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Mp1 22e9

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The MP1-22E9 is a laboratory instrument designed for the separation and purification of biological samples. It utilizes centrifugal force to separate components based on their density and size. The core function of this equipment is to enable efficient and precise separation of various biomolecules, cells, or other particulate matter from complex mixtures.

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Lab products found in correlation

Recombinant human csf 1, by Thermo Fisher Scientific (1 mentions) Cd11b m1 70, by BioLegend (1 mentions) Cd62p rb40, by BD (1 mentions) Lysm cre, by Jackson ImmunoResearch (1 mentions) Csf2rb, by Jackson ImmunoResearch (1 mentions) Cd4 cre, by Jackson ImmunoResearch (1 mentions) C57bl 6 mice, by Jackson ImmunoResearch (1 mentions) Alf 161, by BioXCell (1 mentions) Sb328437, by Abcam (1 mentions)

5 protocols using mp1 22e9

1

Neutralizing antibody treatment in L2/IKKβca mice

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Starting at 1 month of age, L2/IKKβca mice and littermate controls were given intraperitoneal injections of the GM-CSF neutralizing antibody MP1-22E9, the TNF neutralizing antibody XT3.11, IgG2a control (for MP1-22E9), or IgG1 control (for XT3.11) at doses of 800μg per mouse for MP1-22E9 or 500μg per mouse for XT3.11 (BioXCell, West Hanover, NH). Mice were treated every Monday and Thursday until they reached 1.5 month of age. The following numbers of matched littermate control and mutant mice were injected with neutralizing antibody or control: IgG2a, three pairs; MP1-22E9, three pairs. The following numbers of mutant mice were injected with neutralizing antibody or control: IgG1, four mice; and XT3.11, 4 mice.
Tétreault M.P., Weinblatt D., Ciolino J.D., Klein-Szanto A.J., Sackey B.K., Victor C.T., Karakasheva T., Teal V, & Katz J.P. (2016). Esophageal Expression of Active IκB kinase-β in Mice Upregulates Tumor Necrosis Factor and Granulocyte Macrophage Colony-stimulating Factor, Promoting Inflammation and Angiogenesis. Gastroenterology, 150(7), 1609-1619.e11.
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2

Investigating CSF-1 Induction in Mice

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To investigate the induction of CSF-1 in vivo, mice were injected i.v. with freshly prepared hemin (8.8–35 μmol/kg body weight), RBC lysate (17.5 μmol heme/kg body weight), or MDP (InvivoGen, 1 mg/kg body weight/d), while PBS (200 μL/20 g body weight) served as a control. In some experiments, hemin was combined with hemopexin at a 1:1 ratio. For the administration of exogenous CSF-1, mice were injected s.c. in the loose skin over the neck with recombinant human CSF-1 (0.5 mg/kg body weight/d, PeproTech) or PBS as a control for 4 consecutive days. To block endogenous CSF activity, mice were injected i.p. with a blocking antibody against CSF-1 (5A1), CSF-2 (MP1-22E9), or isotype control (1 mg/kg body weight, Bio X Cell). For blockade of CMo migration in vivo, mice were treated with Ultra-LEAF (Low Endotoxin, Azide-Free) blocking antibodies against CD62p (RB40.34, BD), CD106 (M/K-2.7, Bio X Cell), E selectin (9A9, Bio X Cell), CD11b (M1/70, Biolegend), ICAM-1 (YN1/1.7.4, Biolegend), or isotype control (Bio X Cell) (5 mg/kg body weight, i.v.). Mice were sacrificed at various time points after treatment, and blood samples and liver tissues were collected for subsequent analysis.
Liu Y., Su S., Shayo S., Bao W., Pal M., Dou K., Shi P.A., Aygun B., Campbell-Lee S., Lobo C.A., Mendelson A., An X., Manwani D., Zhong H, & Yazdanbakhsh K. (2023). Hemolysis dictates monocyte differentiation via two distinct pathways in sickle cell disease vaso-occlusion. The Journal of Clinical Investigation, 133(18), e172087.
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3

Helminth Infection and Immunity Protocols

Cited 2 times
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Il10−/−, Csf2−/−, Csf2rb−/−, Cd4-Cre, and LysM-Cre mice were obtained from Jackson. C57BL/6 mice were obtained from Jackson or Taconic. Bhlhe40−/− (2 (link), 30 (link)), Bhlhe40GFP+ (3 (link)), and Bhlhe40fl/fl (5 (link)) mice have been reported. Mice were maintained in our specific pathogen free facility. Sex-matched littermates were used for experiments whenever possible. Animal experiments were approved by the Animal Studies Committee of Washington University.
Infective Heligmosomoides polygyrus bakeri third-stage larvae (L3) were prepared as described (13 ) and 200 L3 were given using a 20-gauge gavage needle. Fecal eggs were counted on a McMaster counting chamber (Chalex LLC) (13 ). For rechallenge experiments, infection was cleared with pyrantel pamoate p.o. (2 mg, Columbia Laboratories) on d14 and 15 after primary infection. Mice were rested for 3–4 weeks before reinfection. Blood was collected at d21 post-rechallenge to assess antibody titers. Mice were sacrificed on d17 or 22 of secondary infection for assessment of cellular responses, macroscopic intestinal granulomas, and intestinal worm burden.
For in vivo antibody blockade, mice were injected i.p. with 300 μg of αGM-CSF (Leinco, MP1–22E9), αIL-5 (BioXCell, TRFK5), or control polyclonal rat IgG (Sigma Aldrich I4131) every other day from the day of reinfection.
Jarjour N.N., Bradstreet T.R., Schwarzkopf E.A., Cook M.E., Lai C.W., Huang S.C., Taneja R., Stappenbeck T.S., Van Dyken S.J., Urban JF J.r, & Edelson B.T. (2020). BHLHE40 promotes TH2 cell-mediated anti-helminth immunity and reveals cooperative CSF2RB family cytokines. Journal of immunology (Baltimore, Md. : 1950), 204(4), 923-932.
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4

Immunotherapies in Blastomycosis Infection

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Two hundred and fifty micrograms of anti-IL-1α (BioXcell ALF 161), anti-IL-1β (BioXcell B122), anti-IL-17A (BioXcell 17F3), anti-GM-CSF (BioXcell MP1-22E9) and anti-CD4 (BioXcell GK1.5) were injected i.v retroorbitally at the time of inoculation with B. dermatitidis.
Hernández-Santos N., Wiesner D.L., Fites J.S., McDermott A.J., Warner T., Wüthrich M, & Klein B.S. (2018). Lung epithelial cells coordinate innate lymphocytes and immunity against pulmonary fungal infection. Cell host & microbe, 23(4), 511-522.e5.
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5

Systemic and Local Antibody Treatments for Experimental Autoimmune Uveitis

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For systemic antibody treatment, experimental animals were injected i.p. with the following antibodies: 300 μg of anti-GM-CSF antibody (purified clone MP1–22E9 from BioXcell, or clarified ascites produced by Harlan Bioproducts for Science Inc.), 300 μg of anti–IFN–γ antibody (clone R4–6A2 in the form of ascites produced by Harlan Bioproducts for Science Inc.), 600 μg of anti-IL-17A antibody (clone MM17F3 in the form of ascites from Harlan Bioproducts for Science Inc.) or their respective isotype Ig controls (Rat IgG2a, Rat IgG1, or mouse IgG1). Serum levels of rat IgG2a were determined by ELISA (Invitrogen) to check persisting levels of anti-GM-CSF antibody in circulation. For local antibody treatment, animals were given anti-GM-CSF antibody (100 μg/2 μl/eye), purified from ascites and concentrated, or isotype Ig (Rat IgG2a) on day 10 post-immunization as a single bilateral intravitreal injection. For blocking C–C chemokine receptor type 3 (CCR3) signaling, 200 μg SB328437 (CCR3 antagonist, Abcam), suspended in phosphate-buffered saline (PBS) containing 0.1% tween 80, was administered subcutaneously every day from 1 day before immunization [23 (link)].
Bing S.J., Silver P.B., Jittayasothorn Y., Mattapallil M.J., Chan C.C., Horai R, & Caspi R.R. (2020). Autoimmunity to neuroretina in the concurrent absence of IFN-γ and IL-17A is mediated by a GM-CSF-driven eosinophilic inflammation. Journal of autoimmunity, 114, 102507.
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