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APC anti-mouse CD45 antibody

RRID:AB_312976

Antibody ID

AB_312976

Target Antigen

CD45 See NCBI gene mouse

Proper Citation

(BioLegend Cat# 103111, RRID:AB_312976)

Clonality

monoclonal antibody

Comments

Applications: FC

Clone ID

Clone 30-F11

Host Organism

rat

Vendor

BioLegend Go To Vendor

Cat Num

103111

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()

Sensory Neurons Co-opt Classical Immune Signaling Pathways to Mediate Chronic Itch.

  • Oetjen LK
  • Cell
  • 2017 Sep 21

Literature context:


Abstract:

Mammals have evolved neurophysiologic reflexes, such as coughing and scratching, to expel invading pathogens and noxious environmental stimuli. It is well established that these responses are also associated with chronic inflammatory diseases, including asthma and atopic dermatitis. However, the mechanisms by which inflammatory pathways promote sensations such as itch remain poorly understood. Here, we show that type 2 cytokines directly activate sensory neurons in both mice and humans. Further, we demonstrate that chronic itch is dependent on neuronal IL-4Rα and JAK1 signaling. We also observe that patients with recalcitrant chronic itch that failed other immunosuppressive therapies markedly improve when treated with JAK inhibitors. Thus, signaling mechanisms previously ascribed to the immune system may represent novel therapeutic targets within the nervous system. Collectively, this study reveals an evolutionarily conserved paradigm in which the sensory nervous system employs classical immune signaling pathways to influence mammalian behavior.

Funding information:
  • NCATS NIH HHS - UL1 TR000448()
  • NCI NIH HHS - P30 CA091842()
  • NCRR NIH HHS - S10 RR027552()
  • NHLBI NIH HHS - T32 HL007317()
  • NIAMS NIH HHS - K08 AR065577()
  • NIAMS NIH HHS - R01 AR070116()
  • NIAMS NIH HHS - R21 AR068012()
  • NIAMS NIH HHS - R56 AR064294()
  • NIDDK NIH HHS - P30 DK052574()
  • NIDDK NIH HHS - R01 DK103901()
  • NIGMS NIH HHS - R01 GM101218()
  • NINDS NIH HHS - R01 NS042595()

Dicer Deficiency Differentially Impacts Microglia of the Developing and Adult Brain.

  • Varol D
  • Immunity
  • 2017 Jun 20

Literature context:


Abstract:

Microglia seed the embryonic neuro-epithelium, expand and actively sculpt neuronal circuits in the developing central nervous system, but eventually adopt relative quiescence and ramified morphology in the adult. Here, we probed the impact of post-transcriptional control by microRNAs (miRNAs) on microglial performance during development and adulthood by generating mice lacking microglial Dicer expression at these distinct stages. Conditional Dicer ablation in adult microglia revealed that miRNAs were required to limit microglial responses to challenge. After peripheral endotoxin exposure, Dicer-deficient microglia expressed more pro-inflammatory cytokines than wild-type microglia and thereby compromised hippocampal neuronal functions. In contrast, prenatal Dicer ablation resulted in spontaneous microglia activation and revealed a role for Dicer in DNA repair and preservation of genome integrity. Accordingly, Dicer deficiency rendered otherwise radio-resistant microglia sensitive to gamma irradiation. Collectively, the differential impact of the Dicer ablation on microglia of the developing and adult brain highlights the changes these cells undergo with time.

Funding information:
  • NINDS NIH HHS - R37 NS041280(United States)