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PerCP/Cyanine5.5 anti-mouse CD3 antibody

RRID:AB_1595597

Antibody ID

AB_1595597

Target Antigen

CD3 See NCBI gene mouse

Proper Citation

(BioLegend Cat# 100217, RRID:AB_1595597)

Clonality

monoclonal antibody

Comments

Applications: FC

Clone ID

Clone 17A2

Host Organism

rat

Vendor

BioLegend Go To Vendor

Cat Num

100217

Publications that use this research resource

A Combination of Ontogeny and CNS Environment Establishes Microglial Identity.

  • Bennett FC
  • Neuron
  • 2018 Jun 27

Literature context:


Abstract:

Microglia, the brain's resident macrophages, are dynamic CNS custodians with surprising origins in the extra-embryonic yolk sac. The consequences of their distinct ontogeny are unknown but critical to understanding and treating brain diseases. We created a brain macrophage transplantation system to disentangle how environment and ontogeny specify microglial identity. We find that donor cells extensively engraft in the CNS of microglia-deficient mice, and even after exposure to a cell culture environment, microglia fully regain their identity when returned to the CNS. Though transplanted macrophages from multiple tissues can express microglial genes in the brain, only those of yolk-sac origin fully attain microglial identity. Transplanted macrophages of inappropriate origin, including primary human cells in a humanized host, express disease-associated genes and specific ontogeny markers. Through brain macrophage transplantation, we discover new principles of microglial identity that have broad applications to the study of disease and development of myeloid cell therapies.

Funding information:
  • NCI NIH HHS - P30 CA016672(United States)
  • NCI NIH HHS - R01 CA216054()
  • NCRR NIH HHS - S10 RR025518()
  • NIA NIH HHS - P50 AG047366()
  • NIDA NIH HHS - R37 DA015043()
  • NIMH NIH HHS - K08 MH112120()
  • NIMH NIH HHS - L30 MH108106()
  • NIMH NIH HHS - T32 MH019938()
  • NINDS NIH HHS - F31 NS078813()
  • NINDS NIH HHS - K08 NS075144()
  • NINDS NIH HHS - K08 NS085324()
  • NINDS NIH HHS - K08 NS091527()
  • NINDS NIH HHS - P30 NS069375()

Interleukin-15 Complex Treatment Protects Mice from Cerebral Malaria by Inducing Interleukin-10-Producing Natural Killer Cells.

  • Burrack KS
  • Immunity
  • 2018 Apr 17

Literature context:


Abstract:

Cerebral malaria is a deadly complication of Plasmodium infection and involves blood brain barrier (BBB) disruption following infiltration of white blood cells. During experimental cerebral malaria (ECM), mice inoculated with Plasmodium berghei ANKA-infected red blood cells develop a fatal CM-like disease caused by CD8+ T cell-mediated pathology. We found that treatment with interleukin-15 complex (IL-15C) prevented ECM, whereas IL-2C treatment had no effect. IL-15C-expanded natural killer (NK) cells were necessary and sufficient for protection against ECM. IL-15C treatment also decreased CD8+ T cell activation in the brain and prevented BBB breakdown without influencing parasite load. IL-15C induced NK cells to express IL-10, which was required for IL-15C-mediated protection against ECM. Finally, we show that ALT-803, a modified human IL-15C, mediates similar induction of IL-10 in NK cells and protection against ECM. These data identify a regulatory role for cytokine-stimulated NK cells in the prevention of a pathogenic immune response.

Funding information:
  • Department of Health - NIHR-RP-011-053(United Kingdom)
  • NIAID NIH HHS - R21 AI100088()
  • NIAID NIH HHS - T32 AI007425()

Bone Marrow Myeloid Cells Regulate Myeloid-Biased Hematopoietic Stem Cells via a Histamine-Dependent Feedback Loop.

  • Chen X
  • Cell Stem Cell
  • 2017 Dec 7

Literature context:


Abstract:

Myeloid-biased hematopoietic stem cells (MB-HSCs) play critical roles in recovery from injury, but little is known about how they are regulated within the bone marrow niche. Here we describe an auto-/paracrine physiologic circuit that controls quiescence of MB-HSCs and hematopoietic progenitors marked by histidine decarboxylase (Hdc). Committed Hdc+ myeloid cells lie in close anatomical proximity to MB-HSCs and produce histamine, which activates the H2 receptor on MB-HSCs to promote their quiescence and self-renewal. Depleting histamine-producing cells enforces cell cycle entry, induces loss of serial transplant capacity, and sensitizes animals to chemotherapeutic injury. Increasing demand for myeloid cells via lipopolysaccharide (LPS) treatment specifically recruits MB-HSCs and progenitors into the cell cycle; cycling MB-HSCs fail to revert into quiescence in the absence of histamine feedback, leading to their depletion, while an H2 agonist protects MB-HSCs from depletion after sepsis. Thus, histamine couples lineage-specific physiological demands to intrinsically primed MB-HSCs to enforce homeostasis.

Funding information:
  • NCI NIH HHS - P30 CA013696()
  • NCI NIH HHS - R35 CA197745()
  • NCRR NIH HHS - S10 RR027050()
  • NHLBI NIH HHS - R01 HL115145()
  • NIDDK NIH HHS - R01 DK048077()
  • NIGMS NIH HHS - GM087476(United States)
  • NIH HHS - S10 OD012351()
  • NIH HHS - S10 OD020056()
  • NIH HHS - S10 OD021764()

IL-6/Stat3-Dependent Induction of a Distinct, Obesity-Associated NK Cell Subpopulation Deteriorates Energy and Glucose Homeostasis.

  • Theurich S
  • Cell Metab.
  • 2017 Jul 5

Literature context:


Abstract:

Natural killer (NK) cells contribute to the development of obesity-associated insulin resistance. We demonstrate that in mice obesity promotes expansion of a distinct, interleukin-6 receptor (IL6R)a-expressing NK subpopulation, which also expresses a number of other myeloid lineage genes such as the colony-stimulating factor 1 receptor (Csf1r). Selective ablation of this Csf1r-expressing NK cell population prevents obesity and insulin resistance. Moreover, conditional inactivation of IL6Ra or Stat3 in NK cells limits obesity-associated formation of these myeloid signature NK cells, protecting from obesity, insulin resistance, and obesity-associated inflammation. Also in humans IL6Ra+ NK cells increase in obesity and correlate with markers of systemic low-grade inflammation, and their gene expression profile overlaps with characteristic gene sets of NK cells in obese mice. Collectively, we demonstrate that obesity-associated inflammation and metabolic disturbances depend on interleukin-6/Stat3-dependent formation of a distinct NK population, which may provide a target for the treatment of obesity, metaflammation-associated pathologies, and diabetes.

Funding information:
  • NHLBI NIH HHS - P01 HL096571(United States)
  • PHS HHS - HHSN268201100037C(United States)