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Anti-Mouse CD127 PE 100 ug antibody

RRID:AB_465844

Antibody ID

AB_465844

Target Antigen

Mouse CD127 PE 100 ug mouse

Proper Citation

(Thermo Fisher Scientific Cat# 12-1271-82, RRID:AB_465844)

Clonality

monoclonal antibody

Comments

Applications: Flow (0.25 µg/test)

Clone ID

Clone A7R34

Host Organism

rat

Vendor

Thermo Fisher Scientific Go To Vendor

Cat Num

12-1271-82

Publications that use this research resource

Dye-Independent Methods Reveal Elevated Mitochondrial Mass in Hematopoietic Stem Cells.

  • de Almeida MJ
  • Cell Stem Cell
  • 2017 Dec 7

Literature context:


Abstract:

Hematopoietic stem cells (HSCs) produce most cellular energy through glycolysis rather than through mitochondrial respiration. Consistent with this notion, mitochondrial mass has been reported to be low in HSCs. However, we found that staining with MitoTracker Green, a commonly used dye to measure mitochondrial content, leads to artefactually low fluorescence specifically in HSCs because of dye efflux. Using mtDNA quantification, enumeration of mitochondrial nucleoids, and fluorescence intensity of a genetically encoded mitochondrial reporter, we unequivocally show here that HSCs and multipotential progenitors (MPPs) have higher mitochondrial mass than lineage-committed progenitors and mature cells. Despite similar mitochondrial mass, respiratory capacity of MPPs exceeds that of HSCs. Furthermore, although elevated mitophagy has been invoked to explain low mitochondrial mass in HSCs, we observed that mitochondrial turnover capacity is comparatively low in HSCs. We propose that the role of mitochondria in HSC biology may have to be revisited in light of these findings.

Funding information:
  • NCI NIH HHS - 1R21CA175560-01(United States)
  • NCI NIH HHS - R01 CA167289()
  • NCRR NIH HHS - S10 RR027050()
  • NIA NIH HHS - R01 AG029626()
  • NIA NIH HHS - R01 AG055910()
  • NIH HHS - S10 OD020056()

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)