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Biotin anti-mouse CD3 antibody

RRID:AB_2563946

Antibody ID

AB_2563946

Target Antigen

CD3 See NCBI gene mouse

Proper Citation

(BioLegend Cat# 100243, RRID:AB_2563946)

Clonality

monoclonal antibody

Comments

Applications: FC

Clone ID

Clone 17A2

Host Organism

rat

Vendor

BioLegend Go To Vendor

Cat Num

100243

Publications that use this research resource

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()

Immunosuppression via Loss of IL2rγ Enhances Long-Term Functional Integration of hESC-Derived Photoreceptors in the Mouse Retina.

  • Zhu J
  • Cell Stem Cell
  • 2017 Mar 2

Literature context:


Abstract:

Loss of photoreceptors is a common endpoint in degenerative retinal diseases. Human pluripotent stem cells provide a potential source for photoreceptor replacement, but, even in mouse models, the efficiency and efficacy of transplantation-based repair remains poor. In this study, we examined the degree to which immune rejection contributes to these disappointing outcomes using an immunodeficient IL2 receptor γ (IL2rγ)-null mouse model. Our results show that prevention of cell rejection in the normal and degenerating retinal environment significantly improves long-term survival and integration of hESC-derived donor retinal cells. Transplanted cells are able to differentiate into mature photoreceptors expressing various opsins and can functionally integrate into congenitally blind mice. Our work suggests that even though the retina is often considered immune-privileged, suppression of host immune-mediated cell rejection may well be a useful approach for improving long-term integration of transplanted cells with a view to successful clinical outcomes.