Dendritic Cell and NK Cell Reciprocal Cross Talk Promotes Gamma Interferon-Dependent Immunity to Blood-Stage<i>Plasmodium chabaudi</i>AS Infection in Mice

Ing, Rebecca; Stevenson, Mary M.

doi:10.1128/iai.00994-08

Cited by 83 publications

(94 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A line of evidence indicates that NK cells can regulate DC function and that NK-DC cross-regulation plays an important role in dictating the quality and the quantity of the adaptive immune responses (16)(17)(18)(19)(20)(21). A recent study showed that NK cells can enhance the capacity of DC to present parasitic Ags via the NKG2D receptor pathway (21).…”

mentioning

confidence: 99%

NK Cells Promote Type 1 T Cell Immunity through Modulating the Function of Dendritic Cells during Intracellular Bacterial Infection

Jiao

Gao

Joyee

et al. 2011

The Journal of Immunology

View full text Add to dashboard Cite

Dendritic cells (DC) play a key role in establishing protective adaptive immunity in intracellular bacterial infections, but the cells influencing DC function in vivo remain unclear. In this study, we investigated the role of NK cells in modulating the function of DC using a murine Chlamydia infection model. We found that the NK cell-depleted mice showed exacerbated disease after respiratory tract Chlamydia muridarum infection, which was correlated with altered T cell cytokine profile. Furthermore, DC from C. muridarum-infected NK-depleted mice (NK−DC) exhibited a less mature phenotype compared with that of DC from the infected mice without NK depletion (NK+DC). NK−DC produced significantly lower levels of both IL-12 and IL-10 than those of NK+DC. Moreover, NK−DC showed reduced ability to direct primary and established Ag-specific Th1 CD4+ T cell responses in DC–T coculture systems. More importantly, adoptive transfer of NK−DC, in contrast to NK+DC, failed to induce type 1 protective immunity in recipients after challenge infection. Finally, NK cells showed strong direct enhancing effect on IL-12 production by DC in an NK–DC coculture system, which was partially reduced by blocking NKG2D receptors signaling and virtually abolished by neutralizing IFN-γ activity. The data demonstrate a critical role of NK cells in modulating DC function in an intracellular bacterial infection.

show abstract

mentioning

confidence: 99%

NK Cells Promote Type 1 T Cell Immunity through Modulating the Function of Dendritic Cells during Intracellular Bacterial Infection

Jiao

Gao

Joyee

et al. 2011

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…NK cells display powerful cytotoxic activities once activated, and are potent producers of pro-inflammatory cytokines including IFN-γ and TNF-α which can contribute to the modulation of adaptive immune responses and direct anti-tumour effects (99)(100)(101) . In the context of inflammatory disease, NK cells have been implicated in the pathogenesis of inflammatory bowel disease and psoriasis (102,103) .…”

Section: Natural Killer Cellsmentioning

confidence: 99%

Obesity-associated cancer: an immunological perspective

et al. 2015

View full text Add to dashboard Cite

Epidemiological studies have established an association between obesity, insulin resistance, type 2 diabetes and a number of cancer types. Research has focused predominantly on altered endocrine factors, growth factors and signalling pathways, with little known in man about the immune involvement in the relevant pathophysiological processes. Moreover, in an era of exciting new breakthroughs in cancer immunotherapy, there is also a need to study the safety and efficacy of immunotherapeutics in the complex setting of inflammatory-driven obesityassociated cancer. This review addresses key immune cell subsets underpinning obesityassociated inflammation and describes how such immune compartments might be targeted to prevent and treat obesity-associated cancer. We propose that the modulation, metabolism, migration and abundance of pro-and anti-inflammatory cells and tumour-specific T cells might be therapeutically altered to both restore immune balance, alleviating pathological inflammation, and to improve anti-tumour immune responses in obesity-associated cancer. Obesity: Cancer: Lymphocytes: Immunotherapeutics: InflammationThe burgeoning global health burden of obesity is of grave concern, affecting over half a billion adults worldwide, with approximately 3·5 million attributable deaths each year (1) . Despite national and international interventions to promote a healthy diet and lifestyle, recent reports predict that global obesity rates show no signs of abating, with predictions that half of all adults will be overweight or obese by 2030 (WHO). The worldwide prevalence of obesity almost doubled in the period 1980-2008. In 1980, 5 % of men and 8 % of women were obese and by 2008, these rates were 10 and 14 %, respectively. In many areas of the western world, the overweight phenotype is now the most prevalent body type. For example, in the USA in 2010 the prevalence of a BMI ≥ 25 was 69·2 %, with 35·9 % of people being obese (BMI ≥ 30) (2)

show abstract

“…Virtually all NK cells in the LN belong to the CD56 bright CD16 2 compartment [35], which respond very efficiently to DC-derived cytokines by proliferation and IFN-c production [33,[36][37][38][39][40][41]. In turn, IFN-c promotes DC maturation and sustains Th1 immune responses by providing a conditioning signal that increases the capacity of DC to produce interleukin (IL)212 [21][22][23]42]. In contrast, the CD56 dim CD16 1 NK cell subset enriched in peripheral blood expresses homing receptors for inflamed tissues and rapidly mediates cytotoxicity, which can be enhanced by DC-derived IL-12 [38,41].…”

Section: Introductionmentioning

confidence: 99%

“…In the early phases of an immune response, DC encounter LN-NK cells, that is, before antigen-driven activation of na€ ıve T cells [23,34]. NK cells comprise various subsets that differ in function, phenotype, and tissue localization.…”

Section: Introductionmentioning

confidence: 99%

“…These include maturation of dendritic cells (DC), migration of DC to draining lymph nodes (LN), recruitment of T, B, and natural killer (NK) cells by releasing chemokines, activation of NK cells to produce interferon-gamma (IFN-c), being essential for Th1 priming [21][22][23], and finally antigen presentation and costimulation. This results in clonal expansion and differentiation of naive toward memory/effector T cells [24][25][26][27].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Mesenchymal Stromal Cells Prevent Allostimulation In Vivo and Control Checkpoints of Th1 Priming: Migration of Human DC to Lymph Nodes and NK Cell Activation

et al. 2015

View full text Add to dashboard Cite

Although the immunomodulatory potency of mesenchymal stromal cells (MSC) is well established, the mechanisms behind are still not clear. The crosstalk between myeloid dendritic cells (mDC) and natural killer (NK) cells and especially NK cell-derived interferon-gamma (IFN-c) play a pivotal role in the development of type 1 helper (Th1) cell immune responses. While many studies explored the isolated impact of MSC on either in vitro generated DC, NK, or T cells, there are only few data available on the complex interplay between these cells. Here, we investigated the impact of MSC on the functionality of human mDC and the consequences for NK cell and Th1 priming in vitro and in vivo. In critical limb ischemia patients, who have been treated with allogeneic placenta-derived mesenchymal-like stromal cells (PLX-PAD), no in vivo priming of Th1 responses toward the major histocompatibility complex (MHC) mismatches could be detected. Further in vitro studies revealed that mDC reprogramming could play a central role for these effects. Following crosstalk with MSC, activated mDC acquired a tolerogenic phenotype characterized by reduced migration toward CCR7 ligand and impaired ability to stimulate NK cell-derived IFN-c production. These effects, which were strongly related to an altered interleukin (IL)212/IL-10 production by mDC, were accompanied by an effective prevention of Th1 priming in vivo. Our findings provide novel evidence for the regulation of Th1 priming by MSC via modulation of mDC and NK cell crosstalk and show that off-the-shelf produced MHCmismatched PLX-PAD can be used in patients without any sign of immunogenicity. STEM CELLS 2015;33:3087-3099 SIGNIFICANCE STATEMENTWhile MHC-mismatched mesenchymal stromal cells (MSC) are already used in clinical trials for tissue regeneration and treatment of immune-related disorders, these studies did not sufficiently address alloreactivity. In the present study, we provide to our knowledge for the first time immunological data from a clinical trial demonstrating that patients treated with MHCunmatched MSC did not develop a memory T cell response specific to the mismatch. Moreover, we demonstrate that MSC control important checkpoints of Th1 priming by inhibiting migration and cytokine production of myeloid dendritic cells resulting in a diminished ability to prime natural killer cells and Th1 cells.

show abstract

Dendritic Cell and NK Cell Reciprocal Cross Talk Promotes Gamma Interferon-Dependent Immunity to Blood-StagePlasmodium chabaudiAS Infection in Mice

Abstract: Dendritic cells (DCs) are important accessory cells for promoting NK cell gamma interferon (IFN-␥) production in vitro in response to

Cited by 83 publications

References 46 publications

NK Cells Promote Type 1 T Cell Immunity through Modulating the Function of Dendritic Cells during Intracellular Bacterial Infection

NK Cells Promote Type 1 T Cell Immunity through Modulating the Function of Dendritic Cells during Intracellular Bacterial Infection

Obesity-associated cancer: an immunological perspective

Mesenchymal Stromal Cells Prevent Allostimulation In Vivo and Control Checkpoints of Th1 Priming: Migration of Human DC to Lymph Nodes and NK Cell Activation

Contact Info

Product

Resources

About