CpG pretreatment enhances antiviral T-cell immunity against cytomegalovirus

Ong, Monique L.; Wikström, Matthew E.; Fleming, Peter; Estcourt, Marie J.; Hertzog, Paul J.; Hill, Geoffrey R.; Andoniou, Christopher E.; Degli-Esposti, Mariapia A.

doi:10.1182/blood-2012-12-471227

Cited by 19 publications

(21 citation statements)

References 25 publications

(26 reference statements)

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“…18 Organs were collected at indicated days postinfection (PI) and processed to determine viral titers by standard plaque assay using M210B4 cells, as described. 19 …”

Section: Virus Infection and Quantitationmentioning

confidence: 99%

“…DCs are essential to generate effector T cells during CMV, 18,19 especially during a primary response. The reduced number of IE1 1 CD8…”

Section: Infection Of Dcs Is Impaired During Gvhdmentioning

confidence: 99%

“…19 Furthermore, we have shown that direct presentation depends upon the capacity of MCMV to efficiently infect DCs, mainly the CD11b 1 subset, 24 with the extent of DC infection being a critical determinant of the magnitude and longevity of antiviral T-cell responses. 18 We have previously shown that MCMV infection of DCs is measurable from day 2, increases at day 4, and is sustained until day 6 PI.…”

mentioning

confidence: 99%

“…18,19 We examined the infection of DCs using a recombinant MCMV-expressing GFP. 25 Spleens were collected from non-GVHD and GVHD mice 2 days PI, and GFP expression in DCs was measured by flow cytometry ( Figure 3D).…”

mentioning

confidence: 99%

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Acute GVHD results in a severe DC defect that prevents T-cell priming and leads to fulminant cytomegalovirus disease in mice

Wikström

Fleming

Kuns

et al. 2015

Blood

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“…18 Organs were collected at indicated days postinfection (PI) and processed to determine viral titers by standard plaque assay using M210B4 cells, as described. 19 …”

Section: Virus Infection and Quantitationmentioning

confidence: 99%

“…DCs are essential to generate effector T cells during CMV, 18,19 especially during a primary response. The reduced number of IE1 1 CD8…”

Section: Infection Of Dcs Is Impaired During Gvhdmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Acute GVHD results in a severe DC defect that prevents T-cell priming and leads to fulminant cytomegalovirus disease in mice

Wikström

Fleming

Kuns

et al. 2015

Blood

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“…Mice were sacrificed 4 d postinfection; spleen and liver were collected, homogenized in cold MEM 2% neonatal calf serum (Life Technologies), and centrifuged at 3000 rpm for 15 min at 4˚C. The supernatants were stored at 280˚C, and viral titers were quantified by standard plaque assay on M210B4 cells, as described (26).…”

Section: Determination Of Virus Growth In Vivomentioning

confidence: 99%

Ly49C Impairs NK Cell Memory in Mouse Cytomegalovirus Infection

Forbes

Scalzo

Degli-Esposti

et al. 2016

The Journal of Immunology

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NK cells possess inhibitory receptors that are responsible for self-MHC class I recognition; beyond their inhibitory function, accumulating evidence indicates that such receptors confer NK cell functional competence through an unclear process termed “licensing.” Ly49C is the main self-specific inhibitory Ly49 receptor in H-2b C57BL/6 (B6) mice. We used B6 Ly49C-transgenic and B6 β2 microglobulin (β2m)-knockout Ly49C-transgenic mice to investigate the impact of licensing through this inhibitory receptor in precursor and mature NK cells. We found that self-specific inhibitory receptors affected NK cell precursor survival and proliferation at particular developmental stages in an MHC class I–dependent manner. The presence of Ly49C impacted the NK cell repertoire in a β2m-dependent manner, with reduced Ly49A+, Ly49G2+, and Ly49D+ subsets, an increased DNAM-1+ subset, and higher NKG2D expression. Licensed NK cells displayed a skewed distribution of the maturation stages, which was characterized by differential CD27 and CD11b expression, toward the mature phenotypes. We found that Ly49C-mediated licensing induced a split effect on NK cell functions, with increased cytokine-production capabilities following engagement of various activating receptors while cytotoxicity remained unchanged. Analysis of licensed NK cell functions in vivo, in a system of mouse CMV infection, indicated that licensing did not play a major role in the NK cell antiviral response during acute infection, but it strongly impaired the generation and/or persistence of memory NK cells. This study unravels multifaceted effects of licensing on NK cell populations and their functions.

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Cytomegalovirus immune evasion of myeloid lineage cells

Brinkmann

Dağ

Hengel

et al. 2015

Med Microbiol Immunol

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Cytomegalovirus (CMV) evades the immune system in many different ways, allowing the virus to grow and its progeny to spread in the face of an adverse environment. Mounting evidence about the antiviral role of myeloid immune cells has prompted the research of CMV immune evasion mechanisms targeting these cells. Several cells of the myeloid lineage, such as monocytes, dendritic cells and macrophages, play a role in viral control, but are also permissive for CMV and are naturally infected by it. Therefore, CMV evasion of myeloid cells involves mechanisms that qualitatively differ from the evasion of non-CMV-permissive immune cells of the lymphoid lineage. The evasion of myeloid cells includes effects in cis, where the virus modulates the immune signaling pathways within the infected myeloid cell, and those in trans, where the virus affects somatic cells targeted by cytokines released from myeloid cells. This review presents an overview of CMV strategies to modulate and evade the antiviral activity of myeloid cells in cis and in trans.

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CpG pretreatment enhances antiviral T-cell immunity against cytomegalovirus

Abstract: Key Points Fully functional CD8 T-cell responses, control of infection, and protection from organ pathology are attained without cross-presentation. Direct presentation generates responses that limit disease and ensure host survival despite the presence of immunomodulatory viral proteins.

Cited by 19 publications

References 25 publications

Acute GVHD results in a severe DC defect that prevents T-cell priming and leads to fulminant cytomegalovirus disease in mice

Acute GVHD results in a severe DC defect that prevents T-cell priming and leads to fulminant cytomegalovirus disease in mice

Ly49C Impairs NK Cell Memory in Mouse Cytomegalovirus Infection

Cytomegalovirus immune evasion of myeloid lineage cells

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