Vitamin D-binding protein Antibodies

Vitamin D-binding protein (GC)

Involved in vitamin D transport and storage, scavenging of extracellular G-actin, enhancement of the chemotactic activity of C5 alpha for neutrophils in inflammation and macrophage activation. .

Gene Information

Human
Gene Name:	GC
Uniprot:	P02774
Entrez:	2638

Family

Belongs to:
ALB/AFP/VDB family

Alternative Names

DBP; DBP/GC; DBP-MAF; DBPVDBG; EC 6.3.1.5; Gc; gc-globulin; Gc-MAF; GRD3; group-specific component (vitamin D binding protein); Group-specific component; hDBP; VDB; VDBG; VDBP; Vitamin D BP; vitamin D-binding alpha-globulin; vitamin D-binding protein

Molecular Weight

Mass (kDA):
52.918 kDA

Genomic Context

Human
Location:	4q13.3
Sequence:	4; NC_000004.12 (71741693..71805520, complement)

Tissue Specificity

Expressed in the liver. Found in plasma, ascites, cerebrospinal fluid and urine.

Subcellular Localizations

Secreted.

Diseases

• Cytomegalovirus Infections
• Mycoplasma Pneumonia
• Shwachman Syndrome
• Dyslipidemias
• Coronary Heart Disease
• Atresia
• Microvillous Inclusion Disease
• Encephalitis, St. Louis
• Pelvic Inflammatory Disease
• Essential Fatty Acid Deficiency
• Infertility
• Diffuse Scleroderma

• Immunologic Deficiency Syndromes
• Hemorrhage
• Severe Combined Immunodeficiency
• Neoplasms
• Headache
• Malaria

Pathways

• Transport
• Ovulation
• Luteinization
• Secretion
• Cell Adhesion
• Female Gonad Development
• Cell Proliferation
• Cell Development
• Gluconeogenesis
• Endocytosis
• Oocyte Maturation
• Membrane Fusion
• Glomerular Filtration

• Senescence
• Eclosion
• Flocculation
• Protein Folding
• Gonad Development
• Pathogenesis
• Exocytosis

PTMs

• Phosphorylation

• Deglycosylation

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

Best Uses Of The GC Marker

The GC Marker is an immunoglobulin-derived protein that induces GCs dominated by B cells. It also stimulates memory cells such as IgG+ and IgA+ - to engage in new GC reactions. This article will look at how the GC Marker is useful for these processes. The most significant uses for it are covered in this article. It also explains how the GC Marker can stimulate B cells, IgG+, and IgA+ T cell to engage in GC reactions.

GC Marker can induce GCs dominated B cells

FcRL1 is brought into the immunological synapse through FcRL1's BCR ligation. FcRL1 is recruited to the SH2 domain kinase, c-Abl, upon ligation of BCRs. This increases B cell activation. B cells lacking FcRL1 show decreased activation of plasma cells as well as GC cells. This is not the case in mice without FcRL1.

This discovery could result in more effective and safer vaccines. It could also open the door to treatments for a wide variety of illnesses including B cell tumors and autoimmune diseases. These findings require further study. Researchers can use the Boster Bio GC marker to identify the antigen that triggers B cells that are GC-dominated and other immune responses.

GCs form when B cells express their antigen receptors. Cells produce VLA4, which stabilizes the initial interactions with DCs bearing antigens. Induced GCs recognize the antigen through an immune synapse that is specialized. However, despite these differences B cells are not able to recognize antigens that are infiltrated into tissues.

A combination of factors can trigger this reaction. The BCR is the first. It has two functions in this process: to activate T cells and trigger the GCs that are dominated by B cells. Memory B cells can develop into long-lived plasma cells. They also produce memory B cells. These memory B cells are capable of entering the GC dark zone. They can undergo additional SHM and selection.

Furthermore, a thorough understanding of BCR signalling could lead to more effective vaccines. Studies into the molecular mechanism that drive BCR signalling could lead to improved vaccines or other immunological treatments. Immunologists will soon be able identify and treat illnesses with high accuracy and precision using innovative tools such as the Boster Bio GC marker.

Induction of GCs through IRF4-mediated signalling could be accomplished even in the absence of antigen. This signalling is crucial for the development of broad neutralizing antibodies. IRF4 levels that are induced by a GC marker can help guide HIV vaccine design. However, prolonged activation of this pathway may cause a decline in the number of GC B cells which could be a sign of T cells activated by antigens.

The microenvironment that surrounds the B cell follicle influences its fate. Infectious organisms may send signals that indicate imminent danger to the host, which are interpreted by the innate immune receptors. Pathogen-associated molecular pattern blocks B cells from processing antigens or sending them into processing chambers. If they are exposed CpG-stimulated cells, infection-associated B cells are less likely to seek assistance from T cells.

Induced memory B cells in mice leads to the formation of a large proportion of antigen-specific memory cells (MBCs) and the differentiation of these cells. This results in an entirely unique repertoire of antibodies that guard against the lethal effects of heterosubtypic H5N1 virus. Furthermore, variant proteins of Dengue virus stimulate primarily IgM memory B cells, which have the largest V gene repertoire. These findings highlight the role of a variety of memory B cell populations in the development of immunity.

IgG+ and IgA+ memory cells are able to engage in new GC reactions

In addition, they play a role in class switching and affinity maturation GCs play a major part in B cell differentiation. Due to their affinity maturation B cells in the GC undergo extensive somatic mutations of the genes that make antibodies. The result of this hypermutation is de novo autoreactivity or enhanced affinity of the autoantibody-producing B cells. To stop autoreactivity in memory plasma and B cells, tolerance checkpoints have been suggested.

The mechanism for affinity maturation isn't fully understood. This process takes place when the memory B cells respond to the original antigen. The memory B cell might not recognize the intruder when this happens. If the antigen is changed or the memory B cells are more specific, they may not be able to recognize it. These memory B cells are therefore capable of engaging in new GC reactions.

The study also shows that IgG+ and IgA+ blood B cells come from the same GC pathway. While they are generally regarded as a homogeneous B cell population, they differ greatly in their self-reactivity and poly-reactivity. IgA+ memory cells also have significantly lower self-reactive antibodies. These findings have important implications for the development of IgG+ memory B cells as well as the dysregulation of the immune system in certain autoimmune diseases.

IgG+ and IgA+ cell population are characterized by a low germline variety of Ig gene. Only the functional segments of the Ig gene are accessible to recombination within a number of species of animals. After exposure to these allergens, IgG+ or IgA+ memory cell can participate in new GC reactions.

These B cells can initiate new GC reactions when they encounter an antigen from another country. The B cells may migrate between the two zones, go through multiple cycles of somatic hypermutation and participate in class switch recombination. The ultimate goal of the germinal center is to produce memory cells that are highly sensitive to the antigen they first encounter.

The researchers used FITC-conjugated anti-human IgG antibodies to study the binding of this polymer to antigen. The HEp-2 cells have been examined using an Axio Imager 2(Zeiss), ApoTome.2 system. The images were taken at x40 with the acquisition time of 7000 milliseconds. The filters were then incubated for 2 hours with biotynilated Tritilum vera lectin in order to study N-glycan content.

In the primary immune response, B cells express IgM as the first antibody, and then IgG+ and IgA+, and then shift to IgG+ and IgA+ cells shortly afterward. This is the main immune response. It lasts approximately 30 minutes and is marked by high levels IgM. The second phase is when B cells release IgG and IgA+ memories cells. They then participate in new GC reactions.

It is also able to engage in new GC reactions

GCs produce two types of long-lived "Ab memory" that are circulating memory B cells and PC-secreting high-affinity Ab. Certain Tfh cells can differentiate into long-lived memory, Tfh, which completes the memories derived from GCs. These cells provide layered protection against infection. However, they are typically small in numbers. For this reason, it is essential to know the fundamental mechanisms behind GCs.

MBCs circulate throughout the body and trigger secondary GC reactions swiftly. These MBCs are also capable of producing Ab-secreting cells, which feed forward secondary responses. These reactions are enhanced by new GCs because MBCs from fresh donors possess a greater affinity for the variant pathogen and are more likely to have antigen encounters, and establish protective Abs in the correct class much faster than during the initial response.

B cell proliferation is the first phase of the GC reaction. At this stage B cells purposefully alter the DNA encoding the epitope-binding component of the antigen-binding receptor. The resulting mutations increase ability of B cells to recognize the antigen they are targeting and, as a result, thwart the attempts of the pathogen to escape. The remaining B cells are involved in affinity maturation and are recruited to participate in the GC response.

Reactivated memory cells are a subset of GC-B cells. These memory cells are distinct from the adult immune system and can be cultivated into new germinal centres. They usually express the CCR6 chemokine receptor, which is essential for the correct positioning of memory B cells and optimal recall responses. GC B cells that express Ephrin-B1-positive-S1PR2low phenotypes are the same as memory precursor cells.