During HIV-1 infection most blood dendritic cells are not productively infected and can induce allogeneic CD4+ T cells clonal expansion

Cameron, Paul; Forsum, Urban; Teppler, Hedy; Granelli‐Piperno, Angela; Steinman, Ralph M.

doi:10.1111/j.1365-2249.1992.tb03066.x

Cited by 116 publications

(25 citation statements)

References 45 publications

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“…6 Similarly, HIV-infected DCs were poor stimulators of allogeneic T cells. 5 Our results do not exclude the possibility that direct infection plays a role in vivo; however, the percentage of HIV-infected DCs in vivo is always very low, 36,37 making it highly unlikely that HIV infection of DCs could explain the extent of defective APC function in HIV-infected donors. Our results thus provide an alternative mechanism, in which defective APC function arises from CD4 ϩ T-cell dysregulation, without a requirement of infection of the affected APCs.…”

Section: Discussionmentioning

confidence: 68%

Failure of HIV-exposed CD4+ T cells to activate dendritic cells is reversed by restoration of CD40/CD154 interactions

Zhang

Lifson

Chougnet

2006

Blood

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Because interactions between activated CD4 ؉ T cells and antigen-presenting cells (APCs) are crucial for optimal APC function, defective CD4 ؉ T-cell activation may contribute to APC dysregulation in HIV infection. Here, we show that CD4 ؉ T cells exposed during stimulation to noninfectious HIV having functional envelope glycoproteins failed to provide activation signals to autologous dendritic cells (DCs). Consequently, important DC functions, including production of immunoregulatory cytokines (interleukin-12 p40 and interleukin-10) and up-regulation of costimulatory molecules (CD86, CD40, CD83), as well as the capacity to stimulate naive allogeneic T cells, were all adversely affected. The blunted upregulation of CD154 in CD4 ؉ T cells that were activated in the presence of noninfectious viruses is likely to be the major underlying mechanism for these defects. Addition of recombinant trimeric CD154 could restore production of cytokines by DCs cocultured with HIV-exposed T cells. Moreover, the functional defects mediated by coculture with HIV-exposed T cells were similar to those following antibody blockade of CD40-CD154 interactions. HIV-mediated blunted CD154 expression may thus play an important role in the suppression of cell-mediated immunity seen in HIV

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Section: Discussionmentioning

confidence: 68%

Failure of HIV-exposed CD4+ T cells to activate dendritic cells is reversed by restoration of CD40/CD154 interactions

Zhang

Lifson

Chougnet

2006

Blood

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“…Highly purified populations of myeloid and plasmacytoid DCs from blood of untreated patients contained HIV-1 provirus (25), whereas no proviral DNA or viral particles were found in peripheral blood DCs from HIV-1-infected individuals treated with highly active antiretroviral therapy (26). In vivo, after seroconversion, when anti-HIV-IgGs appeared, productively infected DCs are rarely detected (27).…”

Section: H Uman Immunodeficiency Virus Attaches To Immature Dendriticmentioning

confidence: 99%

IgG Opsonization of HIV Impedes Provirus Formation in and Infection of Dendritic Cells and Subsequent Long-Term Transfer to T Cells

Wilflingseder

Bánki

Garcia

et al. 2007

The Journal of Immunology

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Already at initial phases of infection, HIV is coated with complement fragments. During the chronic phase, when HIV-specific IgGs appear, the virus circulates immune complexed with IgG and complement. Thus, we studied the interaction of dendritic cells (DCs) and DC-T cell cocultures with complement (C)-opsonized and C-IgG-opsonized HIV. HIV infection of monocyte-derived DCs and circulating BDCA-1-positive DCs was significantly reduced upon the presence of virus-specific but non-neutralizing IgGs. DCs exposed to C-Ig-HIV or IgG-opsonized HIV showed an impaired provirus formation and p24 production and a decreased transmission rate to autologous nonstimulated T cells upon migration along a chemokine gradient. This reduced infectivity was also observed in long-term experiments, when T cells were added delayed to DCs exposed to IgG-coated HIV without migration. Similar kinetics were seen when sera from HIV-1-infected individuals before and after seroconversion were used in infection assays. Both C- and C-IgG-opsonized HIV were captured and targeted to a tetraspanin-rich endosome in immature DCs, but differed with respect to MHC class II colocalization. The reduced infection by IgG-opsonized HIV is possibly due to interactions of virus-bound IgG with FcγRIIb expressed on DCs. Therefore, the intracellular fate and transmission of immune-complexed HIV seems to differ depending on time and opsonization pattern.

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“…97,98 This decreased expression of HIV receptor and coreceptors has been implicated in less productive HIV replication in DCs as compared with CD4 + T cells. 99 Apart from these HIV receptor and coreceptor, DCs also possess C-type lectin receptors (CLRs). One such CLR is DC-SIGN, which is able to interact with HIV in vivo and are thus suggested to play a key role in HIV dissemination by DC in vivo.…”

Section: Role Of Dendritic Cells In Hiv Infectionmentioning

confidence: 99%

Immunobiology of human imunodeficiency virus infection

Tripathi¹,

Agrawal²

2007

Indian J Med Microbiol

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The copies of the journal to members of the association are sent by ordinary post. The editorial board, association or publisher will not be responsible for non-receipt of copies. If any of the members wish to receive the copies by registered post or courier, kindly contact the journal's / publisher's offi ce. If a copy returns due to incomplete, incorrect or changed address of a member on two consecutive occasions, the names of such members will be deleted from the mailing list of the journal. Providing complete, correct and up-to-date address is the responsibility of the members. Copies are sent to subscribers and members directly from the publisher's address; it is illegal to acquire copies from any other source. If a copy is received for personal use as a member of the association/society, one cannot resale or giveaway the copy for commercial or library use. AbstractAfter the discovery of human immunodeÞ ciency virus (HIV) and its role in the causation of most devastating epidemic acquired immune deÞ ciency syndrome (AIDS), there has been an increasing trend to decipher the mechanism of infection and to understand why it cannot be controlled by our immune system. By evolution, our immune system has been empowered and enough trained to recognize, elicit immune response and remove antigens and pathogens from the body. Simultaneously, HIV has also gained enough mechanism to escape the natural immune response. On one hand, it downregulates HLA class I antigens, which may present viral antigens to speciÞ c CD8 + T cells; on the other hand, the viral genome get mutated very readily under the selection pressure of speciÞ c cytotoxic T lymphocytes. The high mutation rate and convertibility of its genotype makes it a moving target and poses a prime hurdle in vaccine development. This review explains how HIV enters into the cell, how it resists the host immune response and how HIV manages to escape from it and establish in the human body.

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During HIV-1 infection most blood dendritic cells are not productively infected and can induce allogeneic CD4+ T cells clonal expansion

Cited by 116 publications

References 45 publications

Failure of HIV-exposed CD4+ T cells to activate dendritic cells is reversed by restoration of CD40/CD154 interactions

Failure of HIV-exposed CD4+ T cells to activate dendritic cells is reversed by restoration of CD40/CD154 interactions

IgG Opsonization of HIV Impedes Provirus Formation in and Infection of Dendritic Cells and Subsequent Long-Term Transfer to T Cells

Immunobiology of human imunodeficiency virus infection

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