Anti-phospholipid antibodies and CD5+ B cells in HIV infection

Abstract

This cross-sectional study evaluates the correlation between anti-phospholipid antibodies and CD5+ B cells in 110 patients infected with HIV-1. There were 89.1% of the patients who had IgG antibodies against cardiolipin and phosphatidylserine. The prevalence of IgM and IgA antibodies was < 22%. AIDS was associated with lower frequencies of IgM antibodies against cardiolipin (P = 0.05) and IgG-antibodies against cardiolipin and phosphatidylserine (P = 0.011). Drug users had higher IgM antibodies against phospholipids than patients from other risk groups (P = 0.02). A history of thromboembolic events was not accompanied by higher levels of anti-phospholipid antibodies (P > 0.2). No correlation between anti-phospholipid antibodies and CD5+ B cells was detected. Percentage part of CD5+ B lymphocytes was elevated in all patients and absolute CD4+ T lymphocyte counts and HIV p24 antigen were inversely correlated. In advanced disease a significant reduction of anti-phospholipid antibodies was contrasted with persistent elevation of CD5+ B lymphocytes. These observations may reflect immunological dysfunction involving apoptosis and endothelial damage rather than polyclonal B cell hyperstimulation. A possible explanation would be that in HIV infection an increased rate of spontaneous apoptosis in peripheral blood lymphocytes is accompanied by functional and structural changes of mitochondria. Therefore, structurally altered mitochondrial phospholipids could serve as antigen to induce specific humoral immune responses.

Alterations of self-reactive antibody repertoires in HIV disease: An insight into the role of T cells in the selection of autoreactive B cells

“…HLA molecules, CD95, phospholipids, human ␤2 glycoprotein-1, neutrophil cytoplasmic antigens, are frequently observed in untreated HIV-infected individuals [3][4][5][6][7][8][9]. Disturbances in mechanisms of self-recognition were shown to parallel the progression of HIV-1 infection [3,23].…”

“…Alterations of the B cell compartment include polyclonal B cell activation [1,2] and high levels of self-reactive antibodies in serum [3][4][5][6][7][8][9]. Natural antibodies of the IgM, IgG, and IgA isotype that are reactive with a stages of HIV infection using quantitative immunoblotting followed by multiparametric statistical analysis of the data.…”

Mucosal Plasma Cell Repertoire During HIV-1 Infection

“…Indeed, the proportion of plasma cells expressing IgM was elevated in the duodenal lamina propria of HIV-1-infected patients. One might speculate that an influx of B-1 B cells, purported to be elevated in the blood of HIV-1-infected patients (87), into the intestinal lamina propria could account for these differences in IgM-producing plasma cells. In this context, the preferential usage of V H 4 genes by B-1 B cells (88) could then account for both the decreased V H 3 expression and the increased V H 4 expression that we measured in lamina propria IgM-producing plasma cells.…”

MRI characteristics of patients with antiphospholipid syndrome and multiple sclerosis

“…We postulate that the generation of APLAs during the course of MS may be related to widening B-cell stimulation and epitope spreading triggered by tissue injury. Recent observations in HIV patients suggest that generation of APLA may be triggered by apoptosis, release of cellular phospholipids and endothelial damage rather than polyclonal B cell hyperstimulation [13]. There are several mechanisms by which phospholipid-containing epitopes derived from cellular and intracellular membranes may become immunogenic in MS [12,16].…”