Deficiency of the autologous mixed lymphocyte reaction in patients with classic hemophilia treated with commercial factor VIII concentrate. Correlation with T cell subset distribution, antibodies to lymphadenopathy-associated or human T lymphotropic virus, and analysis of the cellular basis of the deficiency.

Smolen, Josef S.; Bettelheim, Peter; Köller, Ursula; McDougal, Sarah J; Graninger, W; Luger, Thomas A.; Knapp, Walter; Lechner, Klaus

doi:10.1172/jci111896

Cited by 31 publications

(7 citation statements)

References 49 publications

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“…A number of studies have reported that PBL from AIDS patients [l] or from asymptomatic, HIV-seropositive (HIV+) individuals who exhibit > 400 CD4+ cells/mm3 [2][3][4][5][6][7][8], are unresponsive in vitro to stimulation with recall or autologous antigens, but retain response activity to HLA alloantigens (Allo) and T cell mitogens. Specifically, Lane et al…”

Section: Introductionmentioning

confidence: 99%

Functional dichotomy of CD4⁺ T helper lymphocytes in asymptomatic human immunodeficiency virus infection

Clerici

Via²,

Lucey

et al. 1991

Eur J Immunol

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The majority of asymptomatic, human immune deficiency virus seropositive (HIV+) individuals exhibit a defect in CD4+ T helper cell (Th) function that is selective for responses to recall antigens, but not to HLA alloantigens. The CD4-dependent Th response to HLA alloantigens (Allo) can be mediated by two distinct Th pathways: self-restricted CD4+ Th that recognize allogeneic determinants processed and presented by autologous or self accessory or antigen-presenting cells (sAC); and allo-restricted, CD4+ Th that recognize allogeneic determinants directly on allogeneic accessory or antigen-presenting cells (aAC). In contrast, the Th response to recall antigens requires CD4+ Th and sAC and is therefore limited to the major histocompatibility complex (MHC) self-restricted pathway. Peripheral blood leukocytes from 56 asymptomatic HIV+ patients that exhibited a selective defect in CD4+ Th function were analyzed to determine whether the Th response to Allo was entirely functional, or whether one of the CD4-mediated components of the Allo Th response was also defective. By depletion of AC and/or CD8+ Th subsets (to analyze CD4+ Th function), we demonstrated that HIV+ patients who were selectively deficient in Th function to recall antigens were also unresponsive to Allo presented by autologous AC (HLA self-restricted Th pathway), but retained Allo Th activity presented by allogeneic AC (allo-restricted CD4+ Th pathway). These findings indicate that the CD4+ Th defect seen in the majority of asymptomatic, HIV+ individuals is not limited to recall antigens, but also extends to the component of the response to HLA alloantigens that involves the self-restricted, CD4+ Th pathway. Thus, the Th defect observed in asymptomatic, HIV+ patients does not involve a CD4+ Th defect per se, but is limited to the HLA self-restricted component of Th function.

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Section: Introductionmentioning

confidence: 99%

Functional dichotomy of CD4⁺ T helper lymphocytes in asymptomatic human immunodeficiency virus infection

Clerici

Via²,

Lucey

et al. 1991

Eur J Immunol

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“…Therefore no conclusions can be drawn regarding the infectivity of the samples tested, because the amount of infectious agent may be beneath the quäntities detectable by the antigen Elisa. In high percentages of haemophiliacs receiving eommercial clotting concentrates which have not been tested for anti-HIV antibodies and heat inactivated, transmission of the virus has been described, resulting in the development of antibodies to HIV and exacerbation of AIDS (13,14,15). HIV has been isolated from peripheral blood and other body fluids of most patients with pre-AIDS, and from a considerable number of patients with the fully developed picture of AIDS.…”

Section: Discussionmentioning

confidence: 99%

Incidence of Anti HIV Antibodies and Viral Antigen in Standard and Control sera

Köller¹,

Rumpold²,

Schindler³

et al. 1987

Clinical Chemistry and Laboratory Medicine

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Summary:Most material used for control and calibration in a clinical laboratory is based on pool sera of human origin, guaranteed to be HBsAg-free. Since little Information is available on the potential infectivity of HIV, the causative agent of acquired immunodeficiency syndrome (AIDS), 54 control and calibration sera, in routine use, were investigated for the incidence of antibodies to HIV by means of Elisa. Sixteen test specimens (= 30%) gave positive or borderline Elisa results and were further analysed by immunoblotting, resulting in 15 samples all recognizing gp 160 and partially the p 24, p 31, p 55, p 64 and gp 120 band. Only one sample with borderline Elisa result was negative by this assay. Furthermore, all sera were examined for the presence of viral antigen by a solid phase Elisa. All samples under investigation gave negative antigen Elisa results. Bearing in miiid that the sensitivity of this assay is limited to 10 g/l of viral antigen, no conclusion on infectivity should be drawn. The high incidence of HlV-antibodies in the sera investigated demands that this material should be handled with special care by laboratory personnel.

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“…Defective interleukin-2 production as the hallmark of qualitative lymphocyte defects in HIV infection Early and complex T helper (Th) cells defects have been described in HW infected individuals. [1][2][3][4][5][6] We have analysed the qualitative defects of HW infection by examining in vitro antigenand mitogen-stimulated interleukin (IL)-2 production by PBMC of H1V+ individuals. PBMC were stimulated in vitro with recall antigens (influenza virus, tetanus toxoid, or HIV peptides); HLA alloantigens (ALLO); or phytohaemagglutinin (PHA).…”

Section: Cacorresponding Authormentioning

confidence: 99%

The breakdown of the cytokine network subsequent to human immunodeficiency virus infection

Clerici

Villa

Trabattoni

et al. 1995

Mediators of Inflammation

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The acquired immunodeflciency syndrome (AIDS) is a clinically multifaceted disease induced by infection with the human immunodeficiency virus (HIV). HIV infection results in a complex pattern of immunologic alterations that leads to the development of AIDS in the majority of HIV seropositive (HIV+) individuals. The reduction in CD4 T lymphocyte counts is the hallmark of HIV infection; nevertheless, long before the reduction in CD4 counts reaches critical levels, a series of profound and complex defects that impair the function of CD4 T lymphocytes can be detected. Thus, HIV infection is characterized by quantitative and qualitative defects affecting CD4 T lymphocytes. It was suggested recently that programmed cell death (PCD) is an important mechanism leading to CD4 depletion in HIV infection, and that susceptibility of peripheral lymphocytes to PCD is differentially regulated by diverse cytokines. Thus, type 1 cytokines would protect CD4 lymphocytes against PCD, whereas type 2 cytokines would not protect against, and could augment, PCD. We suggest that the qualitative alterations of the immune response provoke the CD4 depletion characteristic of HIV disease via type 2 cytokinemediated augmentation of PCD, and are therefore ultimately responsible for the progression of HIV infection. Finally, we summarize recent data showing that three correlates of disease progression: emergence of HIV strains with syncitium-inducing ability (SI), type 1-to-type 2 cytokine shift, and CD4 depletion, are significantly associated, suggesting a complex interconnected virologic-immunologic pathogenesis of HIV infection.

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Cited by 31 publications

References 49 publications

Functional dichotomy of CD4⁺ T helper lymphocytes in asymptomatic human immunodeficiency virus infection

Functional dichotomy of CD4⁺ T helper lymphocytes in asymptomatic human immunodeficiency virus infection

Incidence of Anti HIV Antibodies and Viral Antigen in Standard and Control sera

The breakdown of the cytokine network subsequent to human immunodeficiency virus infection

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Cited by 31 publications

References 49 publications

Functional dichotomy of CD4+ T helper lymphocytes in asymptomatic human immunodeficiency virus infection

Functional dichotomy of CD4+ T helper lymphocytes in asymptomatic human immunodeficiency virus infection

Incidence of Anti HIV Antibodies and Viral Antigen in Standard and Control sera

The breakdown of the cytokine network subsequent to human immunodeficiency virus infection

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Product

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Functional dichotomy of CD4⁺ T helper lymphocytes in asymptomatic human immunodeficiency virus infection

Functional dichotomy of CD4⁺ T helper lymphocytes in asymptomatic human immunodeficiency virus infection