Dendritic cell subsets in health and disease

Ueno, Hideki; Klechevsky, Eynav; Morita, Rimpei; Aspord, Caroline; Cao, Tinghua; Matsui, Toshimichi; Pucchio, Tiziana Di; Connolly, John E.; Fay, Joseph W.; Pascual, Virginia; Palucka, A. Karolina; Banchereau, Jacques

doi:10.1111/j.1600-065x.2007.00551.x

Cited by 382 publications

(384 citation statements)

References 369 publications

(640 reference statements)

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“…They are found in all tissues including blood and lymphoid organs [6][7][8][9][10][11][12]. In peripheral tissues, DCs are found in an immature stage specialized in the capture of antigens.…”

Section: Introductionmentioning

confidence: 99%

Dendritic cells and cytokines in human inflammatory and autoimmune diseases

Blanco

Palucka

Pascual

et al. 2008

Cytokine & Growth Factor Reviews

459

362

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Dendritic cells (DCs) produce cytokines and are susceptible to cytokine-mediated activation. Thus, interaction of resting immature DCs with TLR ligands, for example nucleic acids, or with microbes leads to a cascade of pro-inflammatory cytokines and skewing of T cell responses. Conversely, several cytokines are able to trigger DC activation (maturation) via autocrine, for example TNF and plasmacytoid DCs, and paracrine, for example type I IFN and myeloid DCs, pathways. By controlling DC activation, cytokines regulate immune homeostasis and the balance between tolerance and immunity. The increased production and/or bioavailability of cytokines and associated alterations in DC homeostasis have been implicated in various human inflammatory and autoimmune diseases. Targeting these cytokines with biological agents as already is the case with TNF and IL-1 represents a success of immunology and the coming years will expand the range of cytokines as therapeutic targets in autoinflammatory and autoimmune pathology.

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Section: Introductionmentioning

confidence: 99%

Dendritic cells and cytokines in human inflammatory and autoimmune diseases

Blanco

Palucka

Pascual

et al. 2008

Cytokine & Growth Factor Reviews

459

362

View full text Add to dashboard Cite

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“…D endritic cells (DC) are the most potent APCs in the immune system and act as a link between innate and adaptive immunity (1,2). DC reside as immature cells in peripheral tissues, where they monitor their environment for danger signals, capture pathogens, and migrate to draining lymph nodes.…”

mentioning

confidence: 99%

HIV-1 Capture and Antigen Presentation by Dendritic Cells: Enhanced Viral Capture Does Not Correlate with Better T Cell Activation

Rodriguez-Plata

Urrutia

Cardinaud

et al. 2012

The Journal of Immunology

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During HIV-1 infection, dendritic cells (DC) facilitate dissemination of HIV-1 while trying to trigger adaptive antiviral immune responses. We examined whether increased HIV-1 capture in DC matured with LPS results in more efficient Ag presentation to HIV-1–specific CD4+ and CD8+ T cells. To block the DC-mediated trans-infection of HIV-1 and maximize Ag loading, we also evaluated a noninfectious integrase-deficient HIV-1 isolate, HIVNL4-3ΔIN. We showed that higher viral capture of DC did not guarantee better Ag presentation or T cell activation. Greater HIVNL4-3 uptake by fully LPS-matured DC resulted in higher viral transmission to target cells but poorer stimulation of HIV-1–specific CD4+ and CD8+ T cells. Conversely, maturation of DC with LPS during, but not before, viral loading enhanced both HLA-I and HLA-II HIV-1–derived Ag presentation. In contrast, DC maturation with the clinical-grade mixture consisting of IL-1β, TNF-α, IL-6, and PGE2 during viral uptake only stimulated HIV-1–specific CD8+ T cells. Hence, DC maturation state, activation stimulus, and time lag between DC maturation and Ag loading impact HIV-1 capture and virus Ag presentation. Our results demonstrate a dissociation between the capacity to capture HIV-1 and to present viral Ags. Integrase-deficient HIVNL4-3ΔIN was also efficiently captured and presented by DC through the HLA-I and HLA-II pathways but in the absence of viral dissemination. HIVNL4-3ΔIN seems to be an attractive candidate to be explored. These results provide new insights into DC biology and have implications in the optimization of DC-based immunotherapy against HIV-1 infection.

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“…cDCs work as powerful APCs and effi cient tissue sentinels that preferentially express TLR 3, 4, 5, 6 and 8, which results in the production of large amounts of TNF-α, IL-1, IL-6 and IL-10 upon activation (Liu 2005;Diebold 2008). cDC can be further subdivided in different subsets depending on whether they reside in peripheral tissues, secondary lymphoid organs or circulate in blood stream, in addition circulating cDCs express different surface markers such as CD1a, CD16 and CD34 that allow even further differentiation (Ueno, Klechevsky et al 2007). Conversely, pDCs can circulate in the blood stream and express low levels of MHC class II, CD86, undetectable levels of CD 80 and have a limited capacity to activate T lymphocytes (Liu 2005).…”

Section: Molecular Interactions At the Dc-t Cell Interface That Contrmentioning

confidence: 99%

Contribution of dendritic cell/T cell interactions to triggering and maintaining autoimmunity

2011

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Under healthy conditions, there is a balance between tolerance to self-tissue constituents and immunity against foreign antigens. Autoimmunity diseases (AD) take place when that equilibrium is disrupted and the immune response is directed to self-antigens, leading to injury or destruction of host tissues. The mechanisms conducing to the loss of immune tolerance remain largely unknown. The recent appearance of biological therapies has contributed to signifi cant reduction in morbidity. However, currently available therapies are associated with important side effects and work only as palliative treatments. Dendritic cells (DCs) have emerged as key players in developing and maintaining adaptive immunity due to their capacity to prime and modulate T cell function. Therefore, because DCs work as central modulators of immune tolerance, it is likely that alterations in their function can lead to the onset of autoimmune-infl ammatory diseases. By modulating DC function, novel pathways in antigen-specifi c tolerance could be established. In this article, the possible contribution of altered DC-T cell interactions to the onset of autoimmunity are discussed. In addition, we expand on the notion that some of the functions of these cells could be relevant targets for intervening therapies aimed to restore the balance or even prevent the loss of tolerance.

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Dendritic cell subsets in health and disease

Cited by 382 publications

References 369 publications

Dendritic cells and cytokines in human inflammatory and autoimmune diseases

Dendritic cells and cytokines in human inflammatory and autoimmune diseases

HIV-1 Capture and Antigen Presentation by Dendritic Cells: Enhanced Viral Capture Does Not Correlate with Better T Cell Activation

Contribution of dendritic cell/T cell interactions to triggering and maintaining autoimmunity

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