CD155 Immune Checkpoint Molecule for Drug Development

CD155 is an adhesion molecule that is upregulated during tumor progression and promotes the proliferation and migration of tumor cells through multiple pathways. At Creative Biolabs, we aim to provide you with the theoretical support and technical assistance necessary for your research on immune checkpoint-related studies.

Key Member	Names	Source	Functions
CD155	Poliovirus receptor, NECL-5	Monocytes, macrophages, thymocytes and CNS neurons	Mediates NK adhesion and triggers its function, participates in mediating tumor cell invasion and migration, and is also an attachment receptor for poliovirus.

A schematic diagram illustrating the mechanisms of TIGIT/CD155. (Wang, 2022) Fig.1. Mechanisms of TIGIT/CD155.^1,2

Structure and Expression of CD155

CD155 is a significant member of the immunoglobulin superfamily, characterized by the presence of immunoglobulin-like domains V, C1, and C2 in its extracellular region. Notably, four splice isoforms of CD155 (α, β, γ, and δ) have been successfully identified. While CD155 is expressed at low levels or not at all in most healthy tissues, it exhibits remarkable overexpression in various human malignant tumors.

Mechanism and Function of CD155

CD155 exerts its influence on tumor cells' proliferation, migration ability, and immune system function through diverse pathways. Specifically, CD155 interacts with CD226, TIGIT, and CD96, resulting in both co-stimulatory and co-inhibitory signals.

Key Member	Features	Source	Functions
CD226	Co-stimulatory	NK cells, T lymphocytes, monocytes, and B cells	Competes with TIGIT for binding to CD155.
TIGIT	Co-inhibitory	T cells and NK cells	Facilitates lymphocyte dysfunction and low reactivity, leading to immune evasion of tumor cells.
CD96	Co-inhibitory	T cells and NK cells	Exerts immunosuppressive actions within the tumor microenvironment. CD96 inhibits the activity of CD8⁺ T cells and induces functional impairment

CD155 and Tumors

CD155's abundant expression in tumor cells contributes to immune evasion strategies, primarily through three CD155-related pathways that inhibit adaptive immunity and T-cell function:

CD155/TIGIT-mediated inhibition of PI3K/MAPK signaling.
CD155/TIGIT-mediated inhibition of NF-κB signaling.
CD155/TIGIT-mediated inhibition of AKT/mTOR signaling.

Moreover, elevated CD155 expression has been associated with enhanced invasive capabilities of tumor cells and their involvement in cell-matrix interactions.

Research on CD155 as an Anti-cancer Intervention

CD155/TIGIT presents itself as a promising target for tumor immunotherapy. Current clinical interventions mainly focus on anti-TIGIT monoclonal antibodies or combination inhibitors. In vitro co-culture studies have demonstrated that anti-TIGIT treatment can effectively eliminate immune suppression of tumor cells by downregulating Arg1 and reducing TGF-β1 secretion.

Our Services

At Creative Biolabs, our commitment extends beyond providing theoretical support and an in-depth understanding of CD155/TIGIT's role in tumors via our support page. We offer comprehensive service projects designed to provide you with technical assistance and diverse service options for the application of immune checkpoint inhibitors in tumor treatments. Contact us today to explore how our state-of-the-art solutions can propel your projects to new heights and revolutionize the way you approach immune checkpoint studies.

References

Wang, Daijun, et al. "Role of CD155/TIGIT in digestive cancers: promising cancer target for immunotherapy." Frontiers in Oncology 12 (2022): 844260.
Under Open Access license CC BY 4.0, without modification.

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