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Anti-Mouse CD4 APC 100 ug antibody

RRID:AB_469320

Antibody ID

AB_469320

Target Antigen

Mouse CD4 APC 100 ug mouse

Proper Citation

(Thermo Fisher Scientific Cat# 17-0041-82, RRID:AB_469320)

Clonality

monoclonal antibody

Comments

Applications: Flow (0.125 µg/test)

Clone ID

Clone GK1.5

Host Organism

rat

Vendor

Thermo Fisher Scientific Go To Vendor

Cat Num

17-0041-82

Publications that use this research resource

Dichotomous Expression of TNF Superfamily Ligands on Antigen-Presenting Cells Controls Post-priming Anti-viral CD4+ T Cell Immunity.

  • Chang YH
  • Immunity
  • 2017 Nov 21

Literature context:


Abstract:

T cell antigen-presenting cell (APC) interactions early during chronic viral infection are crucial for determining viral set point and disease outcome, but how and when different APC subtypes contribute to these outcomes is unclear. The TNF receptor superfamily (TNFRSF) member GITR is important for CD4+ T cell accumulation and control of chronic lymphocytic choriomeningitis virus (LCMV). We found that type I interferon (IFN-I) induced TNFSF ligands GITRL, 4-1BBL, OX40L, and CD70 predominantly on monocyte-derived APCs and CD80 and CD86 predominantly on classical dendritic cells (cDCs). Mice with hypofunctional GITRL in Lyz2+ cells had decreased LCMV-specific CD4+ T cell accumulation and increased viral load. GITR signals in CD4+ T cells occurred after priming to upregulate OX40, CD25, and chemokine receptor CX3CR1. Thus IFN-I (signal 3) induced a post-priming checkpoint (signal 4) for CD4+ T cell accumulation, revealing a division of labor between cDCs and monocyte-derived APCs in regulating T cell expansion.

Funding information:
  • NIA NIH HHS - P01 AG017617(United States)

Cholesterol Accumulation in Dendritic Cells Links the Inflammasome to Acquired Immunity.

  • Westerterp M
  • Cell Metab.
  • 2017 Jun 6

Literature context:


Abstract:

Autoimmune diseases such as systemic lupus erythematosus (SLE) are associated with increased cardiovascular disease and reduced plasma high-density lipoprotein (HDL) levels. HDL mediates cholesterol efflux from immune cells via the ATP binding cassette transporters A1 and G1 (ABCA1/G1). The significance of impaired cholesterol efflux pathways in autoimmunity is unknown. We observed that Abca1/g1-deficient mice develop enlarged lymph nodes (LNs) and glomerulonephritis suggestive of SLE. This lupus-like phenotype was recapitulated in mice with knockouts of Abca1/g1 in dendritic cells (DCs), but not in macrophages or T cells. DC-Abca1/g1 deficiency increased LN and splenic CD11b+ DCs, which displayed cholesterol accumulation and inflammasome activation, increased cell surface levels of the granulocyte macrophage-colony stimulating factor receptor, and enhanced inflammatory cytokine secretion. Consequently, DC-Abca1/g1 deficiency enhanced T cell activation and Th1 and Th17 cell polarization. Nlrp3 inflammasome deficiency diminished the enlarged LNs and enhanced Th1 cell polarization. These findings identify an essential role of DC cholesterol efflux pathways in maintaining immune tolerance.

Funding information:
  • NCRR NIH HHS - S10 RR027050()
  • NHLBI NIH HHS - R01 HL107653()
  • NHLBI NIH HHS - T32 HL007343()