Abnormalities of B-Cell Activation and Immunoregulation in Patients with the Acquired Immunodeficiency Syndrome

Lane, H. Clifford; Masur, Henry; Edgar, L C; Whalen, Gail; Rook, Alain H.; Fauci, Anthony S.

doi:10.1056/nejm198308253090803

Cited by 1,510 publications

(627 citation statements)

References 15 publications

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“…Thus the dramatic increase of circulating IgA in HIVinfected subjects is probably related to both a polyclonal activation of B cells, producing mainly the monomeric form IgA1 isotype [23], and a crossing of sIgA from mucosal origin [35]. Our study also demonstrated that the frequency of IgA isotype antibodies to HIV-1 structural proteins was lower in parotid saliva than in serum, but did not decrease during the course of HIV-1 infection.…”

supporting

confidence: 55%

“…The horizontal line corresponds to the level of albumin above which parotid saliva was considered to be contaminated by blood. [23,24], having been proposed as a surrogate marker to follow the course of HIV infection [25]. In this study, parotid saliva was used to evaluate the variation of IgA and IgG concentrations at the mucosal level during HIV-1 infection.…”

Section: Discussionmentioning

confidence: 99%

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Quantification of IgA and IgG and specificities of antibodies to viral proteins in parotid saliva at different stages of HIV-1 infection

Cartry¹,

Moja²,

Quesnel³

et al. 1997

Clinical and Experimental Immunology

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Paired sera and parotid saliva from 75 HIV‐1‐infected patients, divided in three equal groups with CD4+ cell counts > 500, 200–500 and < 200/mm3, respectively, were analysed for IgG, IgA and secretory IgA (sIgA) concentrations and for IgG and IgA antibody directed to HIV‐1. Twenty‐nine age‐matched HIV− subjects were used as controls. In serum the concentrations of immunoglobulins were significantly increased in HIV‐infected subjects compared with controls, and a progressive increase of IgA and sIgA was noticed while the CD4+ cell count decreased. In contrast, concentrations of IgA and sIgA were not different in parotid saliva between the four subject groups. By an ELISA test directed towards HIV‐1 proteins, 73 of the 75 serum specimens from the HIV‐infected subjects (97%) and 43 of the corresponding saliva (57%) were found positive for specific IgA antibodies to HIV‐1, with an even distribution among the three groups of patients. By Western blotting multiple specificities of IgA to HIV‐1 proteins were not frequently found in patients. By contrast, in spite of an IgG concentration in saliva about 100 times lower than that of IgA, reactivities were significantly higher for IgG than for IgA antibodies, especially to env and to pol HIV‐1 products. Altogether, these data suggest that the regulation of IgA production in HIV‐infected subjects is independent in serum and in parotid saliva. This imbalance of IgA/IgG antibodies to HIV‐1 at the mucosal level appears to be a specific feature of HIV‐1 infection, and may raise important issues in terms of local protection after immunization.

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supporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Quantification of IgA and IgG and specificities of antibodies to viral proteins in parotid saliva at different stages of HIV-1 infection

Cartry¹,

Moja²,

Quesnel³

et al. 1997

Clinical and Experimental Immunology

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“…Recently, persistent immune activation, which is described as elevated T-lymphocyte turnover and apoptosis; polyclonal B-cell activation; increased NK-cell activation and turnover; and dendritic cell activation, 7,14,15 was found to be a hallmark of HIV infection. In fact, it is well associated with CD4 1 T cell counts and HIV viral loads.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effects of chloroquine on the activation of plasmacytoid dendritic cells in SIVmac239-infected Chinese rhesus macaques

Xia

Zhang

et al. 2012

Cell Mol Immunol

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It is currently widely accepted that immune activation in HIV-infected individuals leads to a severe loss of CD4 1 T cells and the progression to AIDS. However, the underlying mechanism of this immune activation remains unclear. Experimental data suggest that the activation of plasmacytoid dendritic cells (pDCs) by plasma viremia may play a critical role in HIV-induced immune activation. In this study, we found that the level of immune activation was higher in the late phase of SIVmac239 infection compared with chronic infection, which suggests that immune activation might be related to disease progression in SIVmac239-infected non-human primate models. Our work also showed that chloroquine could effectively inhibit the activation of pDCs in vitro and in vivo. However, chloroquine treatment of SIVmac239-infected macaques had no significant influence on the Cellular composition of peripheral blood in these animals.

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“…4,82 The broad activation of B lymphocytes in HIV infection is wellcharacterized. [3][4][5][7][8][9] This B cell activation, with the expansion of EBV-infected B cell populations, may be the initial steps in B lineage tumorigenesis and may account for the high frequency of oligoclonal lymphoma observed in these patients. 5 Such a broad lymphocyte activation may predispose to the generation of lymphoma even in the absence of EBV infection.…”

Section: Gammopathy and Plasma Cell Tumors In Aidsmentioning

confidence: 99%

“…[1][2][3][4] Although HIV-infected individuals have deficiencies in CD4-positive T helper cells, and thus might be expected to have problems with B cell activation and immunoglobulin secretion, experimental studies of B lymphocytes in HIV infection have revealed polyclonal B cell activation. 3,5 B cells exposed to HIV in vitro may proliferate 6 or become activated and begin secreting immunoglobulin. 4,7,8 HIV-infected T cells can induce contact-dependent but antigen-independent polyclonal activation of B cells.…”

Section: Introductionmentioning

confidence: 99%

Paraproteinemia, plasmacytoma, myeloma and HIV infection

Fiorino

Atac

1997

Leukemia

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We have identified by MEDLINE search the cases of gammaglobinopathy and plasma cell malignancy in HIV-positive patients reported in the English language literature. The average age at presentation among HIV-positive patients with plasma cell disorders is 33 years, far younger than the average age of presentation in the general population. Some of these patients present with transient paraproteinemias, while others have persistent paraproteins, which may or may not be associated with true plasma cell malignancies. In most cases in which it has been examined, the paraprotein contains high-titer anti-HIV activity. The presence of high-titer anti-HIV activity in the paraproteins of AIDS patients suggests that an antigen-driven process in response to HIV infection may contribute to the early development of plasma cell disorders in these patients. Recent work in plasma cell tumorigenesis has indicated that transformation at a single point in the B lymphocyte lineage can give rise to either lymphoma or myeloma, dependent upon environmental factors such as T cell function, which may be required for directing transformed lymphocytes from lymphoma and towards plasma cell differentiation. This may explain why B lineage oncogenesis in AIDS patients favors the development of lymphoma over that of myeloma.

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Abnormalities of B-Cell Activation and Immunoregulation in Patients with the Acquired Immunodeficiency Syndrome

Cited by 1,510 publications

References 15 publications

Quantification of IgA and IgG and specificities of antibodies to viral proteins in parotid saliva at different stages of HIV-1 infection

Quantification of IgA and IgG and specificities of antibodies to viral proteins in parotid saliva at different stages of HIV-1 infection

Inhibitory effects of chloroquine on the activation of plasmacytoid dendritic cells in SIVmac239-infected Chinese rhesus macaques

Paraproteinemia, plasmacytoma, myeloma and HIV infection

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