Lymphocytotoxic Antibodies Against Peripheral Blood B and T Lymphocytes in Homosexuals With Aids and Arc

Pruzanski, W.; Jacobs, H. S.; Laing, Lorne P.

doi:10.1089/aid.1.1983.1.211

Cited by 30 publications

(9 citation statements)

References 9 publications

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“…In addition, many patients present with polyclonal acti vation of B cells, as manifested by diffuse hypergam maglobulinemia and a variety of antibodies directed against bacterial, viral and sperm-related antigens [11], Similar abnormalities were recorded in patients with ARC and CLS [11,12] and to a lesser extent in symptom-free homosexuals [11][12][13]. We described lymphocytotoxic autoantibodies in all the above groups of patients [6]. These antibodies were directed against both B and T cells [6].…”

Section: Discussionmentioning

confidence: 52%

“…Many such patients also contract a variety of other intercurrent infectious processes. Some of these infections, such as those caused by mycoplasma, cytomegalovirus and Epstein-Barr virus (EBV), are known causes of transient phocytotoxic antibodies have been discovered in AIDS, CLS and ARC patients as well as in symptomfree homosexuals [6,7], In these patients, such anti bodies persist for a long time and seem to be related rather to the HTLV-III viral disease than to the inter current infections. Since CA have a well-known lymphocytotoxic activity [2], it was of interest to search for the existence of CA in AIDS, ARC, CLS and symptom-free homosexuals.…”

Section: Introductionmentioning

confidence: 99%

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Persistent Cold Agglutinins in AIDS and Related Disorders

Pruzanski¹,

Roelcke²,

Donnelly³

et al. 1986

Acta Haematol

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Eighty-one homosexual patients positive for HTLV-III antibody, including 19 with AIDS, 20 with chronic lymphadenopathy syndrome, 10 with AIDS-related complex (ARC) and 32 symptom-free individuals were assessed for the presence of cold agglutinins (CA). In 12 cases, CA were found; 4, 4, 2 and 2, respectively, in each of the above mentioned groups. Seven anti-I,4 anti-i and 1 anti-Gd CA were identified. In 11 of 12 patients, CA were persistent. There were no differences between CA-negative and CA-positive patients with regard to the presence of other antibodies, anemia, frequency of intercurrent infections or development of lymphoproliferative neoplasia. It can be concluded that persistent synthesis of CA may be associated with the HTLV-III infection.

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Section: Discussionmentioning

confidence: 52%

Section: Introductionmentioning

confidence: 99%

Persistent Cold Agglutinins in AIDS and Related Disorders

Pruzanski¹,

Roelcke²,

Donnelly³

et al. 1986

Acta Haematol

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“…+ lymphocytes during late stages of the disease [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17]. Recently, we reported that gp120-containing immune complexes on CD4 + lymphocytes are associated with both dysfunction and depletion of CD4 + blood lymphocytes [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

“…Briefly, 100 l whole blood were incubated with 10 l anti-CD3 (OKT3, all T lymphocytes; Ortho, Raritan, NJ), anti-CD4 (OKT4, helper/ inducer T lymphocytes; Ortho) or anti-CD8 (OKT8, suppressor/ cytotoxic T lymphocytes; Ortho) MoAb for 30 min at 48C. Erythrocytes were lysed by the addition of NH 4 Cl solution for 15 min, the cells were washed with PBS, and 50 l PE-conjugated goat anti-mouse immunoglobulin (Dianova, Hamburg, Germany) were added, together with 50 l FITC-labelled goat anti-human immunoglobulin (Medac, Hamburg, Germany), goat anti-human IgG (Tago, Burlingame, CA), goat anti-human IgM (Medac), rabbit anti-human C3d (Dakopatts, Hamburg, Germany), or 10 l sheep anti-gp120 (Biochrom, Berlin, Germany). The sheep antigp120 was used undiluted, the other antibodies were diluted 1: 40.…”

Section: Introductionmentioning

confidence: 99%

Association of T cell dysfunction with the presence of IgG autoantibodies on CD4+ lymphocytes in haemophilia patients; results of a 10-year study

Daniel

Süsal

Weimer

et al. 1996

Clinical and Experimental Immunology

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HIV induces progressive dysfunction followed by numerical depletion of CD4+ lymphocytes. IgG autoantibodies and gp120‐containing immune complexes have been implicated in the pathogenesis of AIDS. We carried out a longitudinal study in 19 HIV– and 72 HIV+ haemophilia patients over a 10‐year period in order to investigate a possible relationship between the occurrence of autoantibodies and CD4+ lymphocyte changes. IgM, IgG, C3d and gp120 on the surface of CD4+ lymphocytes were determined in heparinized whole blood with flow cytometry and double‐fluorescence. The in vitro response of autoantibody‐coated cells was tested in cell cultures with concanavalin A (Con A), phytohaemagglutinin (PHA), pokeweed mitogen (PWM), anti‐CD3 MoAb or pooled allogeneic stimulator cells (MLC). After a 10‐year follow up, 12 of 71 HIV+ and 16 of 19 HIV– haemophilia patients showed no evidence of immunoglobulins on circulating CD4+ lymphocytes. HIV– haemophilia patients without autoantibodies had CD4+and CD8+ cell counts in the normal range (957 ± 642/μl and 636 ± 405/μl) and normal T cell responses in vitro (mean relative response (RR) ≥ 0.7). In contrast, HIV+ haemophilia patients showed immunological abnormalities which were associated with the autoantibody and immune complex load of CD4+ blood lymphocytes. HIV+ patients without autoantibodies had a mean CD4+ lymphocyte count of 372 ± 274/μl, a mean CD8+ lymphocyte count of 737 ± 435/μl, and normal T lymphocyte stimulation in vitro (mean RR ≥ 0.7). HIV+ patients with complement‐fixing IgM on CD4+ lymphocytes had somewhat lower CD4+ (255 ± 246/μl, P = NS) and CD8+ (706 ± 468/μl, P = NS) lymphocyte numbers, and also normal T lymphocyte stimulation (mean RR ≥ 0.7) in vitro. However, patients with complement‐fixing IgG autoantibodies showed a strong decrease of CD4+ (150 ± 146/μl, P < 0.02) and CD8+ (360 ± 300/μl, P < 0.02) lymphocytes and impaired CD4+ lymphocyte stimulation in vitro with a mean RR of 0.5 ± 0.5 for Con A (P = NS), 0.7 ± 0.8 for PHA (P < 0.03), 0.4 ± 0.4 for PWM (P = NS), 0.8 ± 1.2 for anti‐CD3 MoAb (P < 0.04) and 0.7 ± 1.0 for pooled allogeneic stimulator cells (P = 0.05). Patients with gp120‐containing immune complexes on CD4+ blood lymphocytes demonstrated strongly decreased CD4+ (25 ± 35/μl, P < 0.0001) and CD8+ (213 ± 212/μl, P < 0.006) lymphocyte counts as well as strongly impaired T lymphocyte responses in vitro upon stimulation with PHA (RR 0.2 ± 0.1, P < 0.02), PWM (RR 0.2 ± 0.2, P = 0.05), anti‐CD3 MoAb (RR 0.1 ± 0.1, P < 0.04), and allogeneic stimulator cells (RR 0.2 ± 0.1, P < 0.02). These data led us to speculate that autoantibody formation against CD4+ lymphocytes is an important mechanism in the pathogenesis of AIDS. We hypothesize that autoantibodies against circulating CD4+ lymphocytes inhibit CD4+ cell function, especially the release of cytokines, and induce CD4+ cell depletion. The reduction and dysfunction of CD4+ lymphocytes may be responsible for the CD8+ cell depletion observed in HIV+ patients.

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“…In the first year after infection, many patients develop hypergammaglobulinemia (11)(12)(13), characterized by increased levels of serum antibodies reactive with self antigens (such as T cells and nuclear determinants; foreign antigens such as trinitrophenyl (TNP)l and sheep red blood cells; and HIV viral proteins, including gp160 and p24 [14][15][16][17][18][19][20][21][22]). …”

Section: Introductionmentioning

confidence: 99%

Human immunodeficiency virus infection induces both polyclonal and virus-specific B cell activation.

Shirai¹,

Cosentino²,

et al. 1992

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Peripheral blood lymphocytes (PBL) were obtained from HIV-1-infected patients at different stages of disease. The absolute number of IgM-, IgG-, and IgA-producing lymphocytes per 106 PBL was increased 2.8-, 3.4-, and 1.9-fold, respectively, compared with normal controls. 2-17% of IgG-secreting patient cells reacted with the gpl60 envelope glycoprotein of HIV-1 (a 737-fold increase over background), while 1-9% reacted with p24 (140-fold over background). In addition to this HIV-specific B cell activation, the number of lymphocytes reactive with nonviral antigens such as DNA, myosin, actin, trinitrophenylated keyhole limpet hemocyanin, and ovalbumin was increased by a mean of 17.9-fold. Evidence suggests that the latter changes reflect an HIV-induced polyclonal B cell activation unrelated to the production of anti-HIV antibodies. For example, the proportion of IgG anti-gpl6O-and anti-p24-secreting lymphocytes declined in patients with advanced disease, whereas the number of B cells producing antibodies to non-HIV antigens rose. Moreover, CD4 cell count and T4/T8 ratio showed a significant inverse correlation with the degree of polyclonal activation but not with anti-HIV responsiveness. These observations demonstrate that both quantitative and qualitative changes in B cell activation accompany (and may be predictive of) disease progression in HIV-infected individuals. (J. Clin.

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Lymphocytotoxic Antibodies Against Peripheral Blood B and T Lymphocytes in Homosexuals With Aids and Arc

Cited by 30 publications

References 9 publications

Persistent Cold Agglutinins in AIDS and Related Disorders

Persistent Cold Agglutinins in AIDS and Related Disorders

Association of T cell dysfunction with the presence of IgG autoantibodies on CD4+ lymphocytes in haemophilia patients; results of a 10-year study

Human immunodeficiency virus infection induces both polyclonal and virus-specific B cell activation.

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