Conjugates of dendritic cells and memory T lymphocytes from skin facilitate productive infection with HIV-1

Pope, Melissa; Betjes, Michiel G. H.; Romani, Nikolaus; Hirmand, Haideh; Cameron, Paul; Hoffman, Lloyd A.; Gezelter, Stuart; Steinman, Ralph M.

doi:10.1016/0092-8674(94)90418-9

Cited by 470 publications

(382 citation statements)

References 50 publications

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“…We demonstrated that DCs but not M⌽s exhibit an extraordinary capacity to transmit virus to CD4 ϩ T cells, consistent with previous studies (16,17,28,74,75). In DC:T cell cocultures, viral production increased 1088-fold compared with that in DCs alone.…”

Section: Discussionsupporting

confidence: 79%

Opposite Effects of IL-10 on the Ability of Dendritic Cells and Macrophages to Replicate Primary CXCR4-Dependent HIV-1 Strains

Ancuța

Bakri

Chomont

et al. 2001

The Journal of Immunology

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We investigated the effect of IL-10 on replication of primary CXCR4-dependent (X4) HIV-1 strains by monocyte-derived dendritic cells (DCs) and macrophages (MΦs). MΦs efficiently replicated CXCR4-dependent HIV-1 (X4 HIV-1) strains NDK and VN44, whereas low levels of p24 were detected in supernatants of infected DCs. IL-10 significantly increased X4 HIV-1 replication by DCs but blocked viral production by MΦs as determined by p24 levels and semiquantitative nested PCR. IL-10 up-regulated CXCR4 mRNA and protein expression on DCs and MΦs, suggesting that IL-10 enhances virus entry in DCs but blocks an entry and/or postentry step in MΦs. The effect of IL-10 on the ability of DCs and MΦs to transmit virus to autologous CD4+ T lymphocytes was investigated in coculture experiments. DCs exhibited a greater ability than did MΦs to transmit a vigorous infection to CD4+ T cells despite their very low replication capacity. IL-10 had no effect on HIV-1 replication in DC:T cell cocultures but markedly decreased viral production in MΦ:T cell cocultures. These results demonstrate that IL-10 has opposite effects on the replication of primary X4 HIV-1 strains by DCs and MΦs. IL-10 increases X4-HIV-1 replication in DCs but does not alter their capacity to transmit virus to CD4+ T lymphocytes. These findings suggest that increased levels of IL-10 observed in HIV-1-infected patients with disease progression may favor the replication of X4 HIV-1 strains in vivo.

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Section: Discussionsupporting

confidence: 79%

Opposite Effects of IL-10 on the Ability of Dendritic Cells and Macrophages to Replicate Primary CXCR4-Dependent HIV-1 Strains

Ancuța

Bakri

Chomont

et al. 2001

The Journal of Immunology

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“…Although specific DC/T cell interactions in the periphery have not yet been observed in vivo (except in lymph nodes [26]), the emigration of DC/memory T cell conjugates from skin cultures [24,25] strongly suggests that such interactions could occur. CD40L regulates DC migration from skin to draining lymph node via TNF- § production [27].…”

Section: Discussionmentioning

confidence: 99%

LIGHT, a new TNF superfamily member, is essential for memory T helper cell‐mediated activation of dendritic cells

et al. 2003

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LIGHT is a recently identified member of the TNF superfamily that is up-regulated on activated T cells and can cooperate with CD40L to condition DC for the priming of CTL. In this report, we show that an intracellular pool of LIGHT is found selectively in some CD45RA -CD27 + CD4 + "central" memory T cells and to a greater extent in some CD45RA -CD27 -CD4 + effector memory T cells. LIGHT, like CD40L, is rapidly up-regulated on memory CD4 + T cells upon activation. Unlike CD40L, LIGHT up-regulation on naive T cells is delayed. Stimulation of DC with each subset of memory T cells in the presence of superantigen revealed that CD40L and LIGHT are required for optimal secretion of IL-12. Moreover, effector memory T cells, which can interact with DC in peripheral tissues, contribute to CCR7 induction on DC. LIGHT and CD40L can also regulate IL-12 production by CCR7 + DC capable of migration to lymph nodes. These data suggest that both LIGHT and CD40L may be involved in the maintenance or reactivation of secondary Th1 responses.

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“…The knowledge derived from DC biology about innate and adaptive immune responses, and about their roles in medicine, helps one to think more concretely about the specific driving forces for disease, both pathogenesis and the design of preventions and treatments, e.g. in HIV-1 infection [88,95,96].…”

Section: Dendritic Cells As a Pivotal Force In Medicinementioning

confidence: 99%

Dendritic cells: Understanding immunogenicity

2007

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The impetus for the discovery of dendritic cells in 1972 was to understand immunogenicity, the capacity of an antigenic substance to provoke immunity. During experiments to characterize "accessory" cells that enhanced immunity, we spotted unusual stellate cells in mouse spleen. They had a distinct capacity to form and retract processes or dendrites and were named dendritic cells (DC). DC proved to be different from other cell types and to be peculiarly immunogenic when loaded with antigens. When Langerhans cells were studied, immunogenicity was found to involve two steps: antigen presentation by immature DC and maturation to elicit immunity. Antigenbearing DC were also immunogenic in vivo and were therefore termed "nature's adjuvants". Several labs then learned to generate large numbers of DC from progenitors, which accelerated DC research. Tolerogenicity via DC, including the control of foxp3 + suppressor T cells, was recently discovered. Two areas of current research that I find intriguing are to identify mechanisms for antigen uptake and processing, and for the control of different types of immunity and tolerance. These subjects should be studied in vivo with clinically relevant antigens, so that the activities of DC can be better integrated into the prevention and treatment of disease in patients.

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Conjugates of dendritic cells and memory T lymphocytes from skin facilitate productive infection with HIV-1

Cited by 470 publications

References 50 publications

Opposite Effects of IL-10 on the Ability of Dendritic Cells and Macrophages to Replicate Primary CXCR4-Dependent HIV-1 Strains

Opposite Effects of IL-10 on the Ability of Dendritic Cells and Macrophages to Replicate Primary CXCR4-Dependent HIV-1 Strains

LIGHT, a new TNF superfamily member, is essential for memory T helper cell‐mediated activation of dendritic cells

Dendritic cells: Understanding immunogenicity

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