7069477

CD366 (TIM3) Monoclonal Antibody (8B.2C12), eBioscience™, Invitrogen™

Rat Monoclonal Antibody

Manufacturer: Fischer Scientific

The price for this product is unavailable. Please request a quote

Antigen

CD366 (TIM3)

Concentration

0.5 mg/mL

Classification

Monoclonal

Form

Liquid

Regulatory Status

RUO

Formulation

PBS with 0.09% sodium azide; pH 7.2

Gene Alias

CD366; FLJ14428; Havcr2; HAVcr-2; Hepatitis A virus cellular receptor 2; hepatitis A virus cellular receptor 2 homolog; kidney injury molecule-3; KIM-3; sCD366; soluble CD366; soluble TIM 3; T cell immunoglobulin mucin 3; T cell immunoglobulin mucin-3; T-cell immunoglobulin and mucin domain containing 3; T-cell immunoglobulin and mucin domain-containing protein 3; T-cell immunoglobulin mucin family member 3; T-cell immunoglobulin mucin receptor 3; T-cell membrane protein 3; Tim3; TIM-3; TIMD3; TIMD-3

Gene Symbols

Havcr2

Primary or Secondary

Primary

Content And Storage

4° C

Gene

Havcr2

Clone

8B.2C12

Applications

Flow Cytometry, Immunohistochemistry, Immunoprecipitation

Conjugate

Unconjugated

Host Species

Rat

Target Species

Mouse

Gene Accession No.

Q8VIM0

Gene ID (Entrez)

171285

Isotype

IgG1 κ

Purification Method

Affinity chromatography

Product Type

Antibody

Related Products

Img

Fischer Scientific

7069297

Rat Monoclonal Antibody...

Img

Fischer Scientific

7068095

Mouse Monoclonal Antibody...

Img

Fischer Scientific

7068606

Rat Monoclonal Antibody...

Img

Fischer Scientific

7069506

Rat Monoclonal Antibody...

Img

Fischer Scientific

7068775

Rat Monoclonal Antibody...

Img

Fischer Scientific

7068093

Mouse Monoclonal Antibody...

Img

Fischer Scientific

7068093

Mouse Monoclonal Antibody...

Img

Fischer Scientific

7068931

Mouse Monoclonal Antibody...

Description

  • Description: The 8B.2C12 monoclonal antibody reacts with mouse CD366 (TIM3), a Th1-specific cell surface protein
  • CD366 is a type I transmembrane protein and contains an immunoglobulin and a mucin-like domain in its extracellular portion and a tyrosine phosphorylation motif in its cytoplasmic portion
  • CD366 is expressed selectively by differentiated CD4+ Th1 and CD8+ Tc1, but is absent on Th2 and Tc2
  • Other hematopoietic cell types, including naive T cells, B cells, macrophages and dendritic cells, do not express CD366, at least at the protein level
  • Expression of CD366 is upregulated at a late stage of T cell differentiation on Th1 cells after 3 rounds of in vitro polarization suggesting a role for this molecule in the transport or effector function of Th1 cells rather than a contribution to T cell differentiation
  • In an experimental autoimmune encephalomyelitis (EAE) model, CD366 was shown to be expressed on most CD4+ and CD8+ T cells in the central nervous system at the onset of clinical signs of disease, while less than 2% of CD4+ cells in the periphery expressed CD366 after immunization
  • In this model, in vivo administration of 8B.2C12 resulted in a hyperacute and atypical disease phenotype
  • It is postulated that the engagement of CD366 during T cell activation results in the expansion and activation of macrophages and increased severity of autoimmune disease
  • The Tim gene family may have an important role in the regulation of autoimmunity and allergies
  • TIM3 (Hepatitis A virus cellular receptor 2, HAVCR2, T-cell immunoglobulin, mucin-dmain containing-3) is a 281 amino acid long, Type-1 Th1- specific cell surface glycoprotein expressed on terminally differentiated CD4+Th1 and CD8+Tc1 cells
  • TIM3 consists of an IgV-like domain, a mucin-like domain in the extracellular region, and a conserved Tyrosine phosphorylation motif in the cytoplasmic region
  • TIM3 is involved in macrophage activation and induction of autoimmune diseases
  • Further, TIM3 down-regulates aggressive Th1-mediated immune responses and facilitates in the development of immune tolerance
  • Pathological significance of TIM3 has been attributed to Experimental autoimmune encephalomyelitis (EAE), a Th-1 dependent autoimmune disease, and also enhances the severity of experimental autoimmune encephalomyelitis in mice.