Replication of human immunodeficiency virus type 1 in primary dendritic cell cultures.

Langhoff, Erik; Terwilliger, Ernest F.; Bos, H. J.; Kalland, Karl H.; Poznansky, Mark C.; Bacon, Oliver; Wa, Haseltine

doi:10.1073/pnas.88.18.7998

Cited by 149 publications

(89 citation statements)

References 31 publications

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“…These results appeared to correlate with the greater transcription of HIV genes in 89.6-infected PBMC compared to 89.6-infected DC. In our hands, several of the virus strains tested replicated poorly in DC, including HIV-IIIB, the one strain tested by Patterson & Knight (1987), Langhoff et al (1991), Cameron et al (1992 and ourselves. We observed only marginal p24 antigen production by DC with these strains.…”

Section: Discussionmentioning

confidence: 99%

“…The DC preparations used in these experiments were obtained by metrizamide gradient centrifugation, were partially enriched and contained approximately 50 % monocytes (Knight et al, 1986). Langhoff et al (1991), using a method of enrichment originally described by Young & Steinman (1988), described the susceptibility of DC maintained in PHA-conditioned medium to infection with several HIV clones. These authors reported that fresh DC produced much more virus (>~ 10-fold) than did activated T lymphocytes or monocytes.…”

Section: Discussionmentioning

confidence: 99%

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CD4-independent infection of human peripheral blood dendritic cells with isolates of human immunodeficiency virus type 1

Chehimi

Prakash

Shanmugam

et al. 1993

Journal of General Virology

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

CD4-independent infection of human peripheral blood dendritic cells with isolates of human immunodeficiency virus type 1

Chehimi

Prakash

Shanmugam

et al. 1993

Journal of General Virology

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“…Studies of exogenous infection of dendriiic cells have similarly suffered from the lack of specific dendritic cell markers and incomplete purification. Infection ofdendritic cell-enriched populations has been reported [39][40][41] although the potent APC function of dendritic cells may allow for rapid expansion and infection of trace numbers of Tcells. Although scveraireport.s indicated that epidermal dendriiic ceils (Langerhans ceils) are infected, recent reports find these dendriiic celis to be uninfected [42,43], Our dala would suggest that blood dendritic cells are unlikely to contribute to CD4 loss by infection and direct transmission of virus during lhe initiation of CD4' T cell clonal expansion.…”

Section: Some Implications Of These Findingsmentioning

confidence: 99%

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

Cameron

Forsum

Teppler

et al. 1992

Clinical and Experimental Immunology

116

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SUMMARYWe have considered the possibility that antigen-presenting cells of the dendritic celi lineage may be iniected in vivo and spread HiV-1 al the time dendritic cells initiate the clonal expansion of antigenspecific T cells. Dendritic ceils were isolated from 25 HIV-1-infected subjects (CDC stages II IV). Fewer dendritic eells were recovered from most infected subjects. Reduced numbers of total non-T cells were also found in these patients, so that preferential toss of dendritic cells did not occur.

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“…Several studies demonstrate that blood DCs are susceptible to HIV infection in vitro, 16,17 but the question of infection in vivo has remained controversial. [18][19][20][21] Similarly, there are conflicting reports regarding the ability of DCs from HIV-1-infected patients to stimulate T-lymphocyte proliferation.…”

Section: Introductionmentioning

confidence: 99%

“…Evidence of infection would be important as it would provide a mechanism to explain DC loss and might facilitate infection of T lymphocytes during antigen presentation. Down-regulation of T-lymphocyte stimulatory capacity together with reduced numbers would severely suppress cell-mediated immunity and contribute to the immunosuppression seen in HIV-1 infection.Several studies demonstrate that blood DCs are susceptible to HIV infection in vitro, 16,17 but the question of infection in vivo has remained controversial. [18][19][20][21] Similarly, there are conflicting reports regarding the ability of DCs from HIV-1-infected patients to stimulate T-lymphocyte proliferation.…”

mentioning

confidence: 99%

Dysfunction and infection of freshly isolated blood myeloid and plasmacytoid dendritic cells in patients infected with HIV-1

Donaghy

Gazzard

Gotch

et al. 2003

Blood

242

233

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Recently it has been shown that the 2 populations of blood dendritic cells (DCs), termed plasmacytoid (pcDCs) and myeloid (myDCs), are reduced in HIV-1 infection. This study aimed to determine whether these 2 populations are targets for HIV-1 infection and whether their ability to stimulate T-lymphocyte proliferation is affected. Highly purified populations of myDCs and pcDCs were isolated from the blood of antiretroviral treatmentnaive patients and assessed for the level of HIV provirus by polymerase chain reaction (PCR). We show that both populations are targets for HIV-1 infection as indicated by the presence of provirus in 12 of 14 pcDC and 13 of 14 myDC samples tested. A proportion of this provirus is integrated in myDCs. The ability of both myDCs and pcDCs from HIV-1-infected patients to stimulate allogeneic T-lymphocyte proliferation in a 6-day mixed leukocyte reaction was severely impaired, IntroductionPrimary adaptive immune responses are initiated by dendritic cells (DCs) through the presentation of antigen to T lymphocytes. DCs are also important stimulators of innate immune responses. 1,2 DCs constitute about 1% of the mononuclear cell population of blood and can be divided into 2 major subpopulations that are phenotypically and functionally distinct. 3,4 Myeloid DCs (myDCs) express CD11c, CD13, CD33, and the receptor for granulocyte-macrophage colony-stimulating factor (GM-CSF) and secrete interleukin 12 (IL-12). They are precursors of classical antigen-presenting cells, including Langerhans cells and dermal and interstitial DCs. 5 By contrast, plasmacytoid DCs (pcDCs) are CD11c Ϫ ; lack myeloid markers but express CD68, CD36, IL-3 receptor-␣ (IL-3R␣), immunoglobulin-like transcript 3 (ILT3); and produce high amounts of interferon-␣ (IFN-␣), 6,7 a potent inhibitor of HIV-1 replication. 8 Unlike myDCs, which migrate to the tissues and intercept invading pathogens before migrating to the lymph nodes, pcDCs migrate directly from blood to the secondary lymphoid tissue where they differentiate into cells originally termed plasmacytoid T cells on the basis of their extensive endoplasmic reticulum. 9,10 It has long been known that during HIV-1 infection there is a progressive decline in CD4 T-lymphocyte numbers, and in the later stages of disease there is loss of HIV-specific cytotoxic Tlymphocyte activity. 11 Recently, we and others have reported that there is also a progressive loss in the number of blood DCs. [12][13][14][15] However, to fully understand the role of DCs in the pathogenesis of HIV-1, it is important to determine whether the 2 DC populations are targets for HIV-1 infection and whether their ability to stimulate T lymphocytes in infected individuals is affected. Evidence of infection would be important as it would provide a mechanism to explain DC loss and might facilitate infection of T lymphocytes during antigen presentation. Down-regulation of T-lymphocyte stimulatory capacity together with reduced numbers would severely suppress cell-mediated immunity and contribute to the immunosuppr...

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Replication of human immunodeficiency virus type 1 in primary dendritic cell cultures.

Cited by 149 publications

References 31 publications

CD4-independent infection of human peripheral blood dendritic cells with isolates of human immunodeficiency virus type 1

CD4-independent infection of human peripheral blood dendritic cells with isolates of human immunodeficiency virus type 1

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

Dysfunction and infection of freshly isolated blood myeloid and plasmacytoid dendritic cells in patients infected with HIV-1

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