B-cell receptor CD22 Antibodies

B-cell receptor CD22 (CD22)

May be involved in the localization of B-cells in lymphoid tissues. Binds sialylated glycoproteins; among which is CD45.

Preferentially binds to alpha-2,6-linked sialic acid. The sialic acid recognition site could be masked by cis interactions with sialic acids on the same cell surface.

Gene Information

Human
Gene Name:	CD22
Uniprot:	P20273
Entrez:	933

Family

Belongs to:
immunoglobulin superfamily

Alternative Names

B-cell receptor CD22; BL-CAM; B-lymphocyte cell adhesion molecule; CD22 antigenMGC130020; CD22 molecule; CD22; sialic acid binding Ig-like lectin 2; Sialic acid-binding Ig-like lectin 2; Siglec2; Siglec-2; SIGLEC2FLJ22814; T-cell surface antigen Leu-14

Molecular Weight

Mass (kDA):
95.348 kDA

Genomic Context

Human
Location:	19q13.12
Sequence:	19; NC_000019.10 (35329169..35347361)

Tissue Specificity

B-lymphocytes.

Subcellular Localizations

Cell membrane; Single-pass type I membrane protein.

Diseases

• Leukemia
• Lymphoma
• Neoplasms
• B-cell Lymphomas
• Malignant Neoplasms
• Lymphoid Leukemia
• Acute Lymphocytic Leukemia
• Chronic Lymphocytic Leukemia
• Lymphoma, Non-hodgkin
• Tissue Adhesions
• Malignant Paraganglionic Neoplasm
• Burkitt Lymphoma
• Hairy Cell Leukemia

• Autoimmune Reaction
• Autoimmune Diseases
• Leukemia, Myelocytic, Acute
• Lupus Erythematosus, Systemic
• Myeloid Leukemia
• Leukemia, B-cell
• Autoimmunity

Interacting Proteins

• LYN
• PLCG1
• PTPN6
• SYK

Pathways

• Cell Activation
• Pathogenesis
• B Cell Activation
• Cell Adhesion
• Cell Development
• Immune Response
• Cell Differentiation
• Cell Death
• Localization
• Cell Proliferation
• Cell Cycle
• B Cell Differentiation
• Lymphocyte Activation

• Secretion
• Glycosylation
• B Cell Proliferation
• Cytokine Production
• Cell Maturation
• Endocytosis
• Cell Growth

PTMs

• Phosphorylation
• Cleavage
• Glycosylation
• Dephosphorylation
• Deglycosylation
• Biotinylation

• Acetylation
• Ribosylation
• Oxidation
• Iodination
• Methylation
• Sulphation

• Reduction

Research Areas

• Adaptive Immunity
• DNA Repair
• Immunology

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/CD22

Best Uses Of The CD22 Marker

CD22 is an important marker of T cells and regulates B-cell responses to T-cell-independent (TI) antigens of type 2. This paper will discuss the ways CD22 can be used to target pathogenic autoreactive B cells. You might be interested in the benefits of Boster Bio's other products for this ligand. Read on if you are. There are many reasons to use this marker.

Activation of MAPK/ERK by CD22

CD22 is a key signaling molecule which interacts with the sialic acid-containing cell surface ligands, which are found on T cell, B cells, neutrophils monocytes, and red blood cells. This cell surface ligand is bound to antigens that are cell-linked (CLAs), glycoproteins that are soluble, as well as tyrosine-rich proteins. It also interacts with B-cell adhesion receptors that regulate B-cell migration.

The CD22 intracellular domain includes the immunoreceptor activation as well as a tyrosine inhibition motif. It also contains two Ig-like domains. The cytoplasmic domain has a function in attracting effector molecules by phosphorylation of six Tyrosine residues that are conserved. CD22 is expressed both on human CD27+ naive cell lines and on acidgranulocytes of the mouse intestinal. This suggests that this marker for cell surface could play a key role in eosinophil regulation.

Although it is well-known that CD22 is a key activator for MAPK/ERK (although there are many nuances) However, it is not completely understood. Boster Bio developed a monoclonal antibody, epratuzumab, that activates the CD22 marker on B cells. This monoclonal antibody stimulates phosphorylation of the inhibitory co-receptors, Maloney A, Dardon C and Shock A. Although the effect isn't as significant but it is a strong evidence for its role in MAPK/ERK activation.

B cells are responsible for the production of anti-DNA antibodies. They play a crucial role in the process of establishing humoral immunity. The presence of anti-dsDNA antibodies in blood is a symptom of SLE. A lack of normal activation of B cells results in autoantibodies, antigen-presenting T-cells, as well as pro-inflammatory cytokines. However, the inflammatory response to these antigens is not always effective.

The CD22 molecule blocks the BCR complex's recognition antigen signal. Studies have demonstrated that mice lacking CD22 showed mild activation as well as an increased number of mature B cell. In addition, B cells which were CD22-deficient showed increased IgM secretion and MHC class II molecule expression. The CD22 molecules is a potent therapeutic target for blood cancers, as well as autoimmune diseases.

Emab boosts the immune response and blocks B-cell activation. It also increases CD22 Tyrosine phosphorylation on Tyr822 which is a key regulatory component on the cell's surface. The CD22 molecule also recruits Grb2, an SH2 adaptor protein that negatively regulates BCR driven events.

The CD22 inhibitor Epratuzumab humanized anti-CD22 IgG1 monoclonal antibody that increases the phosphorylation of CD22. It is the first monoclonal antibody targeting this molecule in clinical trials but its mechanism of effect is still unclear. The anti-CD22 antibody Huki CD22 mouse also has human CD22 rather than murine CD22. They are therefore able to target CD22 molecules without affecting development of B-cells.

The anti-inflammatory properties of Nocardia rubra skulleleton promote T cell differentiation to activate B-cells as as T-cells. This anti-inflammatory agent also promotes the disengagement of T cells from APCs. This triggers TH2 immune response. Additionally, rIL-5 is discovered to enhance the expansion of T cells into clonal form.

Regulation of B-cell response in response to T cell-independent (TI2) type 2 antigens

Cross-linking of mIg receptors from responding B cells and antigen-loaded dendritic cells may be a vital component of T-cell-independent immune response regulation. While these interactions are crucial for initiating the signal transduction process, it isn't enough to promote the proliferation and differentiation of the B cells that respond. These interactions may also cause an unfavourable feedback loop which could result in decreased production of antigen-specific antibodies.

In addition memory B cells require polysaccharide immunization to be able to respond to a secondary challenge by polysaccharide-specific antigens. This requires both an T-cell as well as a Polysaccharide antibody. Antigens that are antigens can induce a variety of immune responses which include cytokinesis.

PKCd mediates the class switch to IgG3 in the response of TI-2. It enhances AID expression during the TD response and is needed for crosslinking of the TI-2 BCR. Many transcription factors cooperate to trigger AID during the TD response. It is crucial that B-cell responses to antigens of TI-2 are managed.

In the absence of any specific T cell assistance germinal center development is blocked, which favors the formation of extra follicular plasma cells. The development of memory cells in mice is similar to that of humans. It is possible that memory B cells are not found in mice. It is important to remember that memory B cells are a tiny part of the immune system. Therefore, they are often not recognized.

T cell-independent antigens are not able to prime individuals for an immune secondary response so they need to be boosted. This is not the case with T-I2 antigens. During the boosting period, memory B cells were unable to detect TNP-specific memory cells. Consequently, this result can be attributed to the in-situ generation of plasma cells with a short lifespan.

The diminution of T-independent antibody responses in mice is due to the depletion of macrophages, not to a decrease in the number of immunocompetent cells. Carbonyl iron treatment did not alter the number of th lymphocytes. Macrophages treated with anti-th, or radiation therapy may restore the responsiveness to T-independent antigens in mice.

CD22 can be targeted to attack pathogenic autoreactive T cells

The immune system is dependent upon CD22. It is expressed on a variety of B cells including mature ones and regulates signaling through TLRs or BCRs. It also regulates the thresholds for signaling in B cells in development and could play a significant role in central selection and tolerance induction. Therefore, Boster Bio targets pathogenic B cells via CD22.

B cells are essential to protecting the body against pathogens. However they also play an important part in the immune system that causes autoimmune diseases. They are responsible for the production of Ab directed against self-Ags, presenting them as antigens and secreting pro-inflammatory cytokines. In addition, B cells may become hyperresponsive, which results in an altered selection and inefficient signaling through TLRs. The targeting of CD22 could be a viable strategy to suppress B cells that are autoreactive.

Although the CD22 molecules is widely recognized as an adhesion molecule Eugene Butcher's lab discovered that it also plays a role in the gut-associated lymphoid system. Peyer's patches are lymphoid tissue found in the gut. They house numerous B cells that are responsive to intestinal Ags. CD22 ligands can be detected on the cells of the endothelial layer in capillaries as well as high-endothelial veins (HEVs) of capillaries. Mice deficient in CD22 have a lower homing rate to the PP.

CD22-mediated endocytosis is also inhibited by antibodies. CD22 engagement by antibodies also triggers activation of SHP-1, Grb2, and may encourage co-localization of the endosomes together with TLRs. In other terms, Boster Bio targets pathogenic B cells that are auto-reactive using CD22 by targeting the CD22 binding signal. This could be an effective tool for future preclinical research.

Although the CD22 polymorphism does not have any connection with susceptibility or RA but it can affect the production of cytokines in situations where TLR and BCR stimulation are applied. This suggests that targeting CD22 by blocking this protein might restore the production of IL-10 by regulatory B cells, which is a crucial molecule in SLE. It could also block the activation of the PRDM1/Blimp1 receptor downstream from TLR7 which can restore IL-10 production by regulatory B cells, a major Cytokine in SLE.

The Chimeric Antigen Receptor (CAR) T-cell therapy that has specifically targeted CD22 has been proven in pre-B-cell acutely lymphoblastic leukemia. The treatment has also demonstrated significant results in patients who had previously failed to respond with chemotherapy. This treatment may not be as efficient as the CD19-directed immunotherapy. More studies are required to verify the efficacy of the drug.

The treatment also stops the expansion of CD22-/ B cells in patients with known 11q23 rearrangement. It has been demonstrated that CD22-/B cells show a rapid expansion and hyperproliferation antibodies in patients with all kinds of cancers. This is the only one of its kind that targets B cells that are pathogenic and autoreactive by CD22.