The plasma cofactor and anticardiolipin antibodies.
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Biomedical subjects
Publications and source records attributed to W Barcellini.
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The association between antiphospholipid antibodies (aPL) and arterial or venous thrombosis, fetal loss and thrombocytopenia defines the so-called "antiphospholipid syndrome" (APS). Despite serial studies in recent years, a clear pathogenetic mechanism(s) has not yet been demonstrated. Several authors have investigated the interaction between aPL and the membranes of blood cells (endothelial cells and platelets) involved in coagulation. aPL is also thought to affect the balance between the procoagulant and anticoagulant states by interacting with plasma or tissue cofactors. Finally, the strong association between aPL and experimental animal models of fetal loss supports a direct pathogenetic role for aPL in inducing a poor pregnancy outcome in APS women.
The natural course of human immunodeficiency type 1 (HIV-1) infection varies considerably. The identification of laboratory disease markers has become critically important to patient management. This study, carried out on 37 patients with primary HIV-1 infection (PHI), shows that, along with plasma HIV-1 RNA and CD4+ T cell counts, evaluation of plasma levels of some immune activation markers (sCD30, TNF-alpha, and sTNFR-I) may help to identify patients at risk of a more rapid disease progression, suggesting that immune activation is among the factors who determine the rate of disease progression. Early combination antiviral therapy significantly decreased levels of virus load and of immune activation markers, suggesting that it may reduce the extent of immune activation through the suppression of HIV-1 replication. Among others, sCD30 could be a more sensitive marker of immune activation, and it might be also useful in the monitoring of the response to antiviral therapy.
The immune system is able to recognize and neutralize potentially harmful agents, conferring to the organism resistance to infectious and malignant diseases. The authors have reviewed the literature and identified a group of substances able to enhance and/or reduce different immune functions, both in an experimental model and in occupational and environmental human exposure. The group includes several polyhalogenated hydrocarbons, particularly polychlorinated biphenyls, polybrominated biphenyls, tetrachloro-dibenzo-p-dioxin (TCDD), some metals like lead, cadmium and mercury, pesticides, i.e. dithiocarbamates and organotin compounds, organic solvents. The observed changes are usually slight and do not allow prognostic conclusion. In this study, the authors propose a 3-level rank of tests suitable for the immune evaluation of individuals occupationally exposed to xenobiotics, divided into three levels, as follows: tier 1: immunoglobulin classes (IgG, IgA, IgM), complement fractions (C3, C4), rheumatoid factor, and non-organ specific autoantibodies (AMA, SMA, ANA); CD3, CD4, CD8, CD57, CD20, HLA-DR; CD3/HLA-DR positive lymphocyte subsets; tier 2: determination of the mitotic response of peripheral blood lymphocytes to phytohaemoagglutinin, anti-CD3 monoclonal antibody, phorbol-myristate-acetate (PMA) and polyclonal immunoglobulin production after stimulation with pokeweed mitogen; tier 3: cytokine production with and without mitogen stimulation. The approach is "step by step" and assumes the need of a closely integrated and comparative evaluation of the findings obtained. The protocol could be used in research fields; moreover, some of the tests could be useful in the monitoring of persons exposed in the environment or in the workplace to immunotoxic substances or to biological agents.