B cell activation and human immunodeficiency virus infection. V. Phenotypic and functional alterations in CD5+ and CD5? B cell subsets

Abstract

B cell dysregulation is a hallmark of human immunodeficiency virus infection. Since B lymphocytes comprise two distinct subpopulations, CD5+ and CD5- cells, we addressed their individual phenotypic and functional behavior. Seropositive patients with both limited and advanced disease progression had an increased percentage of peripheral blood CD5+ B cells, compared to seronegative controls (20.1 +/- 2.1 and 22.7 +/- 5.7, respectively, vs 17.0 +/- 3.4 in controls); however, due to the lymphopenia and reduced number of circulating B cells in infected individuals, the absolute number of CD19+CD5+ lymphocytes was actually reduced. Although HIV-specific antibodies were synthesized spontaneously in vitro only by CD5- B cells, a 10-fold lower degree of spontaneous, non-HIV-specific activation was also displayed by unstimulated CD5+ B cells. These findings indicate that B cell dysregulation during HIV infection involves both the CD5- and the CD5+ B cell compartments; moreover, in view of the putative role of CD5+ B cells in autoimmune phenomena and IL-10 production, these data reinforce the possibility that B cell dysfunction might be causally involved in AIDS pathogenesis.

Intravenous ganciclovir consistently induces remission of persistent Epstein–Barr encephalitis in an HIV-1-infected patient

“…The dysregulation of plasma cells that occurs in HIV infection and immune reconstitution syndrome may make the development of autoantibodies to factor VIII more common in HIV-infected patients [8][9][10][11][12][13].…”

Effects of CD2 locus control region sequences on gene expression by retroviral and lentiviral vectors

“…At different times after infection, cells were pelleted, washed, fixed, and labeled, where appropriate, with a phycoerythrin-labeled anti-HLA class I monoclonal antibody (mAb) (DAKO, Glostrup, Denmark) or with a PC5-labeled anti-human CD3 mAb (Coulter). Two-color immunofluorescence was carried out as reported 25 and was analyzed using the PRISM parameter of the Elite cytofluorometer; the negative control setting for each monoclonal antibody was determined by using labeled immunoglobulin of the corresponding isotype. Mock-transduced cell lines served as the negative control for EGFP-expression analysis.…”

Mechanisms of hypergammaglobulinemia and impaired antigen-specific humoral immunity in HIV-1 infection

“…1 Polyclonal B-cell activation is demonstrated by hypergammaglobulinemia and spontaneous antibodies' (Abs) production by cultured peripheral lymphocytes 2,3 ; additional signs of B-cell abnormality are the high incidence of B-cell tumors 4 and the deregulated expression of several surface molecules like Fas, Fas ligand (FasL), CD5, CD21, and CD27. [5][6][7][8] B-cell hyperactivity is also accompanied by functional defects since humoral immune responses following immunization are severely impaired in HIV-1-infected subjects and B lymphocytes from patients are poorly responsive to in vitro stimulation. [9][10][11] Several mechanisms may account for the B-cell abnormalities in HIV-1 infection.…”