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Figure 3 G, H. Tumor infiltrating cells in Lenti-HPV-07-vaccinated mice. Figure 4 F. Expression of PDL1 on tumor cells in Lenti-HPV-07-vaccinated mice.

ABSTRACT: C57BL/6 mice were engrafted s.c. with 1.10(6) TC-1 cells and injected with 1.1(9) TU of Ctrl Lenti or Lenti-HPV-07 (n = 7/group). Intratumoral CD8+ T cells were analyzed for the expression of exhaustion markers or TCF-1. Tumor cellls were studied for expression of PDL-1.

ORGANISM(S): Mus musculus (mouse)

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PROVIDER: S-BSST1102 | biostudies-other |

REPOSITORIES: biostudies-other

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Figure 4C. Tumor infiltrating immune cells in Lenti-HPV-07-vaccinated mice.

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Figure 3 A, B, D, E, F. Tumor infiltrating T cells in Lenti-HPV-07-vaccinated mice.

Project description: Not available

| S-BSST1101 | biostudies-other

Figure 4A B. Features of tumor cells and tumor infiltrating innate immune cells in Lenti-HPV-07-vaccinated mice.

Project description: Not available

| S-BSST1103 | biostudies-other

Figure 2 B and D. Characterization of Lenti-HPV-07-induced T-cell effectors by Intracellular Cytokine Staining (ICS) in mice immunized with Lenti-HPV-07

Project description: Not available

| S-BSST1100 | biostudies-other

Figure 7. Long-lasting antitumor T-cell memory induced by a single Lenti-HPV-07 vaccination

Project description: Not available

| S-BSST1108 | biostudies-other

Figure 6D. Effect of Lenti-HPV-07 immunotherapy on lung T cells in C57BL/6 with metastatic TC-1 tumors

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Tumor-infiltrating myeloid cells induce tumor cell resistance to cytotoxic T cells in mice.

Project description:Cancer immunotherapeutic approaches induce tumor-specific immune responses, in particular CTL responses, in many patients treated. However, such approaches are clinically beneficial to only a few patients. We set out to investigate one possible explanation for the failure of CTLs to eliminate tumors, specifically, the concept that this failure is not dependent on inhibition of T cell function. In a previous study, we found that in mice, myeloid-derived suppressor cells (MDSCs) are a source of the free radical peroxynitrite (PNT). Here, we show that pre-treatment of mouse and human tumor cells with PNT or with MDSCs inhibits binding of processed peptides to tumor cell-associated MHC, and as a result, tumor cells become resistant to antigen-specific CTLs. This effect was abrogated in MDSCs treated with a PNT inhibitor. In a mouse model of tumor-associated inflammation in which the antitumor effects of antigen-specific CTLs are eradicated by expression of IL-1? in the tumor cells, we determined that therapeutic failure was not caused by more profound suppression of CTLs by IL-1?-expressing tumors than tumors not expressing this proinflammatory cytokine. Rather, therapeutic failure was a result of the presence of PNT. Clinical relevance for these data was suggested by the observation that myeloid cells were the predominant source of PNT in human lung, pancreatic, and breast cancer samples. Our data therefore suggest what we believe to be a novel mechanism of MDSC-mediated tumor cell resistance to CTLs.

| S-EPMC3195459 | biostudies-literature

Mismatch repair proteins expression and tumor-infiltrating T-cells in colorectal cancer.

Project description:Microsatellite instability (MSI) and tumor mutational burden (TMB) are indicators of the tumor mutational load, which can lead to immune cell recruitment. By contrast, the number of tumor-infiltrating T cells (TITs) is indicative of the host immune response to tumor cells. The present study evaluated if the expression of mismatch repair (MMR) proteins can be used as a precise tool to assess immunogenicity in the tumor microenvironment. A total of 73 colorectal cancer cases were enrolled in the present study. MMR protein expression was assessed using four-antibodies immunohistochemistry (IHC) targeting MLH1, MSH2, MSH6 and PMS2. TIT was assessed through IHC by counting CD3+ and CD8+ cells in tumor. The enrolled cases were classified into four groups according to MMR and TIT status i) Mismatch repair-proficient (pMMR) and a high number of TITs (pMMR/TIT-H); ii) pMMR and a low number of TITs (pMMR/TIT-L); iii) mismatch repair-deficient (dMMR) and TIT-H (dMMR/TIT-H); and iv) dMMR/TIT-L]. The present study evaluated the clinicopathological characteristics of the four groups, in addition to the difference of TMB. TMB analysis was counted the number of the somatic mutations through multi-genes panel using next-generation sequencing. Clinicopathological characteristics, including age, sex, pathological depth of invasion and lymph node metastasis, were not found to be statistically different between dMMR/TIT-H and dMMR/TIT-L groups. Tumors among pMMR/TIT-H group were associated with poorly differentiation compared with those in pMMR/TIT-L group (P=0.025). The median TMB among the dMMR/TIT-H group was the highest in four groups but the median TMB was <10 muts/Mb in dMMR/TIT-L, pMMR/TIT-H and pMMR/TIT-L groups, respectively. However, one tumor in the pMMR/TIT-H group showed high TMB. The present findings suggest that assessing MMR status alone may not be sufficient to precisely evaluate the antitumor immune response in the tumor microenvironment.

| S-EPMC9533364 | biostudies-literature

Increased expression of adenosine A3 receptor in tumor-infiltrating natural killer cells.

Project description: Not available

| S-EPMC8027170 | biostudies-literature

Liprin-α1 Expression in Tumor-Infiltrating Lymphocytes Associates with Improved Survival in Patients with HPV-Positive Oropharyngeal Squamous Cell Carcinoma.

Project description:BackgroundLiprin-α1 is a scaffold protein involved in cell adhesion, motility, and invasion in malignancies. Liprin-α1 inhibits the expression of metastatic suppressor CD82 in cancers such as oral carcinoma, and the expression of these proteins has been known to correlate negatively. The role of these proteins has not been previously studied in human papillomavirus (HPV)-related head and neck cancers. Our aim was to assess the clinical and prognostic role of liprin-α1 and CD82 in HPV-positive oropharyngeal squamous cell carcinoma (OPSCC) in comparison to HPV-negative OPSCC.MethodsThe data included 139 OPSCC patients treated at the Helsinki University Hospital (HUS) during 2012-2016. Immunohistochemistry was utilized in HPV determination and in biomarker assays. Overall survival (OS) was used in the survival analysis.ResultsStronger expression of liprin-α1 in tumor-infiltrating lymphocytes (TILs) was linked to lower cancer stage (p < 0.001) and HPV positivity (p < 0.001). Additionally, we found an association between elevated expression of liprin-α1 and weak expression of CD82 in tumor cells (p = 0.029). In survival analysis, we found significant correlation between favorable OS and stronger expression of liprin-α1 in TILs among the whole patient cohort (p < 0.001) and among HPV-positive patients (p = 0.042).ConclusionsIncreased liprin-α1 expression in the TILs is associated with favorable prognosis in OPSCC, especially among HPV-positive patients.

| S-EPMC10513983 | biostudies-literature

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