Neutrophils Transport Antigen from the Dermis to the Bone Marrow, Initiating a Source of Memory CD8+ T Cells

Duffy, Darragh; Perrin, Hélène; Abadie, Valérie; Benhabilès, Nora; Boissonnas, Alexandre; Liard, Christelle; Descours, Benjamin; Reboulleau, Damien; Bonduelle, Olivia; Verrier, Bernard; Rooijen, Nico van; Combadière, Christophe; Combadière, Béhazine

doi:10.1016/j.immuni.2012.11.002

Cited by 28 publications

(38 citation statements)

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“…Neutrophils reportedly have difficulties in priming CD4 T cells compared with CD8 T cells after vaccinia infection (13); in our model, we observe no CD4 T-cell response to GPN in NYVAC-Cor in NYVAC-C Δ3-infected mice.…”

Section: Discussioncontrasting

confidence: 62%

“…In contrast, VACVinfected neutrophils cannot induce a CD8 T-cell proliferative response in BM in the absence of myeloid APCs (13). When mice were NYVAC-GFP-or NYVAC-GFP Δ3-infected, we did not detect GFP + -infected neutrophils in secondary lymphoid organs, which would suggest indirect neutrophil infection.…”

Section: Discussioncontrasting

confidence: 56%

“…To determine the functional profile of CD4 and CD8 T cells, we measured levels of IFN-γ, TNF-α, and IL-2 as well as of lysosomal-associated membrane protein-1 (LAMP-1 or CD107a) as a surrogate marker for induction of killing. We determined the magnitude of the T-cell response as the number of T cells that expressed IFN-γ and/or TNF-α and/or IL-2 and/or CD107a and the polyfunctionality of the response as T cell's capacity to express more than one of these activation markers (13).…”

Section: Nyvac-c δ3 Enhances the Hiv-specific T-cell Response Throughmentioning

confidence: 99%

“…In the presence of a granulocyte macrophage-colony-stimulating factor (GM-CSF) (10), tumor necrosis factor (TNF)-α, interleukin (IL)-4 (11), or interferon (IFN)-γ (12), neutrophils can adopt an antigen-presenting cell (APC) phenotype, thus triggering T-cell activation. In the context of VACV infection, neutrophils generate virus-specific memory CD8 T cells, transporting antigens from the dermis to the bone marrow (BM) (13). It is nonetheless not known how VACV modulates neutrophil recruitment, the factors involved, or the significance in immune response triggering.…”

mentioning

confidence: 99%

“…Total RNA was extracted using RNeasy Mini Kit (Qiagen) and was treated with DNase I recombinant, RNase-free. Subsequently, first-strand cDNA was synthesized with Oligo (dT) [12][13][14][15][16][17][18] primers (Invitrogen) using SuperScriptIII Reverse transcriptase (Invitrogen) following the manufacturer's protocol, and cDNA was used for PCR amplification. The primers K7RinternalFwd-Bam and K7RinternalRev-Not used for amplification of K7R cDNA were the same as for cloning and are described in Table S1.…”

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confidence: 99%

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NFκB activation by modified vaccinia virus as a novel strategy to enhance neutrophil migration and HIV-specific T-cell responses

Pilato¹,

Mejías-Pérez²,

Zonca

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Neutrophils are antigen-transporting cells that generate vaccinia virus (VACV)-specific T-cell responses, yet how VACV modulates neutrophil recruitment and its significance in the immune response are unknown. We generated an attenuated VACV strain that expresses HIV-1 clade C antigens but lacks three specific viral genes (A52R, K7R, and B15R). We found that these genes act together to inhibit the NFκB signaling pathway. Triple ablation in modified virus restored NFκB function in macrophages. After virus infection of mice, NFκB pathway activation led to expression of several cytokines/chemokines that increased the migration of neutrophil populations (Nα and Nβ) to the infection site. Nβ cells displayed features of antigen-presenting cells and activated virus-specific CD8 T cells. Enhanced neutrophil trafficking to the infection site correlated with an increased T-cell response to HIV vector-delivered antigens. These results identify a mechanism for poxvirus-induced immune response and alternatives for vaccine vector design.

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Section: Discussioncontrasting

confidence: 62%

Section: Discussioncontrasting

confidence: 56%

Section: Nyvac-c δ3 Enhances the Hiv-specific T-cell Response Throughmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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NFκB activation by modified vaccinia virus as a novel strategy to enhance neutrophil migration and HIV-specific T-cell responses

Pilato¹,

Mejías-Pérez²,

Zonca

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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CXCR4, but not CXCR3, drives CD8⁺ T‐cell entry into and migration through the murine bone marrow

et al. 2019

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The BM serves as a blood‐forming organ, but also supports the maintenance and immune surveillance function of many T cells. Yet, in contrast to other organs, little is known about the molecular mechanisms that drive T‐cell migration to and localization inside the BM. As BM accumulates many CXCR3‐expressing memory CD8+ T cells, we tested the involvement of this chemokine receptor, but found that CXCR3 is not required for BM entry. In contrast, we could demonstrate that CXCR4, which is highly expressed on both naive and memory CD8+ T cells in BM, is critically important for homing of all CD8+ T‐cell subsets to the BM in mice. Upon entry into the BM parenchyma, both naïve and memory CD8+ T cells locate close to sinusoidal vessels. Intravital imaging experiments revealed that CD8 T cells are surprisingly immobile and we found that they interact with ICAM‐1+VCAM‐1+BP‐1+ perivascular stromal cells. These cells are the major source of CXCL12, but also express key survival factors and maintenance cytokines IL‐7 and IL‐15. We therefore conclude that CXCR4 is not only crucial for entry of CD8+ T cells into the BM, but also controls their subsequent localization toward BM niches that support their survival.

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Peripheral and systemic antigens elicit an expandable pool of resident memory CD8⁺ T cells in the bone marrow

et al. 2019

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BM has been put forward as a major reservoir for memory CD8+ T cells. In order to fulfill that function, BM should “store” memory CD8+ T cells, which in biological terms would require these “stored” memory cells to be in disequilibrium with the circulatory pool. This issue is a matter of ongoing debate. Here, we unequivocally demonstrate that murine and human BM harbors a population of tissue‐resident memory CD8+ T (TRM) cells. These cells develop against various pathogens, independently of BM infection or local antigen recognition. BM CD8+ TRM cells share a transcriptional program with resident lymphoid cells in other tissues; they are polyfunctional cytokine producers and dependent on IL‐15, Blimp‐1, and Hobit. CD8+ TRM cells reside in the BM parenchyma, but are in close contact with the circulation. Moreover, this pool of resident T cells is not size‐restricted and expands upon peripheral antigenic re‐challenge. This works extends the role of the BM in the maintenance of CD8+ T cell memory to include the preservation of an expandable reservoir of functional, non‐recirculating memory CD8+ T cells, which develop in response to a large variety of peripheral antigens.

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Neutrophils Transport Antigen from the Dermis to the Bone Marrow, Initiating a Source of Memory CD8+ T Cells

Cited by 28 publications

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NFκB activation by modified vaccinia virus as a novel strategy to enhance neutrophil migration and HIV-specific T-cell responses

NFκB activation by modified vaccinia virus as a novel strategy to enhance neutrophil migration and HIV-specific T-cell responses

CXCR4, but not CXCR3, drives CD8⁺ T‐cell entry into and migration through the murine bone marrow

Peripheral and systemic antigens elicit an expandable pool of resident memory CD8⁺ T cells in the bone marrow

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Neutrophils Transport Antigen from the Dermis to the Bone Marrow, Initiating a Source of Memory CD8+ T Cells

Cited by 28 publications

References 0 publications

NFκB activation by modified vaccinia virus as a novel strategy to enhance neutrophil migration and HIV-specific T-cell responses

NFκB activation by modified vaccinia virus as a novel strategy to enhance neutrophil migration and HIV-specific T-cell responses

CXCR4, but not CXCR3, drives CD8+ T‐cell entry into and migration through the murine bone marrow

Peripheral and systemic antigens elicit an expandable pool of resident memory CD8+ T cells in the bone marrow

Contact Info

Product

Resources

About

CXCR4, but not CXCR3, drives CD8⁺ T‐cell entry into and migration through the murine bone marrow

Peripheral and systemic antigens elicit an expandable pool of resident memory CD8⁺ T cells in the bone marrow