Induction of Functional Human Macrophages from Bone Marrow Promonocytes by M-CSF in Humanized Mice

Li, Yan; Chen, Yi‐Ping Phoebe; Zheng, Dahai; Lu, Yin; Chionh, Yok Hian; Wong, Lawson L. S.; Tan, Shaohua; Tan, Thiam Chye; Chan, Jerry Kok Yen; Alonso, Sylvie; Dedon, Peter C.; Lim, Bing; Chen, Jianzhu

doi:10.4049/jimmunol.1300742

Cited by 40 publications

(42 citation statements)

References 29 publications

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“…In the BRG model, injection of human IL-3 and GM-CSF increased myeloid engraftment within the lung and led to increased innate responses to virus infection (50). Treatment of NSG Hu-SRC-SCID mice with M-CSF led to decreased viral transcript levels early after infection and was associated with a burst of inflammatory cytokines, such as IL-6 and TNF at 48 hours post infection (51). …”

Section: Infectious Disease In Humanized Micementioning

confidence: 99%

Humanized Mouse Models of Clinical Disease

Walsh

Kenney

Jangalwe

et al. 2017

Annu. Rev. Pathol. Mech. Dis.

442

384

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Immunodeficient mice engrafted with functional human cells and tissues, i.e., “humanized mice”, have become increasingly important as small pre-clinical animal models for the study of human diseases. Since the description of immunodeficient mice bearing mutations in the IL2 receptor common gamma chain (IL2rgnull) in the early 2000’s, investigators have been able to engraft murine recipients with human hematopoietic stem cells that develop into functional human immune systems. These mice can also be engrafted with human tissues such as islets, liver, skin, and most solid and hematologic cancers. Humanized mice are permitting significant progress in studies of human infectious disease, cancer, regenerative medicine, graft versus host disease, allergies, and immunity. Ultimately, use of humanized mice may lead to the implementation of truly “personalized” medicine in the clinic. This review discusses recent progress in the development and use of humanized mice, and highlights their utility for the study of human diseases.

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Section: Infectious Disease In Humanized Micementioning

confidence: 99%

Humanized Mouse Models of Clinical Disease

Walsh

Kenney

Jangalwe

et al. 2017

Annu. Rev. Pathol. Mech. Dis.

442

384

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“…For example, human myeloid cells have been found to be less than 5–10% of what is found in humans[reviewed in (9)]. Although some studies report that these myeloid cells are reasonably functional (90;109), other studies have described these myeloid cells as phenotypically immature and functionally defective (110). Furthermore, human NK cell maturation, function and homeostasis are also defective in humanized mice owing in part, to NK cell susceptibility to phagocytosis by murine macrophages (98) (discussed below) and lack of trans-presentation hIL15-hIL15Rα(111).…”

Section: Current Strategies For Improving Engraftment Of Human Hematomentioning

confidence: 99%

“…al. reported that hydrodynamic delivery of a plasmid encoding for human M-CSF enhanced the generation of mature and functional monocytes and tissue-associated macrophages in Hu-HSC-NSG mice (109). The use of transgenic technology is another approach that is currently being used to enhance expression of human cytokines and growth factors in immuno-deficient mice.…”

Section: Current Strategies For Improving Engraftment Of Human Hematomentioning

confidence: 99%

Use of Humanized Mice to Study the Pathogenesis of Autoimmune and Inflammatory Diseases

Koboziev

Jones-Hall

Valentine

et al. 2015

Inflammatory Bowel Diseases

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Animal models of disease have been used extensively by the research community for the past several decades to better understand the pathogenesis of different diseases as well as assess the efficacy and toxicity of different therapeutic agents. Retrospective analyses of numerous preclinical intervention studies using mouse models of acute and chronic inflammatory diseases reveal a generalized failure to translate promising interventions or therapeutics into clinically-effective treatments in patients. Although several possible reasons have been suggested to account for this generalized failure to translate therapeutic efficacy from the laboratory bench to the patient’s bedside, it is becoming increasingly apparent that the mouse immune system may not adequately recapitulate the immuno-pathological mechanisms observed in human diseases. Indeed, it is well-known that >80 major differences exist between mouse and human immunology; all of which contribute to significant differences in immune system development, activation and responses to challenges in innate and adaptive immunity. This inconvenient reality has prompted investigators to attempt to humanize the mouse immune system in order to address important, human-specific questions that are impossible to study in patients. The successful long-term engraftment of human hemato-lymphoid cells in mice would provide investigators with a relatively inexpensive, small animal model to study clinically-relevant mechanisms as well as facilitate the evaluation of human-specific therapies in vivo. The discovery that targeted mutation of the IL-2 receptor common gamma chain in lymphopenic mice allows for the long-term engraftment of functional human immune cells has advanced greatly our ability to humanize the mouse immune system. The objective of this review is to present a brief overview of the recent advances that have been made in the development and use of humanized mice with special emphasis on autoimmune and chronic inflammatory diseases. In addition, we discuss current challenges and possible solutions for utilizing these unique mouse models to define the human-specific immuno-pathological mechanisms responsible for the induction and perpetuation of chronic gut inflammation.

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“…M-CSF mediates the survival and proliferation of precursors of the monocyte and macrophage lineage and their differentiation into mature phagocytes [1,2]. Macrophages, in relation to the immune response, exist as phagocytes and antigen-presenting cells [3,4].…”

Section: Biological Effect Of Macrophage Colony-stimulating Factor (Mmentioning

confidence: 99%

“…Macrophages, in relation to the immune response, exist as phagocytes and antigen-presenting cells [3,4]. Furthermore, the activity of macrophages is associated with the regulation of many biological processes and is dependent on the actual macrophage phenotype induced under various inflammatory conditions [1]. Macrophages play an important role in homeostasis, autoimmunization, and first defense during infection.…”

Section: Biological Effect Of Macrophage Colony-stimulating Factor (Mmentioning

confidence: 99%

Effect of Macrophage Colony-Stimulating Factor Receptor c-Fms Antibody on Lipopolysaccharide-Induced Pathological Osteoclastogenesis and Bone Resorption

Kimura

Kitaura

Ishida

et al. 2015

Interface Oral Health Science 2014

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Lipopolysaccharide (LPS) is a major component of Gram-negative bacteria cell walls and is a well-known potent inducer of inflammation and pathogens of inflammatory bone loss. Formation of osteoclasts is highly dependent on the presence of macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor kappa-B ligand (RANKL). Recent reports indicate that biological preparations, including anti-RANKL antibody and anti-tumor necrosis factor-α antibody, positively influence rheumatoid arthritis and osteoporosis. In this study, we aimed to investigate whether the M-CSF receptor c-Fms antibody would inhibit the formation of osteoclasts. C57BL6/J mice were injected with either LPS, LPS and anti-c-Fms antibody, anti-c-Fms antibody, or PBS into the supracalvariae. Animals were sacrificed and calvariae fixation and demineralization were performed. Histological sections of calvariae were stained for tartrate-resistant acid phosphatase (TRAP). In mice administered with both LPS and the anti-cFms antibody, osteoclast numbers were lower than those in mice administered with LPS alone. Moreover, levels of TRACP-5b, a bone resorption marker in mice serum, were lower in mice administered with both LPS and the anti-c-Fms antibody than in mice administered with LPS alone. These results suggest that M-CSF and its receptor are potential therapeutic targets in LPS-induced osteoclastogenesis, and that the anti-c-Fms antibody might be useful for inhibition of inflammation-induced bone erosion. In this study, we describe and discuss the effect the anti-c-Fms antibody has on pathological osteoclastogenesis and bone resorption.

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Induction of Functional Human Macrophages from Bone Marrow Promonocytes by M-CSF in Humanized Mice

Cited by 40 publications

References 29 publications

Humanized Mouse Models of Clinical Disease

Humanized Mouse Models of Clinical Disease

Use of Humanized Mice to Study the Pathogenesis of Autoimmune and Inflammatory Diseases

Effect of Macrophage Colony-Stimulating Factor Receptor c-Fms Antibody on Lipopolysaccharide-Induced Pathological Osteoclastogenesis and Bone Resorption

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