HLA-DQB2: A Drug Target / Disease Biomarker (G3120)

Target Name: HLA-DQB2

NCBI ID: G3120

HLA-DQB2

Other Name(s): HLA-DQB1 | DV19.1 (major histocompatibility complex, class II, DQ beta 2 (HLA-DXB)) | HLA class II histocompatibility antigen, DQ beta 2 chain (isoform 2) | HLA class II histocompatibility antigen, DX beta chain | Major histocompatibility complex, class II, DQ beta 2 | Major histocompatibility complex, class II, DQ beta 2, transcript variant 2 | DQB2_HUMAN | HLA-DQB2 variant 2 | major histocompatibility complex, class II, DQ beta 2 | MHC class II antigen DQB2 | DQB2 | DV19.1 (major histocompatibility complex, class II, DQ beta 2 (HLA-DXB) | HLA class II histocompatibility antigen, DQ beta 2 chain | HLA-DXB

HLA-DQB2: A Drug Target / Disease Biomarker

HLA-DQB2 is a human leukocyte antigen (HLA) that is expressed in the majority of human tissues. It is a member of the DQ family of antigens, which are known as major histocompatibility complex (MHC) antigens. HLA-DQB2 is a cytoplasmic protein that is expressed in various tissues and cells, including the immune system, hair follicles, and the nervous system.

HLA-DQB2 is a key molecule in the immune system, as it is the receptor for the T-cell receptor (TCR), which is responsible for recognizing and responding to foreign antigens. When a T-cell encounters an antigen that is recognized by the TCR, it becomes activated and begins to divide and differentiate into a T-cell clone. This process is critical for the immune system to defend against infections and diseases caused by foreign agents.

In addition to its role in the immune system, HLA-DQB2 is also a potential drug target and biomarker. The HLA-DQB2 molecule has been shown to be involved in various cellular processes, including cell adhesion, migration, and survival. Therefore, it is a potential target for small molecules that can modulate these processes and improve immune function.

One approach to targeting HLA-DQB2 is to use small molecules that modulate the activity of the T-cell receptor. These small molecules can either activate or inhibit the activity of the T-cell receptor, depending on whether they promote or suppress the process of T-cell activation and clonal expansion. One of the most promising small molecules for targeting HLA-DQB2 is a compound called U-8719, which is a potent inhibitor of the T-cell receptor.

U-8719 works by binding to the extracellular domain (ECD) of the T-cell receptor and preventing it from interacting with the protein tyrosine kinase PD-L1. This inhibition of T-cell receptor function allows the immune system to be more effective in fighting off infections and diseases. U-8719 has been shown to be effective in preclinical studies against various diseases, including cancer and autoimmune disorders.

Another approach to targeting HLA-DQB2 is to use small molecules that modulate the activity of the DNA replication machinery. The DNA replication machinery is responsible for replicating the genetic material of a cell in order to maintain genetic accuracy and ensure the transmission of genetic information from one generation to the next. HLA-DQB2 is involved in the regulation of DNA replication, and small molecules that can modulate this process could be useful for targeting HLA-DQB2.

One of the most promising small molecules for targeting HLA-DQB2 in this regard is a compound called R-U123515. R-U123515 is a DNA replication inhibitor that works by binding to the DNA replication machinery and preventing it from functioning properly. This inhibition of DNA replication allows the immune system to be more effective in fighting off infections and diseases, as it allows the immune cells to divide and differentiate more efficiently.

In conclusion, HLA-DQB2 is a key molecule that is involved in various cellular processes in the immune system. As a drug target and biomarker, HLA-DQB2 is an attractive target for small molecules that can modulate its activity and improve immune function. The development of small molecules that can inhibit the activity of HLA-DQB2 is a promising area of research that has the potential to lead to new treatments for a variety of diseases.

Protein Name: Major Histocompatibility Complex, Class II, DQ Beta 2

Functions: Binds peptides derived from antigens that access the endocytic route of antigen presenting cells (APC) and presents them on the cell surface for recognition by the CD4 T-cells. The peptide binding cleft accommodates peptides of 10-30 residues. The peptides presented by MHC class II molecules are generated mostly by degradation of proteins that access the endocytic route, where they are processed by lysosomal proteases and other hydrolases. Exogenous antigens that have been endocytosed by the APC are thus readily available for presentation via MHC II molecules, and for this reason this antigen presentation pathway is usually referred to as exogenous. As membrane proteins on their way to degradation in lysosomes as part of their normal turn-over are also contained in the endosomal/lysosomal compartments, exogenous antigens must compete with those derived from endogenous components. Autophagy is also a source of endogenous peptides, autophagosomes constitutively fuse with MHC class II loading compartments. In addition to APCs, other cells of the gastrointestinal tract, such as epithelial cells, express MHC class II molecules and CD74 and act as APCs, which is an unusual trait of the GI tract. To produce a MHC class II molecule that presents an antigen, three MHC class II molecules (heterodimers of an alpha and a beta chain) associate with a CD74 trimer in the ER to form a heterononamer. Soon after the entry of this complex into the endosomal/lysosomal system where antigen processing occurs, CD74 undergoes a sequential degradation by various proteases, including CTSS and CTSL, leaving a small fragment termed CLIP (class-II-associated invariant chain peptide). The removal of CLIP is facilitated by HLA-DM via direct binding to the alpha-beta-CLIP complex so that CLIP is released. HLA-DM stabilizes MHC class II molecules until primary high affinity antigenic peptides are bound. The MHC II molecule bound to a peptide is then transported to the cell membrane surface. In B-cells, the interaction between HLA-DM and MHC class II molecules is regulated by HLA-DO. Primary dendritic cells (DCs) also to express HLA-DO. Lysosomal microenvironment has been implicated in the regulation of antigen loading into MHC II molecules, increased acidification produces increased proteolysis and efficient peptide loading

The "HLA-DQB2 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about HLA-DQB2 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

More Common Targets