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Mixed cryoglobulinemia: a model of virus-related disease in internal medicine
Franco Dammacco1, Gianfranco Lauletta, Michele Montrone
1Department of Biomedical Seiences and Human Oncology, Section of Internal Medicine and Clinical Oncology, University of Bari Medical Sehool, Bari, Italy. f.dammacco@dimo.uniba.it
Abstract:
Like other hepatotropic viruses, hepatitis C virus (HCV) exhibits the property of inducing hepatocellular damage, possibly through induction of immune mechanisms that lead to hepatocellular necrosis. The early activated mechanisms include production of non-specific and specific antibodies, which represent the first line of defence against invading foreign pathogens. As a consequence, circulating immune complexes are promptly formed and antigen uptake and processing by specialized cells are enhanced. A major fraction of circulating immunoglobulins (Igs) are part of the spectrum of so-called "natural" antibodies, which include anti-idiotypic antibodies and molecules with rheumatoid factor (RF) activity. They mainly belong to the IgM class, are polyclonal and have no intrinsic pathogenetic potential. In 20-30% of HCV-infected patients, RFs share characteristics of high affinity molecules, are monoclonal in nature, and result in the production of cold-precipitating immune complexes and mixed cryoglobulinemia (MC). The persistent production of monoclonal RF molecules implies the existence of a further mechanism capable of restricting the reactivity and reflects a distinct selection of a cell population that can be maintained throughout life because it is continuously exposed to antigen pressure. Either polyclonal or monoclonal profiles of B-cell expansion are demonstrable in the liver of the majority of HCV-infected patients. The frequent detection of oligoclonal B cell expansion may, indeed, represent a key pathobiologic feature which sustains non-malignant B-cell lymphoproliferation. The preferential expansion of one clone would in turn lead to a monoclonal pattern, which could favor stochastic oncogenic events. Thus, it can be postulated that HCV is the stimulus not only for the apparent benign lymphoproliferative process underlying a wide spectrum of clinical features, but also for the progression to frank lymphoid malignancy in a subgroup of patients.
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