High expression of CX3CL1 by tumor cells correlates with a good prognosis and increased tumor-infiltrating CD8+ T cells, natural killer cells, and dendritic cells in breast carcinoma

2012 ◽  
Vol 106 (4) ◽  
pp. 386-392 ◽  
Author(s):  
Min Ho Park ◽  
Ji Shin Lee ◽  
Jung Han Yoon
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Breast Carcinoma ◽  
Natural Killer Cells ◽  
Natural Killer ◽  
Tumor Cells ◽  
Cd8 T Cells ◽  
Good Prognosis ◽  
High Expression ◽  
Killer Cells

scholarly journals Next-Generation Immunotherapies to Improve Anticancer Immunity

2021 ◽  
Vol 11 ◽  
Author(s):  
Yaoyao Shi ◽  
Katarzyna Tomczak ◽  
June Li ◽  
Joshua K. Ochieng ◽  
Younghee Lee ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Natural Killer Cells ◽  
Natural Killer ◽  
Tumor Cells ◽  
Checkpoint Inhibitors ◽  
Cytotoxic T Cells ◽  
Cell Subset ◽  
Cytotoxic T Cell ◽  
Killer Cells

Checkpoint inhibitors are widely used immunotherapies for advanced cancer. Nonetheless, checkpoint inhibitors have a relatively low response rate, work in a limited range of cancers, and have some unignorable side effects. Checkpoint inhibitors aim to reinvigorate exhausted or suppressed T cells in the tumor microenvironment (TME). However, the TME contains various other immune cell subsets that interact to determine the fate of cytotoxic T cells. Activation of cytotoxic T cells is initiated by antigen cross-presentation of dendritic cells. Dendritic cells could also release chemokines and cytokines to recruit and foster T cells. B cells, another type of antigen-presenting cell, also foster T cells and can produce tumor-specific antibodies. Neutrophils, a granulocyte cell subset in the TME, impede the proliferation and activation of T cells. The TME also consists of cytotoxic innate natural killer cells, which kill tumor cells efficiently. Natural killer cells can eradicate major histocompatibility complex I-negative tumor cells, which escape cytotoxic T cell–mediated destruction. A thorough understanding of the immune mechanism of the TME, as reviewed here, will lead to further development of more powerful therapeutic strategies. We have also reviewed the clinical outcomes of patients treated with drugs targeting these immune cells to identify strategies for improvement and possible immunotherapy combinations.

Increased Expression of Fractalkine is Correlated with a Better Prognosis and an Increased Number of Both CD8+ T Cells and Natural Killer Cells in Gastric Adenocarcinoma

2008 ◽  
Vol 15 (6) ◽  
pp. 1775-1782 ◽  
Author(s):  
Miki Hyakudomi ◽  
Takeshi Matsubara ◽  
Ryoji Hyakudomi ◽  
Tetsu Yamamoto ◽  
Shoichi Kinugasa ◽  
...  
Keyword(s):  
T Cells ◽  
Natural Killer Cells ◽  
Natural Killer ◽  
Gastric Adenocarcinoma ◽  
Cd8 T Cells ◽  
Killer Cells

CD27low Natural Killer Cells Prolong Allograft Survival in Mice by Controlling Alloreactive CD8+ T Cells in a T-Bet–Dependent Manner

2015 ◽  
Vol 99 (2) ◽  
pp. 391-399 ◽  
Author(s):  
Margareta Lantow ◽  
Elke Eggenhofer ◽  
Manije Sabet-Baktach ◽  
Philipp Renner ◽  
Jordi Rovira ◽  
...  
Keyword(s):  
T Cells ◽  
Natural Killer Cells ◽  
Natural Killer ◽  
Cd8 T Cells ◽  
Dependent Manner ◽  
Allograft Survival ◽  
Killer Cells

Glatiramer acetate (Copaxone) inhibits natural killer cells lysis of tumor cells but enhances their killing of autologous and allogeneic immature and mature dendritic cells.

2008 ◽  
Vol 22 (S2) ◽  
pp. 465-465
Author(s):  
Azzam A Maghazachi ◽  
Kristin L Sand ◽  
Cecilia B Becerra ◽  
Johannes Rolin ◽  
Eirunn Knudsen
Keyword(s):  
Dendritic Cells ◽  
Natural Killer Cells ◽  
Natural Killer ◽  
Tumor Cells ◽  
Glatiramer Acetate ◽  
Killer Cells

scholarly journals Autoimmunity, hypogammaglobulinemia, lymphoproliferation, and mycobacterial disease in patients with activating mutations in STAT3

Blood ◽  
2015 ◽  
Vol 125 (4) ◽  
pp. 639-648 ◽  
Author(s):  
Emma M. Haapaniemi ◽  
Meri Kaustio ◽  
Hanna L. M. Rajala ◽  
Arjan J. van Adrichem ◽  
Leena Kainulainen ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Natural Killer Cells ◽  
Natural Killer ◽  
Mycobacterial Disease ◽  
Killer Cells ◽  
Activating Mutations ◽  
Key Points ◽  
Stat3 Mutations

Key Points Germline activating STAT3 mutations were detected in 3 patients with autoimmunity, hypogammaglobulinemia, and mycobacterial disease. T-cell lymphoproliferation, deficiency of regulatory and helper 17 T cells, natural killer cells, dendritic cells, and eosinophils were common.

scholarly journals Metabolic Remodeling in Glioma Immune Microenvironment: Intercellular Interactions Distinct From Peripheral Tumors

2021 ◽  
Vol 9 ◽  
Author(s):  
Runze Qiu ◽  
Yue Zhong ◽  
Qingquan Li ◽  
Yingbin Li ◽  
Hongwei Fan
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Tumor Microenvironment ◽  
Natural Killer Cells ◽  
T Lymphocytes ◽  
Regulatory T Cells ◽  
Natural Killer ◽  
Cytotoxic T Lymphocytes ◽  
Glioma Cells ◽  
Killer Cells

During metabolic reprogramming, glioma cells and their initiating cells efficiently utilized carbohydrates, lipids and amino acids in the hypoxic lesions, which not only ensured sufficient energy for rapid growth and improved the migration to normal brain tissues, but also altered the role of immune cells in tumor microenvironment. Glioma cells secreted interferential metabolites or depriving nutrients to injure the tumor recognition, phagocytosis and lysis of glioma-associated microglia/macrophages (GAMs), cytotoxic T lymphocytes, natural killer cells and dendritic cells, promoted the expansion and infiltration of immunosuppressive regulatory T cells and myeloid-derived suppressor cells, and conferred immune silencing phenotypes on GAMs and dendritic cells. The overexpressed metabolic enzymes also increased the secretion of chemokines to attract neutrophils, regulatory T cells, GAMs, and dendritic cells, while weakening the recruitment of cytotoxic T lymphocytes and natural killer cells, which activated anti-inflammatory and tolerant mechanisms and hindered anti-tumor responses. Therefore, brain-targeted metabolic therapy may improve glioma immunity. This review will clarify the metabolic properties of glioma cells and their interactions with tumor microenvironment immunity, and discuss the application strategies of metabolic therapy in glioma immune silence and escape.

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