Rapid progress in the field of cancer immunotherapy is a result of advances in our understanding of immune marker expression, antigen presentation, and the cell-mediated immune response involving CD3+ T-lymphocytes. T-cells are crucial to the body’s immune response to cancer, both endogenously and following therapeutic intervention. A T-cell marker panel that can identify subsets of tumor-associated T-cells allows scientists to identify and target subpopulations of T-cells playing unique roles in the immune response against a tumor.
CD4+ and CD8+ T-cells participate in the anti-tumor immune response at the site of the tumor or in the periphery, such as in tumor-draining lymph nodes. Among the T-cells localized to the tumor, some enter the tumor as naïve cells and undergo maturation within the tumor 1. Others are primed in the periphery and subsequently traffic to the site of the tumor to participate in the effector or memory response against an established tumor 2. Adhesion molecules including CD31 3, CD43 4 and CD44 5 help regulate the migration of these T-cells.
Within the tumor microenvironment, a positive prognosis is usually conferred to patients bearing solid tumors with a high CD8+ T-cell infiltrate 6, as tumor-infiltrating cytotoxic T-cells are the crucial mediator of anti-tumor immune responses. However, CD8+ T-cell activity can be regulated within the tumor microenvironment. Myeloid cells, CD4+ helper T-cells, and tumor cells can modulate the level of both maturation and activation of a CD8+ T-cell. Among many, T-cell exhaustion and anergy are major challenges to the maintenance of anti-tumor immune responses 7, and can be monitored via changes to cell surface molecules.
In parallel, CD4+ T-cells can support an ongoing immune response against solid tumors through the promotion of a Th1-skewed microenvironment that primes CD8+ T-cells. Th17-polarized CD4+ T-cells, too, have recently been shown in mouse models to promote anti-tumor immune responses, possibly due to their memory-like phenotype. However, depending on both the type of cancer and the phenotype of the T-cells, CD4+ T-cells may confer either a positive or negative prognosis. While helper and memory CD4+ T-cells bolster the inflammatory response, regulatory T-cells suppress ongoing immune responses and can promote tumor progression 8.
T-cell marker research is crucial to our understanding of how the immune response to a tumor is affected. Being able to categorize subsets of T-cells based on their physiologic localization and maturation state in a variety of human cancer types and corresponding mouse models will improve the ability to target crucial T-cell subsets for activation or inhibition at different stages of tumor progression. Additionally, characterizing molecules that may function as novel immune checkpoints or exhaustion markers within the context of cancer, including CD5 9, can build on the successes of anti-CTLA4 and anti-PD-1 therapies, translating this field into the clinic yet again.
Our current T-cell marker portfolio consists of these polyclonal and monoclonal – including our new recombinant rabbit monoclonal antibodies (RmAbs) – products:
T-Cell Regulation/Immune Checkpoints
Studies show only 50% of antibodies can be trusted to work the way they’re designed to.* That’s where Bethyl is different. We have been producing antibodies that deliver reliable results for over 45 years. Our antibodies are manufactured and validated on-site to ensure target specificity and sensitivity. Validation is a continuous process at Bethyl, and we routinely evaluate new lots side-by-side with old lots to ensure lot-to-lot consistency. If a product doesn’t meet our standards, it doesn’t leave our facility. Interested in learning more about our validation process? Click here.