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Human Leukocyte Antigen (HLA) class I and class II molecules, along with various immune cell antigens, constitute a diverse group of cell surface proteins critical for immune surveillance and response. HLA class I molecules (HLA-A, -B, -C) are expressed on all nucleated cells and present endogenous peptides to CD8+ cytotoxic T cells, while HLA class II molecules (HLA-DR, -DP, -DQ) are primarily expressed on professional antigen-presenting cells to present exogenous peptides to CD4+ helper T cells [1]. The additional immune cell antigens component encompasses a vast array of Cluster of Differentiation (CD) markers, such as CD3, CD19, and CD20, as well as immune checkpoints like PD-1 and CTLA-4, which serve as vital regulatory nodes in the immune system [2]. These molecules are primary targets in oncology, where monoclonal antibodies and CAR-T cell therapies are designed to either deplete specific cell populations or unleash the immune system against tumors [3]. In the context of transplantation and autoimmunity, these antigens are targeted to suppress unwanted immune activation and prevent graft rejection [1]. Due to their central role in immune signaling, therapeutic modulation of these targets requires precise control to avoid severe adverse effects like cytokine release syndrome or profound immunosuppression [3].
Modulation of antigen presentation, T-cell activation inhibition, B-cell depletion, and immune checkpoint blockade.
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