An extensive monoclonal antibody panel for the phenotyping of leukocyte subsets in the common marmoset and the cotton-top tamarin

Brok, Herbert; Hornby, Rebecca J.; Griffiths, Gareth; Scott, Leah; Hart, Bert A. ’t

doi:10.1002/1097-0320(20011201)45:4<294::aid-cyto10002>3.0.co;2-c

Cited by 55 publications

(48 citation statements)

References 25 publications

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“…Lethally irradiated (50 gray) EBVtransformed marmoset B cells from stably growing lines maintained in 75-cm 2 tissue culture flasks (Greiner) were used as APC. Lines of interest were characterized by the expression of T cell-specific cell surface markers by flow cytometry using cross-reactive mAbs raised against human CD markers (20). Isotype controls were kindly provided by J. Miller (Chemicon International).…”

Section: Generation Of Mog Peptide-reactive Tclmentioning

confidence: 99%

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Fast Progression of Recombinant Human Myelin/Oligodendrocyte Glycoprotein (MOG)-Induced Experimental Autoimmune Encephalomyelitis in Marmosets Is Associated with the Activation of MOG34–56-Specific Cytotoxic T Cells

Kap

Smith

Jagessar

et al. 2008

The Journal of Immunology

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The recombinant human (rh) myelin/oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) model in the common marmoset is characterized by 100% disease incidence, a chronic disease course, and a variable time interval between immunization and neurological impairment. We investigated whether monkeys with fast and slow disease progression display different anti-MOG T or B cell responses and analyzed the underlying pathogenic mechanism(s). The results show that fast progressor monkeys display a significantly wider specificity diversification of anti-MOG T cells at necropsy than slow progressors, especially against MOG34–56 and MOG74–96. MOG34–56 emerged as a critical encephalitogenic peptide, inducing severe neurological disease and multiple lesions with inflammation, demyelination, and axonal injury in the CNS. Although EAE was not observed in MOG74–96-immunized monkeys, weak T cell responses against MOG34–56 and low grade CNS pathology were detected. When these cases received a booster immunization with MOG34–56 in IFA, full-blown EAE developed. MOG34–56-reactive T cells expressed CD3, CD4, or CD8 and CD56, but not CD16. Moreover, MOG34–56-specific T cell lines displayed specific cytotoxic activity against peptide-pulsed B cell lines. The phenotype and cytotoxic activity suggest that these cells are NK-CTL. These results support the concept that cytotoxic cells may play a role in the pathogenesis of multiple sclerosis.

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Section: Generation Of Mog Peptide-reactive Tclmentioning

confidence: 99%

“…After 7 days, cells were harvested and stained with the fluorescein-labeled monoclonal Ab used for the phenotyping of human MNC subsets that are known to cross-react with marmoset MNC (20). Proliferating cells were identified by the dilution of CFSE.…”

Section: Phenotype Of Mog 34 -56 -And Mog 74 -96 -Reactive T Cellsmentioning

confidence: 99%

Fast Progression of Recombinant Human Myelin/Oligodendrocyte Glycoprotein (MOG)-Induced Experimental Autoimmune Encephalomyelitis in Marmosets Is Associated with the Activation of MOG34–56-Specific Cytotoxic T Cells

Kap

Smith

Jagessar

et al. 2008

The Journal of Immunology

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“…This relative proximity in comparison with mice is reflected by the relatively high cross-reaction of mAbs raised against CD markers of human leukocytes with leukocytes of marmosets (Jagessar et al, 2013a;Brok et al, 2001). This makes the marmoset a potentially useful model for the safety and efficacy evaluation of biological therapeutics, mAbs for example, which for specificity reasons cannot be tested in lower species.…”

Section: Validation Of the Marmoset Eae Model With Clinically Relevanmentioning

confidence: 99%

The common marmoset (<i>Callithrix jacchus</i>): a relevant preclinical model of human (auto)immune-mediated inflammatory disease of the brain

et al. 2016

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Abstract. The increasing prevalence of chronic autoimmune-mediated inflammatory disorders (AIMIDs) in aging human populations creates a high unmet need for safe and effective medications. However, thus far the translation of pathogenic concepts developed in animal models into effective treatments for the patient has been notoriously difficult. The main reason is that currently used mouse-based animal models for the pipeline selection of promising new treatments were insufficiently predictive for clinical success. Regarding the high immunological similarity between human and non-human primates (NHPs), AIMID models in NHPs can help to bridge the translational gap between rodent and man. Here we will review the preclinical relevance of the experimental autoimmune encephalomyelitis (EAE) model in common marmosets (Callithrix jacchus), a small-bodied neotropical primate. EAE is a generic AIMID model projected on the human autoimmune neuro-inflammatory disease multiple sclerosis (MS).

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“…53 PBMCs were isolated by Ficoll (LSM Lymphocyte Separation Medium; ICN Biomedicals, Aurora, OH) and cells were cultured in 25 mmol/L HEPESbuffered RPMI 1640 (Life Technologies, Glasgow, UK) supplemented with 10% fetal calf serum (ICN Biomedicals), penicillin, and streptomycin (Invitrogen, Paisley, UK), Glutamax (Invitrogen), and ␤-mercaptoethanol (Invitrogen). sPGN was sonicated for 20 minutes and immediately added to the culture.…”

Section: Stimulation Of Peripheral Blood Mononuclear Cells (Pbmcs) Anmentioning

confidence: 99%

Phagocytes Containing a Disease-Promoting Toll-Like Receptor/Nod Ligand Are Present in the Brain during Demyelinating Disease in Primates

Visser

Melief

Riel

et al. 2006

The American Journal of Pathology

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An extensive monoclonal antibody panel for the phenotyping of leukocyte subsets in the common marmoset and the cotton-top tamarin

Cited by 55 publications

References 25 publications

Fast Progression of Recombinant Human Myelin/Oligodendrocyte Glycoprotein (MOG)-Induced Experimental Autoimmune Encephalomyelitis in Marmosets Is Associated with the Activation of MOG34–56-Specific Cytotoxic T Cells

Fast Progression of Recombinant Human Myelin/Oligodendrocyte Glycoprotein (MOG)-Induced Experimental Autoimmune Encephalomyelitis in Marmosets Is Associated with the Activation of MOG34–56-Specific Cytotoxic T Cells

The common marmoset (<i>Callithrix jacchus</i>): a relevant preclinical model of human (auto)immune-mediated inflammatory disease of the brain

Phagocytes Containing a Disease-Promoting Toll-Like Receptor/Nod Ligand Are Present in the Brain during Demyelinating Disease in Primates

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An extensive monoclonal antibody panel for the phenotyping of leukocyte subsets in the common marmoset and the cotton-top tamarin

Cited by 55 publications

References 25 publications

Fast Progression of Recombinant Human Myelin/Oligodendrocyte Glycoprotein (MOG)-Induced Experimental Autoimmune Encephalomyelitis in Marmosets Is Associated with the Activation of MOG34–56-Specific Cytotoxic T Cells

Fast Progression of Recombinant Human Myelin/Oligodendrocyte Glycoprotein (MOG)-Induced Experimental Autoimmune Encephalomyelitis in Marmosets Is Associated with the Activation of MOG34–56-Specific Cytotoxic T Cells

The common marmoset (&lt;i&gt;Callithrix jacchus&lt;/i&gt;): a relevant preclinical model of human (auto)immune-mediated inflammatory disease of the brain

Phagocytes Containing a Disease-Promoting Toll-Like Receptor/Nod Ligand Are Present in the Brain during Demyelinating Disease in Primates

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The common marmoset (<i>Callithrix jacchus</i>): a relevant preclinical model of human (auto)immune-mediated inflammatory disease of the brain