TCR V alpha 3.2 Monoclonal Antibody (RR3-16), PerCP-eFluor™ 710, eBioscience™, Invitrogen™

Beschreibung

Description: This RR3-16 monoclonal antibody reacts with the mouse T cell receptor (TCR) V alpha 3.2 chain. Composed of an alpha and beta chain, TCR specificity is typically determined by Va, Ja, Vb, Db, and Jb gene rearrangement. The RR3-16 antibody recognizes the V alpha 3.2 chain on T cells from mouse strains bearing the b (e.g., C57BL/6) or c haplotype (e.g., SJL, SWR, and NOD) in the Tcra gene complex. The V alpha 3.2 chain is absent in mice with the a (e.g., Balb/c, AKR, C3H) and d (e.g., DBA/1 and DBA/2) haplotypes. Studies demonstrate that the V alpha 3.2 TCR is more highly expressed on CD8+ T cells. Applications Reported: This RR3-16 antibody has been reported for use in flow cytometric analysis. Applications Tested: This RR3-16 antibody has been tested by flow cytometric analysis of mouse splenocytes. This can be used at less than or equal to 0.125 μg per test. A test is defined as the amount (μg) of antibody that will stain a cell sample in a final volume of 100 μL. Cell number should be determined empirically but can range from 10^5 to 10^8 cells/test. It is recommended that the antibody be carefully titrated for optimal performance in the assay of interest. PerCP-eFluor™ 710 can be used in place of PE-Cy5, PE-Cy5.5 or PerCP-Cy5.5. PerCP-eFluor™ 710 emits at 710 nm and is excited with the blue laser (488 nm). Please make sure that your instrument is capable of detecting this fluorochrome.

For a filter configuration, we recommend using the 685 LP dichroic mirror and 710/40 band pass filter, however the 695/40 band pass filter is an acceptable alternative. Our testing indicates that PerCP-eFluor® 710 conjugated antibodies are stable when stained samples are exposed to freshly prepared 2% formaldehyde overnight at 4°C, but please evaluate for alternative fixation protocols. Excitation: 488 nm; Emission: 710 nm; Laser: Blue Laser. Filtration: 0.2 μm post-manufacturing filtered. The ability of T cell receptors (TCR) to discriminate foreign from self-peptides presented by major histocompatibility complex (MHC) class II molecules is essential for an effective adaptive immune response. TCR recognition of self-peptides has been linked to autoimmune disease. Mutant self-peptides have been associated with tumors. Engagement of TCRs by a family of bacterial toxins know as superantigens has been responsible for toxic shock syndrome. Autoantibodies to V beta segments of T cell receptors have been isolated from patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). The autoantibodies block TH1-mediated inflammatory autodestructive reactions and are believed to be a method by which the immune system compensates for disease. Most human T cells express the TCR alpha-beta and either CD4 or CD8 molecule (single positive, SP). A small number of T cells lack both CD4 and CD8 (double negative, DN). Increased percentages of alpha-beta DN T cells have been identified in some autoimmune and immunodeficiency disorders. Gamma-delta T cells are primarily found within the epithelium. They show less TCR diversity and recognize antigens differently than alpha-beta T cells. Subsets of gamma-delta T cells have shown antitumor and immunoregulatory activity.