Intratumoral Injection of Dendritic Cells Transduced by an SV40-Based Vector Expressing Interleukin-15 Induces Curative Immunity Mediated by CD8+ T Lymphocytes and NK Cells

Cell transfer therapy for cancer has made a rapid progress recently and the immunotherapy has been recognized as the fourth anticancer modality after operation, chemotherapy, and radiotherapy. Lymphocytes used for cell transfer therapy include dendritic cells, natural killer (NK) cells, and T lymphocytes such as tumor-infiltrating lymphocytes (TILs) and cytotoxic T lymphocytes (CTLs). In vitro activated or engineered immune cells can traffic to cancer tissues to elicit persistent antitumor immune response which is very important especially after immunosuppressive treatments such as chemotherapy. In this review, we overviewed recent advances in the exploration of dendritic cells, NK cells, and T cells for the treatment of human cancer cells.

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Urban particulate matter stimulation of human dendritic cells enhances priming of naive CD8 T lymphocytes

Immunology ◽

10.1111/imm.12852 ◽

2017 ◽

Vol 153 (4) ◽

pp. 502-512 ◽

Cited By ~ 11

Author(s):

Paul E. Pfeffer ◽

Tzer R. Ho ◽

Elizabeth H. Mann ◽

Frank J. Kelly ◽

Maria Sehlstedt ◽

...

Keyword(s):

Dendritic Cells ◽

Particulate Matter ◽

T Lymphocytes ◽

Urban Particulate Matter ◽

Cd8 T Lymphocytes ◽

Human Dendritic Cells ◽

Stimulation Of

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Immune Profile of the Normal Maternal-Fetal Interface in Rhesus Macaques and Its Alteration Following Zika Virus Infection

Frontiers in Immunology ◽

10.3389/fimmu.2021.719810 ◽

2021 ◽

Vol 12 ◽

Author(s):

Matilda J. Moström ◽

Elizabeth A. Scheef ◽

Lesli M. Sprehe ◽

Dawn Szeltner ◽

Dollnovan Tran ◽

...

Keyword(s):

T Lymphocytes ◽

Nk Cells ◽

B Lymphocytes ◽

Vertical Transmission ◽

Zika Virus ◽

Peripheral Blood ◽

Congenital Infection ◽

Effector Memory ◽

Cd8 T Lymphocytes ◽

Maternal Fetal Interface

The maternal decidua is an immunologically complex environment that balances maintenance of immune tolerance to fetal paternal antigens with protection of the fetus against vertical transmission of maternal pathogens. To better understand host immune determinants of congenital infection at the maternal-fetal tissue interface, we performed a comparative analysis of innate and adaptive immune cell subsets in the peripheral blood and decidua of healthy rhesus macaque pregnancies across all trimesters of gestation and determined changes after Zika virus (ZIKV) infection. Using one 28-color and one 18-color polychromatic flow cytometry panel we simultaneously analyzed the frequency, phenotype, activation status and trafficking properties of αβ T, γδ T, iNKT, regulatory T (Treg), NK cells, B lymphocytes, monocytes, macrophages, and dendritic cells (DC). Decidual leukocytes showed a striking enrichment of activated effector memory and tissue-resident memory CD4+ and CD8+ T lymphocytes, CD4+ Tregs, CD56+ NK cells, CD14+CD16+ monocytes, CD206+ tissue-resident macrophages, and a paucity of B lymphocytes when compared to peripheral blood. t-distributed stochastic neighbor embedding (tSNE) revealed unique populations of decidual NK, T, DC and monocyte/macrophage subsets. Principal component analysis showed distinct spatial localization of decidual and circulating leukocytes contributed by NK and CD8+ T lymphocytes, and separation of decidua based on gestational age contributed by memory CD4+ and CD8+ T lymphocytes. Decidua from 10 ZIKV-infected dams obtained 16-56 days post infection at third (n=9) or second (n=1) trimester showed a significant reduction in frequency of activated, CXCR3+, and/or Granzyme B+ memory CD4+ and CD8+ T lymphocytes and γδ T compared to normal decidua. These data suggest that ZIKV induces local immunosuppression with reduced immune recruitment and impaired cytotoxicity. Our study adds to the immune characterization of the maternal-fetal interface in a translational nonhuman primate model of congenital infection and provides novel insight in to putative mechanisms of vertical transmission.

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The XC chemokine receptor 1 is a conserved selective marker of mammalian cells homologous to mouse CD8α+ dendritic cells

Journal of Experimental Medicine ◽

10.1084/jem.20100223 ◽

2010 ◽

Vol 207 (6) ◽

pp. 1283-1292 ◽

Cited By ~ 410

Author(s):

Karine Crozat ◽

Rachel Guiton ◽

Vanessa Contreras ◽

Vincent Feuillet ◽

Charles-Antoine Dutertre ◽

...

Keyword(s):

Dendritic Cells ◽

T Cell ◽

T Lymphocytes ◽

Chemokine Receptor ◽

Mammalian Cells ◽

Pathogenic Bacteria ◽

Cd8 T Cell ◽

Specific Marker ◽

Cd8 T Lymphocytes ◽

Chemokine Receptor 1

Human BDCA3+ dendritic cells (DCs) were suggested to be homologous to mouse CD8α+ DCs. We demonstrate that human BDCA3+ DCs are more efficient than their BDCA1+ counterparts or plasmacytoid DCs (pDCs) in cross-presenting antigen and activating CD8+ T cells, which is similar to mouse CD8α+ DCs as compared with CD11b+ DCs or pDCs, although with more moderate differences between human DC subsets. Yet, no specific marker was known to be shared between homologous DC subsets across species. We found that XC chemokine receptor 1 (XCR1) is specifically expressed and active in mouse CD8α+, human BDCA3+, and sheep CD26+ DCs and is conserved across species. The mRNA encoding the XCR1 ligand chemokine (C motif) ligand 1 (XCL1) is selectively expressed in natural killer (NK) and CD8+ T lymphocytes at steady-state and is enhanced upon activation. Moreover, the Xcl1 mRNA is selectively expressed at high levels in central memory compared with naive CD8+ T lymphocytes. Finally, XCR1−/− mice have decreased early CD8+ T cell responses to Listeria monocytogenes infection, which is associated with higher bacterial loads early in infection. Therefore, XCR1 constitutes the first conserved specific marker for cell subsets homologous to mouse CD8α+ DCs in higher vertebrates and promotes their ability to activate early CD8+ T cell defenses against an intracellular pathogenic bacteria.

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Faculty Opinions recommendation of Blood-stage Plasmodium infection induces CD8+ T lymphocytes to parasite-expressed antigens, largely regulated by CD8alpha+ dendritic cells.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1124133.581266 ◽

2008 ◽

Author(s):

Christian Engwerda

Keyword(s):

Dendritic Cells ◽

T Lymphocytes ◽

Blood Stage ◽

Plasmodium Infection ◽

Cd8 T Lymphocytes

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Blood-stage Plasmodium infection induces CD8+ T lymphocytes to parasite-expressed antigens, largely regulated by CD8 + dendritic cells

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.0806727105 ◽

2008 ◽

Vol 105 (38) ◽

pp. 14509-14514 ◽

Cited By ~ 137

Author(s):

R. J. Lundie ◽

T. F. de Koning-Ward ◽

G. M. Davey ◽

C. Q. Nie ◽

D. S. Hansen ◽

...

Keyword(s):

Dendritic Cells ◽

T Lymphocytes ◽

Blood Stage ◽

Plasmodium Infection ◽

Cd8 T Lymphocytes

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Presence of functional dendritic cells in patients chronically infected with hepatitis C virus

Blood ◽

10.1182/blood-2003-04-1339 ◽

2004 ◽

Vol 103 (3) ◽

pp. 1026-1029 ◽

Cited By ~ 111

Author(s):

Randy S. Longman ◽

Andrew H. Talal ◽

Ira M. Jacobson ◽

Matthew L. Albert ◽

Charles M. Rice

Keyword(s):

Dendritic Cells ◽

Hepatitis C Virus ◽

Hepatitis C ◽

T Lymphocytes ◽

Memory T Cells ◽

Immune Repertoire ◽

Cd8 T Lymphocytes ◽

Specific Memory ◽

Chronic Hcv

Abstract The absence of expanded numbers of hepatitis C virus (HCV)-reactive CD8+ T lymphocytes (CTLs) in patients chronically infected with HCV has led to the investigation of dendritic cell (DC) function in this population as a potential cause for this defect. Several studies have shown evidence for impaired monocyte-derived DCs in chronically infected patients. As it is difficult to reconcile these data with the fact that patients with chronic HCV are immune competent, we re-evaluated this finding, carefully assessing phenotypic markers and functional activity of patient DCs as compared with noninfected controls. In contrast to these prior studies, DCs from 13 of 13 chronic HCV patients expressed typical maturation markers. These mature DCs were capable of priming allogeneic T lymphocytes, as well as stimulating influenza-specific memory T cells. This finding is consistent with clinical and immunologic data that the deficit in the patient's immune repertoire is HCV-specific and suggests that refined models are required for understanding the role of DCs in HCV pathogenesis. (Blood. 2004;103:1026-1029)

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