated, in order both to understand the mechanisms of the disease and to formulate new therapeutic approaches. Cytokines are soluble molecules of a communication network among the cells that is responsible for regulating the immune response. This complex network of cytokines begins operating during the initial phase of infection, allowing the development of innate and adaptive immunity, and it not only participates in controlling the virus but also results in damage to the liver, leading ultimately to cirrhosis. Mixed cryoglobulinemia, one of the most serious extrahepatic manifestations of hepatitis C, is also characterized by deregulation of the cytokine network and impaired development of B lymphocytes. The cytokine profile in hepatitis C has been extensively studied and new evidence is continually being reported. Interferon type III, which contributes to antiviral immunity, interleukin-33, one of the youngest members of the interleukin-1 family, the new subtype of T helper lymphocytes producing interleukin 17 and B cell activating factor associated with the cryoglobulinemia of chronic hepatitis C, have all been documented as playing a role. This is a review of recent data derived from basic research and clinical studies on cytokines in the immune response of patients with chronic hepatitis C, and cryoglobulinemia induced by hepatitis C virus. [ABSTRACT FROM AUTHOR]