Investigating T Cell Immunity in Cancer: Achievements and Prospects

Abstract

T cells play a key role in tumour surveillance, both identifying and eliminating transformed cells. However, as tumours become established they form their own suppressive microenvironments capable of shutting down T cell function, and allowing tumours to persist and grow. To further understand the tumour microenvironment, including the interplay between different immune cells and their role in anti-tumour immune responses, a number of studies from mouse models to clinical trials have been performed. In this review, we examine mechanisms utilized by tumour cells to reduce their visibility to CD8+ Cytotoxic T lymphocytes (CTL), as well as therapeutic strategies trialled to overcome these tumour-evasion mechanisms. Next, we summarize recent advances in approaches to enhance CAR T cell activity and persistence over the past 10 years, including bispecific CAR T cell design and early evidence of efficacy. Lastly, we examine mechanisms of T cell infiltration and tumour regression, and discuss the strengths and weaknesses of different strategies to investigate T cell function in murine tumour models.

A potential platform of combining sialic acid derivative-modified paclitaxel cationic liposomes with antibody–drug conjugates inspires robust tumor-specific immunological memory in solid tumors

“…The success of T cell responses depends largely on the ability of T cells to act as effectors and generate long-term antigen-specific memory. 77,78 CD44 is observed on memory T cells, distinguishing them from naive T cells. Memory T cells can be further classified into many phenotypes, 79 such as central memory T cells (T CM , CD3 + CD8 + CD44 + CD62L + ) and effector memory T cells (T EM , CD3 + CD8 + CD44 + CD62L − ), and here we detected a broad phenotype of CD3 + CD8 + CD44 + to verify the generation of memory T cells.…”

T cell effects and mechanisms in immunotherapy of head and neck tumors

“…All nucleated cells express major histocompatibility complex (MHC) class I molecules, and HNCs are no exception [ 27 ]. Once T cells detect the antigen peptide-MHC I complex presented by HNCs, CD8+ T cells are activated to form CTLs, thus destroying tumor cells that present target antigens.…”

“…Once T cells detect the antigen peptide-MHC I complex presented by HNCs, CD8+ T cells are activated to form CTLs, thus destroying tumor cells that present target antigens. In mouse experiments, Malik et al [ 28 ] found that CD8+ T cells isolated from vitiligo patients (patients with vitiligo overexpress CD8+ T cells) could be recognized in vitro and trigger apoptosis of mouse melanoma tumor cells [ 27 , 29 ]. This experiment showed that CTL had a direct killing effect on tumor cells.…”

Immunotherapy Plus Radiotherapy for the Treatment of Sarcomas: Is There a Potential for Synergism?

“… 39 Finally, CD8+ T cells are activated into CTL, becoming the main force that kills tumor cells. 40 , 41 This anti-tumor immune response process is negatively regulated by MDSCs, Treg cells, TAMs (M2 phenotype), and CAFs. 29 , 30 , 42 …”