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Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,6
Online ISSN 1827-1898
Toriani-Terenzi C., Fagiolo E.
From the Laboratory of Immunohematology Catholic University of “Sacro Cuore”, Rome, Italy
Background. AIHA is characterised by the destruction of antibody-coated red blood cells, but the mechanism that initiates the production of autoantibodies remains unclear. We have studied the proliferative response and the spontaneous and mitogen-induced (PHA and OKT3) synthesis of IFN-γ, IL-2 and IL-4 by peripheral blood mononuclear cells from patients with AIHA before any treatment to investigate the activation of Th1 and Th2 subsets.
Methods. Thirteen AIHA patients, both idiopathic and associated with other diseases, were studied by ELISA methods and H3 thymidine incorporation to determine in vitro cytokine production and T cell proliferative response, respectively.
Results. Under basal conditions the proliferative response induced in peripheral blood mononuclear cells was enhanced in AIHA patients suggesting a basal state of hyperactivation. This increase in proliferative response can be related to the basal enhanced levels of IL-2 (p<0.04), a key cytokine, that regulates the growth, differentiation and function of lymphocytes. High IL-2 levels in AIHA patients supernatants, with or without OKT3 stimulation, justify the high basal activation of T lymphocytes. Under basal conditions levels of IFN-γ are decreased and IL-4 levels are increased.
Conclusions. AIHA is characterised by the destruction of antibody-coated red blood cells, but the mechanism that initiates the production of autoantibodies remains unclear. But looking to this data it is possible to suppose that there is a prevalent contribution of Th2 lymphocytes to the pathogenesis of AIHA.