Aberrant Expression of CD27 and Soluble CD27 (sCD27) in HIV Infection and in AIDS-Associated Lymphoma

Widney, Daniel P.; Gundapp, G; Said, Jonathan; Meijden, M van der; Bonavida, Benjamin; Demidem, Aïcha; Trevisan, Chiara; Taylor, Jeremy M. G.; Detels, Roger; Martı́nez-Maza, Otoniel

doi:10.1006/clim.1999.4782

Cited by 84 publications

(71 citation statements)

References 39 publications

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“…The question was asked whether decreased CD27 expression resulted from a specific lack of CD27 expression on B cells, or a decreased generation of CD27-expressing (memory) B cells. Starting with the first possibility, we did not find significantly increased levels of sCD27, consistent with proteolytic cleavage, among the CGD patients, nor did we find intracellular retention of CD27 protein (17,25,26). Next, it was determined whether CD27-negative B cells had previously expressed CD27, as a consequence of differentiation into memory B cells, but that continued expression of this marker was negatively influenced by the defective NADPH oxidase system in CGD B cells.…”

Section: Discussionmentioning

confidence: 79%

“…The first approach taken was based on the observation that in immune-mediated disorders and malignancies, CD27 is proteolytically cleaved from the surface of cells, a process common to members of the TNF superfamily (17,25,26). This possibility was evaluated by measuring sCD27 levels in plasma or serum of 25 CGD patients, and comparing these with the levels found in a reference group of 30 HC.…”

Section: The Mechanism Of Decreased Cd27-positive B Cellsmentioning

confidence: 99%

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Patients with Chronic Granulomatous Disease Have a Reduced Peripheral Blood Memory B Cell Compartment

Bleesing

Souto-Carneiro

Savage

et al. 2006

The Journal of Immunology

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In this study, we have identified an altered B cell compartment in patients with chronic granulomatous disease (CGD), a disorder of phagocyte function, characterized by pyogenic infections and granuloma formation caused by defects in NADPH activity. This is characterized by an expansion of CD5-expressing B cells, and profound reduction in B cells expressing the memory B cell marker, CD27. Both findings were independent of the age, genotype, and clinical status of the patients, and were not accompanied by altered CD5 and CD27 expression on T cells. Focusing on CD27-positive B cells, considered to be memory cells based on somatically mutated Ig genes, we found that the reduction was not caused by CD27 shedding or abnormal retention of CD27 protein inside the cell. Rather, it was determined that CD27-negative B cells were, appropriately, CD27 mRNA negative, consistent with a naive phenotype, whereas CD27-positive B cells contained abundant CD27 mRNA and displayed somatic mutations, consistent with a memory B cell phenotype. Thus, it appears that CGD is associated with a significant reduction in the peripheral blood memory B cell compartment, but that the basic processes of somatic mutation and expression of CD27 are intact. X-linked carriers of CGD revealed a significant correlation between the percentage of CD27-positive B cells and the percentage of neutrophils with normal NADPH activity, reflective of the degree of X chromosome lyonization. These results suggest a role for NADPH in the process of memory B cell formation, inviting further exploration of secondary Ab responses in CGD patients.

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Section: Discussionmentioning

confidence: 79%

Section: The Mechanism Of Decreased Cd27-positive B Cellsmentioning

confidence: 99%

Patients with Chronic Granulomatous Disease Have a Reduced Peripheral Blood Memory B Cell Compartment

Bleesing

Souto-Carneiro

Savage

et al. 2006

The Journal of Immunology

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“…In general, this molecule is expressed on strongly activated T and B cells (4) and some hematological malignancies, such as non-Hodgkin's lymphoma (42). In fact, when PBMCs were isolated and stimulated with phytohemagglutinin, approximately 18 and 32% of the cells became CD70 ϩ after 7 and 12 days of cultivation, respectively (data not shown).…”

Section: Vol 82 2008 Cd70 Expression On Htlv-1-carrying T-cell Linementioning

confidence: 95%

Highly Enhanced Expression of CD70 on Human T-Lymphotropic Virus Type 1-Carrying T-Cell Lines and Adult T-Cell Leukemia Cells

Baba

Okamoto

Hamasaki

et al. 2008

J Virol

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Human T-lymphotropic virus type 1 (HTLV-1) is the etiologic agent of adult T-cell leukemia (ATL).In Japan, the number of HTLV-1 carriers is estimated to be 1.2 million and more than 700 cases of ATL have been diagnosed every year. Considering the poor prognosis and lack of curative therapy of ATL, it seems mandatory to establish an effective strategy for the treatment of ATL. In this study, we attempted to identify the cell surface molecules that will become suitable targets of antibodies for anti-ATL therapy. The expression levels of approximately 40,000 host genes of three human T-cell lines carrying HTLV-1 genomes were analyzed by oligonucleotide microarray and compared with the expression levels of the genes in an HTLV-1-negative T-cell line. The HTLV-1-carrying T-cell lines used for experiments had totally different expression patterns of viral genome. Among the genes evaluated, the expression levels of 108 genes were found to be enhanced more than 10-fold in all of the T-cell lines examined and 11 of the 108 genes were considered to generate the proteins expressed on the cell surface. In particular, the CD70 gene was upregulated more than 1,000-fold and the enhanced expression of the CD70 molecule was confirmed by laser flow cytometry for various HTLV-1-carrying T-cell lines and primary CD4 ؉ T cells isolated from acute-type ATL patients. Such expression was not observed for primary CD4 ؉ T cells isolated from healthy donors. Since CD70 expression is strictly restricted in normal tissues, such as highly activated T and B cells, CD70 appears to be a potential target for effective antibody therapy against ATL.

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“…However, we did not observe a similar positive association between E. coli-induced IL-23 or baseline CD16 ϩ monocyte frequency and activated CD4 ϩ or CD8 ϩ T cell frequencies. The positive associations with plasma sCD27 levels, but lack of association with peripheral blood T cell activation, may be due to the fact that sCD27 is shed from multiple activated cell types, including both T cells and B cells (45)(46)(47). In the setting of untreated infection, therefore, increased proinflammatory monocyte frequencies and cytokine production may reflect more generalized or complex immune activation processes than are reflected by measuring T cell activation markers alone.…”

Section: Fig 5 Percentages Of Cd16mentioning

confidence: 99%

Increased Escherichia coli-Induced Interleukin-23 Production by CD16⁺Monocytes Correlates with Systemic Immune Activation in Untreated HIV-1-Infected Individuals

Manuzak

Dillon

Lee

et al. 2013

J Virol

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The level of microbial translocation from the intestine is increased in HIV-1 infection. Proinflammatory cytokine production by peripheral antigen-presenting cells in response to translocated microbes or microbial products may contribute to systemic immune activation, a hallmark of HIV-1 infection. We investigated the cytokine responses of peripheral blood myeloid dendritic cells (mDCs) and monocytes to in vitro stimulation with commensal enteric Escherichia coli in peripheral blood mononuclear cells (PBMC) from untreated HIV-1-infected subjects and from uninfected controls. Levels of interleukin 23 (IL-23) produced by PBMC from HIV-1-infected subjects in response to E. coli stimulation were significantly higher than those produced by PBMC from uninfected subjects. IL-23 was produced primarily by CD16 ؉ monocytes. This subset of monocytes was increased in frequency and expressed higher levels of Toll-like receptor 4 (TLR4) in HIV-1-infected individuals than in controls. Blocking TLR4 on total CD14؉ monocytes reduced IL-23 production in response to E. coli stimulation. Levels of soluble CD27, an indicator of systemic immune activation, were elevated in HIV-1-infected subjects and were associated with the percentage of CD16؉ monocytes and the induction of IL-23 by E. coli, providing a link between these parameters and systemic inflammation. Taken together, these results suggest that IL-23 produced by CD16؉ monocytes in response to microbial stimulation may contribute to systemic immune activation in HIV-1-infected individuals.

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Aberrant Expression of CD27 and Soluble CD27 (sCD27) in HIV Infection and in AIDS-Associated Lymphoma

Cited by 84 publications

References 39 publications

Patients with Chronic Granulomatous Disease Have a Reduced Peripheral Blood Memory B Cell Compartment

Patients with Chronic Granulomatous Disease Have a Reduced Peripheral Blood Memory B Cell Compartment

Highly Enhanced Expression of CD70 on Human T-Lymphotropic Virus Type 1-Carrying T-Cell Lines and Adult T-Cell Leukemia Cells

Increased Escherichia coli-Induced Interleukin-23 Production by CD16⁺Monocytes Correlates with Systemic Immune Activation in Untreated HIV-1-Infected Individuals

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Aberrant Expression of CD27 and Soluble CD27 (sCD27) in HIV Infection and in AIDS-Associated Lymphoma

Cited by 84 publications

References 39 publications

Patients with Chronic Granulomatous Disease Have a Reduced Peripheral Blood Memory B Cell Compartment

Patients with Chronic Granulomatous Disease Have a Reduced Peripheral Blood Memory B Cell Compartment

Highly Enhanced Expression of CD70 on Human T-Lymphotropic Virus Type 1-Carrying T-Cell Lines and Adult T-Cell Leukemia Cells

Increased Escherichia coli-Induced Interleukin-23 Production by CD16+Monocytes Correlates with Systemic Immune Activation in Untreated HIV-1-Infected Individuals

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Increased Escherichia coli-Induced Interleukin-23 Production by CD16⁺Monocytes Correlates with Systemic Immune Activation in Untreated HIV-1-Infected Individuals