Both plasmacytoid dendritic cells and monocytes stimulate natural killer cells early during human herpes simplex virus type 1 infections

Vogel, Karin; Thomann, Sabrina; Vogel, Benjamin; Schuster, Philipp; Schmidt, Bárbara

doi:10.1111/imm.12337

Cited by 32 publications

(31 citation statements)

References 64 publications

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“…An increase in the HLA-E expression on the cell surface has been shown in monocytes activated by different stimuli, such as IL-27 or IFN-a [35,36]. Accordingly, the expression of HLA-E was low in primary monocytes and strongly up-regulated in MDMs.…”

Section: Discussionmentioning

confidence: 95%

Regulation and trafficking of the HLA-E molecules during monocyte-macrophage differentiation

Camilli¹,

Cassotta²,

Battella³

et al. 2015

Journal of Leukocyte Biology

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HLA-E is a nonclassical HLA-class I molecule whose best known role is to protect from the natural killer cells. More recently, an additional function more similar to that of classical HLA-class I molecules, i.e., antigen presentation to T cells, is emerging. However, much remains to be explored about the intracellular trafficking of the HLA-E molecules. With the use of 3 different cellular contexts, 2 monocytic cell lines, U937 and THP1, and peripheral blood monocytes, we show here a remarkable increase of HLA-E during monocyte-macrophage differentiation. This goes independently from the classical HLA-class I, the main source of HLA-E-specific peptides, which is found strongly up-regulated upon differentiation of peripheral blood monocytes but not at all in the case of U937 and THP1 cell lines. Although in all cases, there was a moderate increase of HLA-E expressed in the cell surface, lysis by natural killer cells is comparably restored by an anti-NKG2A antibody in untreated as well as in PMA-differentiated U937 cells. Instead, the great majority of the HLA-E is retained in the vesicles of the autophagy-lysosome network, where they colocalize with the microtubule-associated protein light chain 3, as well as with the lysosomal-associated membrane protein 1. We conclude that differently from the classical HLA-class I molecules, the primary destination of the newly synthesized HLA-E molecules in macrophages is, rather than the cell membrane, the intracellular autophagy-lysosomal vesicles where they are stored and where they can encounter the exogenous antigens.

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Section: Discussionmentioning

confidence: 95%

Regulation and trafficking of the HLA-E molecules during monocyte-macrophage differentiation

Camilli¹,

Cassotta²,

Battella³

et al. 2015

Journal of Leukocyte Biology

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“…IL-18 produced from activated macrophages induced IFN-γ production by NK cells and protected mice from HSV infections [32]. IFN-γ is also produced from activated macrophages and γδ T cells in response to HSV infections, which further stimulates macrophages to produce TNF-α, which activates NK cells for HSV control [33]. Depletion of macrophages with clodronate liposomes or modulation of the tumor microenvironment with CPA (reducing IFN-γ expression and infiltration of macrophages) improves oHSV intratumoral spread and efficacy in brain tumors [34].…”

Section: Host Responses Against Hsv Infectionmentioning

confidence: 99%

Oncolytic herpes simplex virus interactions with the host immune system

Saha

Wakimoto

Rabkin

2016

Current Opinion in Virology

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Oncolytic viruses (OVs), like oncolytic herpes simplex virus (oHSV), are genetically engineered to selectively replicate in and kill cancer cells, while sparing normal cells. Initial OV infection, cell death, and subsequent OV propagation within the tumor microenvironment leads to a cascade of host responses (innate and adaptive), reflective of natural anti-viral immune responses. These host-virus interactions are critical to the balance between OV activities, anti-viral immune responses limiting OV, and induction of anti-tumor immunity. The host response against oHSV is complex, multifaceted, and modulated by the tumor microenvironment and immunosuppression. As a successful pathogen, HSV has multiple mechanisms to evade such host responses. In this review, we will discuss these mechanisms and HSV evasion, and how they impact oHSV therapy.

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“…In particular, it was shown that functional interactions between DCs and NK cells occur. DCs are required for Ly49H + NK cell accumulation in mouse cytomegalovirus infection and for proper NK cell response in Herpes simplex virus‐1 infection …”

Section: The Interaction Of Nk Cells and Dendritic Cellsmentioning

confidence: 99%

The yin‐yang of the interaction between myelomonocytic cells and NK cells

et al. 2018

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NK cells are innate lymphoid cells, which play a key role in the immune response to cancer and pathogens and participate in the shaping of adaptive immunity. NK cells engage in a complex bidirectional interaction with myelomonocytic cells. In particular, macrophages, dendritic cells and neutrophils promote differentiation and effector function of NK cells and, on the other hand, myelomonocytic cells express triggers of checkpoint blockade (eg PD-L1) and other immunosuppressive molecules, which negatively regulate NK cell function. In addition, NK cells express high levels of IL-1R8, which acts as a checkpoint for IL-18 driven differentiation and activation of NK cells. Evidence suggests that targeting the myeloid cell-NK cell crosstalk unleashes effective anti-tumour and anti-viral resistance.

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Both plasmacytoid dendritic cells and monocytes stimulate natural killer cells early during human herpes simplex virus type 1 infections

Cited by 32 publications

References 64 publications

Regulation and trafficking of the HLA-E molecules during monocyte-macrophage differentiation

Regulation and trafficking of the HLA-E molecules during monocyte-macrophage differentiation

Oncolytic herpes simplex virus interactions with the host immune system

The yin‐yang of the interaction between myelomonocytic cells and NK cells

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