FlowMAb FITC anti-human/monkey MHC class II (HLA-DR)

Catalog #FM0306-FITC
Clone:
L243
Reactivities:
Human, Monkey
As low as $240.00

$240.00 - $350.00

$240.00 - $350.00

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  • 100 µg - $350.00
  • 25 µg - $240.00
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Product Details

The L243 monoclonal antibody reacts with the human and monkey MHC class II, HLA-DR. The transmembrane glycoprotein HLA-DR consists of a 36 kDa chain and a 27 kDa chain. Antigen-presenting cells such as B cells, monocytes, macrophages, thymic epithelial cells, and activated T cells primarily express HLA-DR. HLA-DR is critical for the presentation of peptides to CD4+ T cells. This fluorescein isothiocyanate (FITC)-conjugated version of the antibody is useful for flow cytometry and immunofluorescence, immunohistochemistry (frozen), and immunohistochemistry (paraffin).

Specifications

Isotype Mouse IgG2a, Īŗ
Recommended Isotype Control(s) FlowMAb FITC mouse IgG2a isotype control, unknown specificity
Conjugation FITC
Excitation Source Blue 488 nm
Excitation Max 494 nm
Emission Max 518 nm
Immunogen Human lymphoblastoid B cell line RPMI 8866.9
Reported Applications Flow cytometry
Formulation PBS, pH 7.0
Contains 0.09% Sodium Azide
Production Purified from cell culture supernatant in an animal-free facility
Purification Protein G. Conjugated with fluorescein isothiocyanate under optimal conditions.
Storage The antibody solution should be stored at the stock concentration at 4Ā°C and protected from prolonged exposure to light. Do not freeze.
Flow Cytometry
Kho, S., et al. (2015). "Preserved dendritic cell HLA-DR expression and reduced regulatory T cell activation in asymptomatic Plasmodium falciparum and P. vivax infection" Infect Immun 83(8): 3224-3232. PubMed

Clinical illness with Plasmodium falciparum or Plasmodium vivax compromises the function of dendritic cells (DC) and expands regulatory T (Treg) cells. Individuals with asymptomatic parasitemia have clinical immunity, restricting parasite expansion and preventing clinical disease. The role of DC and Treg cells during asymptomatic Plasmodium infection is unclear. During a cross-sectional household survey in Papua, Indonesia, we examined the number and activation of blood plasmacytoid DC (pDC), CD141(+), and CD1c(+) myeloid DC (mDC) subsets and Treg cells using flow cytometry in 168 afebrile children (of whom 15 had P. falciparum and 36 had P. vivax infections) and 162 afebrile adults (of whom 20 had P. falciparum and 20 had P. vivax infections), alongside samples from 16 patients hospitalized with uncomplicated malaria. Unlike DC from malaria patients, DC from children and adults with asymptomatic, microscopy-positive P. vivax or P. falciparum infection increased or retained HLA-DR expression. Treg cells in asymptomatic adults and children exhibited reduced activation, suggesting increased immune responsiveness. The pDC and mDC subsets varied according to clinical immunity (asymptomatic or symptomatic Plasmodium infection) and, in asymptomatic infection, according to host age and parasite species. In conclusion, active control of asymptomatic infection was associated with and likely contingent upon functional DC and reduced Treg cell activation.