Peranan Lymphocyte Activation Gene-3 (LAG-3) pada Mekanisme “Immune Escape” dalam Karsinoma Sel Skuamosa Oral

Abstract

Oral squamous cell carcinoma (OSCC) is a malignant lesion in the oral cavity with the 6th ranking and a percentage of 90% of the most common malignancies. Malignant lesions have one of the characteristics in the form of immune escape ability, which is the event that tumor cells escape from recognition or attack by the immune system through various mechanisms so that tumor cells can survive and grow rapidly. Immune escape is achieved by using membrane proteins as ligands to bind to the membrane receptors of tumor infiltrating lymphocytes (TIL). Lymphocyte activation gene-3 (LAG-3) and Fibrinogen protein like 1 (FGL1) are potential receptor-ligand pairs involved in this mechanism. High affinity of LAG-3 and FGL1 will increase tumor growth by inhibiting the immune microenvironment. The impact of this binding is in the form of increased production of immunosuppressive cytokines and exhaustion of T cells or T cell dysfunction, thereby reducing T cell activity and promoting immune escape. The aim of this study was to determine the location of LAG-3 expression and its relationship to the immune response mechanism in oral squamous cell carcinoma. The research method used is an analytical observational method with a cross-sectional design. Tumor samples carry out from the Anatomical Pathology Laboratory RSD dr. Soebandi Jember which was recorded from 2017-2022. LAG-3 is declared positive if there is overexpression in lymphocytes and/or tumor cells with immunohistochemistry (IHC) staining. The results showed that LAG-3 expression was found in lymphocyte cells (TIL) and tumor cells of OSCC with different degrees of intensity. Overexpression of LAG-3 is thought to play a role in the immune escape mechanism through suppresing TIL activation by FGL1 which binds to LAG-3 on the TIL surface and also its expression on tumor cells is thought to function for tumor growth and development.