Скачать или смотреть Etigilimab Unveiling the Role of Anti-TIGIT in Cancer Research

https://www.assaygenie.com/anti-tigit...

1. Introduction to Etigilimab:

Etigilimab, also known as MGA271, is a monoclonal antibody that targets TIGIT (T-cell immunoreceptor with Ig and ITIM domains). TIGIT is identified as an "immune checkpoint receptor that dampens immune responses, allowing cancer cells to evade detection." Etigilimab's primary function is to inhibit this receptor, thereby "reactivat[ing] T-cells and NK cells, fostering a robust anti-tumor immune response." Developed by Mereo BioPharma, Etigilimab represents a key effort in cancer research to leverage the body's own immune system to combat malignancies. The article emphasizes that anti-TIGIT therapies like Etigilimab are frequently explored in conjunction with PD-1 or PD-L1 inhibitors to achieve "synergistic effects."

Key Quote: "Etigilimab inhibits TIGIT, a receptor that suppresses T-cell activity, enhancing the immune system's ability to combat tumors."

2. Mechanism of Action:

The core of Etigilimab's efficacy lies in its ability to disrupt the interaction between TIGIT and its ligands, CD155 (PVR) and CD112 (nectin-2), which are commonly found on tumor cells and antigen-presenting cells within the tumor microenvironment. When TIGIT binds to these ligands, it transmits inhibitory signals that suppress the activity and proliferation of T-cells.

By blocking this interaction, "Etigilimab promotes T-cell activation, enhances cytokine production, and restores immune surveillance. Additionally, it boosts NK cell-mediated cytotoxicity, further contributing to its anti-cancer effects."

A crucial aspect of this mechanism involves the competition between TIGIT and CD226 (DNAM-1), a co-stimulatory receptor, for the same ligands. The presence of TIGIT typically diminishes CD226's activation, leading to impaired immune responses. Etigilimab effectively "restores CD226-mediated signaling by preventing TIGIT’s inhibitory binding, thereby enhancing the activation and function of effector T-cells and NK cells."

Preclinical studies have shown that Etigilimab not only increases T-cell proliferation but also boosts the production of vital cytokines for anti-tumor immunity, such as "interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α)." Furthermore, it amplifies the ability of NK cells to destroy tumor cells, indicating a dual mechanism of immune activation.

The article highlights the potential of combining Etigilimab with PD-1/PD-L1 inhibitors: "PD-1 blockade prevents T-cell exhaustion, while TIGIT inhibition restores T-cell and NK cell activity. This complementary interaction addresses multiple pathways of immune suppression, making it a promising strategy in cancer immunotherapy."