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M cells and the follicle-associated epithelium
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Hiroshi Ohno, Marian Neutra, Ifor R. Williams
FAE cells differ from villus cells in their ability to release certain chemokines that attract immune cells toward the FAE and thus to sites of organized lymphoid tissue. In the small intestine of mice and humans, for example, chemokine CCL20, also designated macrophage inflammatory protein-3α (MIP-3α), is constitutively expressed in the FAE but not in the villus epithelium (Figure 15.2). CCL20 attracts subpopulations of DCs and lymphocytes that express the chemokine receptor CCR6. Mice that lack CCR6 have lower numbers of CD11c+ DCs in the subepithelial dome regions of Peyer's patches and have an impaired humoral immune response to orally administered antigen and certain enteropathogenic viruses. Cells of the mouse FAE also express CCL9 (analogous to CCL23 in humans), which attracts CCR1-expressing myeloid DCs, and CXCL16, which attracts CXCR6-expressing B and T lymphocytes into Peyer's patches.
The value of immunotherapy in head and neck cancer
Published in Expert Opinion on Biological Therapy, 2019
Paolo Manca, Luis E. Raez, Matthew Salzberg, Jorge Sanchez, Brian Hunis, Christian Rolfo
The rationale for combining immunotherapy with chemotherapy, radiotherapy or other targeted therapies is based on the ability of standard treatment to enhance tumor antigen release and presentation as synergistic association between these treatments have been proven [3,81,82]. In the particular scenario of radiotherapy, abscopal effect is well described, as well as its association in immune system activation in solid tumors, such as melanoma or NSCLC, therefore promising results are expected in the combination with immunotherapy [83–85]. Sridharan et al. demonstrated that patients with tumors with different histological types, including HNSCC, have different cytokine levels after being treated with radiotherapy with or without concurrent chemotherapy. A reduction in CXCL10 level was observed, which is known to stimulate cancer stem cells and it is associated with poor prognosis. CXCL16 level, which is associated with attracting tumor-infiltrating lymphocytes and NK cells, was increased. These findings support the combination of standard treatment with immunotherapy with promising results thus far [86] and with new studies under development [87,88].
Anti-CD122 antibody restores specific CD8+ T cell response in nonalcoholic steatohepatitis and prevents hepatocellular carcinoma growth
Published in OncoImmunology, 2023
Stéphanie Lacotte, Florence Slits, Beat Moeckli, Andrea Peloso, Stéphane Koenig, Matthieu Tihy, Sofia El Hajji, Quentin Gex, Laura Rubbia-Brandt, Christian Toso
In order to assess the phenotype of the tumor-specific T cells, we analyzed the SIINFEKL-specific CD8+ T cells in the tumor and in the adjacent liver parenchyma (Figure 5c). We found no differences in the percentage of SIINFEKL-specific CD8+ T cells (dextramers+ cells) in ND- and HFD-fed mice (Figure 5d, 12.3% vs 13.3%). Nearly all of the CD8+ dextramers+ cells were in the CD44+ CXCR6+ cell subset in both ND- and HFD-fed mice, meaning that both normal and steatotic livers were able to promote an antigen-specific immune response (Figure 5e, 87.8% vs 81.7%). However, the CD8+ dextramers+ cells from the livers of HFD-fed mice expressed a higher level of PD-1, suggesting a lower immune activity (Figure 5c and f, MFI 12605 vs. 16083). These results were confirmed using the GSE113508 dataset where the gene expression was evaluated in colorectal cancer injected into healthy or fatty livers.19 Colorectal cancer implanted into fatty livers had an increased expression of CXCL16, CXCR6, PD-L1 and PD-1 (Supplementary Figure C). Macrophages and dendritic cells are among the main producers of CXCL16. In order to assess their role in the migration of CD8+ CXCR6+ cells, we depleted them with clodronate liposomes. However, while we achieved a successful depletion of macrophages (0.65% vs 7.97%) and dendritic cells (1.57% vs 9.33%), the migration of CD8+ CXCR6+ cells remained with no measurable change (12% vs 14.37 in total CD8+ CXCR6+ cells and 1.60% vs 1.79% in dextramers+ CXCR6+ cells). This observation suggest that macrophages and dendritic cells are not the only mediators for CXCR6-expressing cell migration into the liver. Interestingly, the depletion of macrophages and dendritic cells correlated with a decreased expression of PD-1 and CD366 (Tim-3) both on CD8+ CXCR6+ cells and CD8+ dextramers+ cells (Supplementary Figure D).
Chemokines as the critical factors during bladder cancer progression: an overview
Published in International Reviews of Immunology, 2021
Amir Sadra Zangouei, Amir Abbas Hamidi, Hamid Reza Rahimi, Ehsan Saburi, Majid Mojarrad, Meysam Moghbeli
CMTM is belonged to the MARVEL domain containing protein family involved in reproduction, immune response, tumorigenesis, and apoptosis induction. It acts as a tumor suppressor gene in different types of cancer, and also regulates the tumor cell migration [89]. CMTM8 is believed to suppress the EGFR signaling pathway, which is up regulated in various malignant tumors [170]. In other tumor types, CMTM8 induced tumor cell apoptosis. Moreover, CMTM8 down regulation by c-MET results in EMT [171]. Levels of CMTM8 protein expression were assessed in BCa patients that showed its down regulation was significantly correlated with advanced tumor grade and stage. CMTM8 ectopic expression also reduced cell viability, migration, and colony formation in BCa cell line [88]. CMTM8 up regulation suppressed the cell proliferation and migration, while induced apoptosis in BCa. There was also significant association between CMTM8 expression, invasion, and patient survival. Moreover, CMTM8 was significantly over expressed in low-grade BCa cell line (RT4) and under expressed in high-grade BCa cell line (T24). The CMTM8 over expression reduced cell proliferation and migration through EGF and SDF1 in T24 cells. CMTM8 down regulation was observed in high grade in comparison with low grade BCa tissues. Decreased CMTM8 expression was associated with poor survival among BCa patients [89]. CXCL16 is a chemokine produced by immune cells, fibroblasts, keratinocytes, and tumor cells [135]. CXCR6 is upregulated following T cells activation. It is also expressed on CD4 + T cells, NK cells, DCs, and innate lymphoid cells [172]. There were higher and lower expressions of CXCR6 and CXCL16 respectively in BCa tissues compared with controls. The CXCL16/CXCR6 expressions were correlated with patients survival. CXCL16 was also associated with lymphovascular invasion. Moreover, there were significant correlations between CXCR6 expression, T stage, and perineural invasion. They concluded that the CXCL16/CXCR6 expression was associated with tumor aggressiveness [90].