The role of CD11c+ hepatic dendritic cells in the induction of innate immune responses

Shu, Shang An; Lian, Zhe Xiong; Chuang, Ya Hui; Yang, Guo Xiang; Moritoki, Yuki; Comstock, Sarah S.; Zhong, Ruiqin; Ansari, Aftab A.; Liu, Y.-J.; Gershwin, M. Eric

doi:10.1111/j.1365-2249.2007.03419.x

Cited by 47 publications

(50 citation statements)

References 32 publications

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“…The proliferative capacities of T and B cells were almost similar between NK-depleted mice and control mice (Table 2). However, DCs from NK-depleted mice could not activate allogenic T cells and HBsAg-specific T cells ( [20], and NK cell-derived cytokines are required for the proper functioning of DCs [21,22]. In this study, DCs from NK-depleted mice produced significantly lower levels of IFN-g, TNF-a and IL-12 compared with those produced by DCs of control mice (Fig.…”

Section: Discussionmentioning

confidence: 56%

Impaired dendritic cell functions because of depletion of natural killer cells disrupt antigen-specific immune responses in mice: restoration of adaptive immunity in natural killer-depleted mice by antigen-pulsed dendritic cell

Yoshida

Akbar

Miyake

et al. 2008

Clinical and Experimental Immunology

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SummaryThe primary aim of this study was to evaluate the role of natural killer (NK) cells on antigen-specific adaptive immune responses. After analysing the mechanism of impaired adaptive immune responses of NK-depleted mice, an immune interventional approach was developed to restore adaptive immunity in NK-depleted mice. NK cells were depleted from mice by administration of anti-asialo GM1 antibody (100 ml/mouse), twice, at an interval of 48 h. Hepatitis B surface antigen (HBsAg) was administered intraperitoneally to normal C57BL/6 mice (control mice) and NK-depleted mice. The levels of antibody to HBsAg (anti-HBs) in the sera and HBsAg-specific lymphocytes in the spleen were assessed. The functions of T lymphocytes, B lymphocytes and dendritic cells (DCs) were evaluated in vitro. HBsAg-pulsed DCs were prepared by culturing spleen DCs with HBsAg for 48 h and administered once to NK-depleted mice. The levels of anti-HBs in the sera and HBsAg-specific lymphocytes were significantly lower in NK-depleted mice compared with control mice (P < 0·05). The functions of T and B lymphocytes were similar between control mice and NK-depleted mice. However, the functions of spleen DC and liver DC were significantly lower in NK-depleted mice compared with control mice (P < 0·05). Administration of HBsAg-pulsed DCs, but not HBsAg, induced HBsAg-specific humoral and cellular immune responses in NK-depleted mice. Our study suggests that cross-talk between NK cells and DCs regulates the magnitude of adaptive immunity. In addition, antigenpulsed immunogenic DCs represent potent immune modulator even if subjects with diminished innate immunity.

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Section: Discussionmentioning

confidence: 56%

Impaired dendritic cell functions because of depletion of natural killer cells disrupt antigen-specific immune responses in mice: restoration of adaptive immunity in natural killer-depleted mice by antigen-pulsed dendritic cell

Yoshida

Akbar

Miyake

et al. 2008

Clinical and Experimental Immunology

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“…Collectively, our data therefore suggest that the GPI-based treatment fuels the generation of alternatively activated anti-inflammatory macrophages (aaM/M2) (62) during African trypanosome infection. However, we do not rule out a possible involvement of other cellular players in the observed induction of TNF, IL-6 and IL-12p40 during the course of infection, because dendritic cells as well as adipocytes were reported to be potent producers of proinflammatory cytokines in response to TLR ligands (63,64).…”

Section: Discussionmentioning

confidence: 99%

A Glycosylphosphatidylinositol-Based Treatment Alleviates Trypanosomiasis-Associated Immunopathology

Stijlemans

Baral

Guilliams

et al. 2007

The Journal of Immunology

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The GPI-anchored trypanosome variant surface glycoprotein (VSG) triggers macrophages to produce TNF, involved in trypanosomiasis-associated inflammation and the clinical manifestation of sleeping sickness. Aiming at inhibiting immunopathology during experimental Trypanosoma brucei infections, a VSG-derived GPI-based treatment approach was developed. To achieve this, mice were exposed to the GPI before an infectious trypanosome challenge. This GPI-based strategy resulted in a significant prolonged survival and a substantial protection against infection-associated weight loss, liver damage, acidosis, and anemia; the latter was shown to be Ab-independent and correlated with reduced macrophage-mediated RBC clearance. In addition, GPI-based treatment resulted in reduced circulating serum levels of the inflammatory cytokines TNF and IL-6, abrogation of infection-induced LPS hypersensitivity, and an increase in circulating IL-10. At the level of trypanosomiasis-associated macrophage activation, the GPI-based treatment resulted in an impaired secretion of TNF by VSG and LPS pulsed macrophages, a reduced expression of the inflammatory cytokine genes TNF, IL-6, and IL-12, and an increased expression of the anti-inflammatory cytokine gene IL-10. In addition, this change in cytokine pattern upon GPI-based treatment was associated with the expression of alternatively activated macrophage markers. Finally, the GPI-based treatment also reduced the infection-associated pathology in Trypanosoma congolense and Trypanosoma evansi model systems as well as in tsetse fly challenge experiments, indicating potential field applicability for this intervention strategy.

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“…Hepatic cDCs express higher levels of TLR2 and TLR4 than splenic cDCs. In response to TLR7 and TLR9 activation, hepatic pDCs produce cytokines such as TNF-α, IL-6 and IL-12, whereas in response to TLR2, TLR3 and TLR4 activation hepatic cDCs produce TNF-α and IL-6 [35].…”

Section: Tlr Expression In Hepatic Cell Populationsmentioning

confidence: 99%

Toll-like receptors in acute liver injury and regeneration

Chen

Sun

2011

International Immunopharmacology

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The role of CD11c+ hepatic dendritic cells in the induction of innate immune responses

Cited by 47 publications

References 32 publications

Impaired dendritic cell functions because of depletion of natural killer cells disrupt antigen-specific immune responses in mice: restoration of adaptive immunity in natural killer-depleted mice by antigen-pulsed dendritic cell

Impaired dendritic cell functions because of depletion of natural killer cells disrupt antigen-specific immune responses in mice: restoration of adaptive immunity in natural killer-depleted mice by antigen-pulsed dendritic cell

A Glycosylphosphatidylinositol-Based Treatment Alleviates Trypanosomiasis-Associated Immunopathology

Toll-like receptors in acute liver injury and regeneration

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