FCGR2A Antibodies

Low affinity immunoglobulin gamma Fc region receptor II-a (FCGR2A)

Binds to the Fc region of immunoglobulins gamma. Low affinity receptor.

By binding to IgG it initiates cellular responses against pathogens and soluble antigens. Promotes phagocytosis of opsonized antigens.

Gene Information

Human
Gene Name:	FCGR2A
Uniprot:	P12318
Entrez:	2212

Family

Belongs to:
No superfamily

Alternative Names

CD32 antigen; CD32a; CD32MGC23887; CDw32fc-gamma-RIIa; Fc fragment of IgG, low affinity IIa, receptor (CD32); Fc fragment of IgG, low affinity IIa, receptor for (CD32); Fc gamma RIIA; FCG2; Fc-gamma RII-a; Fc-gamma-RIIa; FcGR; FCGR2; FCGR2A; FCGR2A1; FcgRIIA; FCRIIA; fcRII-a; IGFR2MGC30032; IgG Fc receptor II-a; Immunoglobulin G Fc receptor II; low affinity immunoglobulin gamma Fc region receptor II-a

Molecular Weight

Mass (kDA):
35.001 kDA

Genomic Context

Human
Location:	1q23.3
Sequence:	1; NC_000001.11 (161505430..161524048)

Tissue Specificity

Found on monocytes, neutrophils and eosinophil platelets.

Subcellular Localizations

Cell membrane; Single-pass type I membrane protein.

Diseases

• Lupus Erythematosus, Systemic
• Autoimmune Reaction
• Autoimmune Diseases
• Arthritis
• Rheumatoid Arthritis
• Inflammation
• Dysequilibrium Syndrome
• Malignant Neoplasms
• Malaria
• Malaria, Falciparum
• Infective Disorder
• Autoimmunity
• Lymphoma

• Ulcer
• Colorectal Cancer
• Colorectal Neoplasms
• Pneumonia
• Nephritis
• Neoplasms
• Mucocutaneous Lymph Node Syndrome

Interacting Proteins

• UBQLN1

Pathways

• Pathogenesis
• Immune Response
• Phagocytosis
• Antibody-dependent Cellular Cytotoxicity
• Platelet Activation
• Secretion
• Inflammatory Response
• Platelet Aggregation
• Cell Activation
• Complement Activation
• Respiratory Burst
• Virulence
• Mast Cell Activation

• Type I Interferon Production
• Cell Maturation
• System Process
• Chemotaxis
• Cholesterol Efflux
• Receptor-mediated Endocytosis
• Cell Proliferation

PTMs

• Phosphorylation

• Oxidation

• Ubiquitination

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/FCGR2A

Best Uses of the FCGR2A Marker

Boster can also receive results from scientists in addition to the many applications of the FCGR2A mark. They can submit results that relate to species, applications, or special samples and be awarded credit for their work. All of these options are available to scientists around the world. The best uses for FCGR2A markers are described in this article. We'll look at only a few. Continue reading to learn more.

Expression of FCGR2A in HNSCC

In the article "Best uses of the FCGR2A marker in the treatment of human neuronal tumors," four researchers (Ciprotti, Ozlem, Tebbutt, and Nussinov) examine the clinical and biological implications of this gene expression marker. The authors, Marika Ciprotti, Avigail Ozlem and Elia Nussinov, present their latest findings.

This study was carried out by researchers from the J Craig Venter Institute, the NIAID, Immunogenet Lab and the Soroka Medical Center, Beer Sheva, Israel. They explain the use of the FCGR2A gene to detect HNSCC. The research team was supported by grants from NIH and the National Institutes of Health (NIH).

Correlation between FCGR2A expression and immune-labeled gene expression

One of the most significant advantages of FCGR2A is its ability to identify precisely IgG-like antibodies. The FCGR2A receptor binds to human IgG1 or IgG3 antibodies. However, FCGR2A polymorphisms can affect its levels and affinity for IgG molecules. A variant of this gene which has histidine in position 131 is able to interact better with IgG2 molecules than its counterpart with IgG1.

FCGR2A is also a benefit because it is sensitive and specific for lung transplantation. This means it has a high success rate. It can also be used to predict the outcome of lung transplantation. The FCGR polymorphism, in conjunction with its ligands, may be used to unravel intricate mechanisms that control the immune response and the outcome of lung allografts. It is possible to develop individual preventative strategies for patients by using the FCGR genotype, as well as ligands.

This marker has its advantages, but it also has its drawbacks. A positive FCGR2A genotype is not guaranteed to prevent the loss of grafts among patients with cystic Fibrosis. In these patients it is possible that the FCGR genotype could be the most effective way to avoid the possibility of a bacterial infection since it helps the LTR to overcome the initial acute rejection. Clinical trials are required to confirm that FCGR2A genotypes can be used to predict the outcome of LTR treatments.

A recent study revealed that FCGR2A polymorphisms were detected in 158 LTRs as well as 184 CTLs. It was found that a combination of genotypes was an indicator of the response to chemotherapy. Researchers discovered that patients with FCGR3A polymorphism were less likely to receive chemotherapy. A significant proportion of patients with cancer had FCGR2A alleles.

The FCGR2A marker is also able to identify patients suffering from early-stage DSA. It is highly sensitive and can be used to detect graft dysfunction. It could also be used to detect patients with low-affinity CD16 F alleles. It is interesting that the FCGR2A marker is available from Boster Bio's online shop. For more details, visit their website.

In a study conducted recently, patients with FCGR2A 158 V/V had significantly longer PFS compared to patients with FCGR3A 158 F/F. This study shows that the FCGR2A polymorphism does not correlate with responses rates. The study also demonstrated that FCGR3A polymorphisms don't predict the course of disease or the outcome. The FCGR2A study suggests that FCGR2A polymorphisms are able to identify patients with B-cell Lymphoma.

Another use of the FCGR2A marker is in the field immune checkpoint cell cytotoxicity. When activated by FcR NK cells can detect inflammatory and cytokines. They also release cytotoxic granules. The FCGR3A polymorphism also influences the effectiveness of IgG immunotherapy to reduce the risk of developing cancer.

Relationship between FCGR2A expression and the grade of tumor in HNSCC

The low survival rate of HNSCC is compounded by significant toxicities associated with current treatment strategies. Immunosuppressive therapy, a promising alternative to conventional chemotherapy, is aimed at enhancing the immune system and reducing tumor growth. The immune system plays an important role in the development and growth of cancer. Tumor cells can evade immune surveillance by using checkpoint pathways to suppress antitumor T-cell responses.

We have determined the relationship between FCGR2A expression and HNSCC grade using data from the HNSCC cohort of the TCGA. We employed a consensus clustering model, which included the cumulative distribution function (k= 2-9) to calculate the overall survival rate of HNSCC patients. The results revealed a strong positive correlation between FCGR2A expression and the grade of tumor.

The TCGA's HNSCC data includes RNA-seq data for 502 patients as well as 44 healthy controls. Clinicopathological information includes tumor grade and TNM staging. We also utilized TCGA's extensive TCGA–Tx db to analyze lncRNA levels in tumor samples. This study has important implications for developing new clinical markers and therapeutic targets.

Several factors contribute to immunosuppression in HNSCC. Inflammation promotes tumor growth, while M1 macrophages aid in the immune response against malignant cells. Tumors with a high proportion of TAMs are more likely to suffer adverse outcomes following surgery and chemotherapy. TAMs can also be associated with poor prognosis. Tregs are commonly overexpressed HNSCC. They inhibit immune responses by secreting IL-10, and using to increase the survival of T cells in the environment. factors.

The immune system of HNSCC is unique, and includes distinct molecular subtypes. The majority of HPV-positive HNSCC are found in atypical tumors. The basal subtype, which is closely associated with lung squamous cells cancer is also associated with carcinogenesis from tobacco. The mesenchymal type has the highest immune infiltration and the most cytolytic activity.

This study found that tumors that had lower levels of CD56dim NK cells infiltration had higher levels of FCGR2A expression in HNSCC. The NK cell infiltration levels in HNSCC were the highest in tumors carrying genetic smoking signatures. These cancers can be treated by immunotherapy that targets immune cells.