INT184006
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
+ IgG2cexpressing ASCs within extrafollicular foci. | |||||||||||||||
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Heightened production of IgG2c is significant, as this isotype is the most efficient IgG subclass for anti-pathogen FcR-mediated effector functions (Nimmerjahn and Ravetch, 2005) and has long been recognized as the predominant isotype elicited by viral infections (Coutelier et al., 1987). | |||||||||||||||
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, PE conjugated; Biolegend, San Diego, CA, USA) and CXCR4 (2B11/CXCR4, rat IgG2b ? | |||||||||||||||
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200, clone HIS24, mouse IgG2b, BD Biosciences), anti-mouse Mac3 (1? | |||||||||||||||
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Briefly, mouse monoclonal antihuman C-C chemokine ligand-2/MCP-1 IgG2b (R&D Systems) was coated onto polystyrene microtitre plates (Nunc-Immunoplate II; BRL, Uxbridge, Middlesex, UK) at a concentration of 2 ? | |||||||||||||||
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The IgG2b anti-murine RAGE mAb was developed by Wyeth (Cambridge, MA, USA). | |||||||||||||||
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For each set, appropriate isotypic control was done (IgG2b,? | |||||||||||||||
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In this paper, we show that TLR agonists significantly enhance the TI-2 antibody response through the elaboration of type I IFN that promotes production of IgG2c by FO B cells. | |||||||||||||||
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These findings strongly suggest that FO B cells are the predominant source of the poly(I:C)-induced IgG2c antibody response to the TI-2 antigen NP-Ficoll.
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S1 shows dose response of poly(I:C) on the production of NP-specific IgG2c and lack of polyclonal IgG2c production. | |||||||||||||||
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S1 shows dose response of poly(I:C) on the production of NP-specific IgG2c and lack of polyclonal IgG2c production. | |||||||||||||||
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Collectively, our findings suggest that in the presence of poly(I:C), a B cell population distinct from MZ B cells is the predominant source of NP-specific IgG2c. | |||||||||||||||
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+ plasma cells that lacked IgM or IgG2c expression (Fig. 2 B) were also observed with poly(I:C) and are likely to be NP-specific IgG3-producing ASCs, as this isotype comprised a significant amount of the response (Fig. 1 B). | |||||||||||||||
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The NP-specific mAb S43-10 (Reth et al., 1978) was used as a positive control for a high-affinity NP-specific IgG2c antibody with an affinities of Kd = 2.4 × 10? | |||||||||||||||
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Later in the course of infection, (day 3540 post-infection) IgG1, IGg2b, IgG3, and IgA were produced. | |||||||||||||||
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A mouse line of mutated gp130 in which the SHP-2/SOCS3-binding site was disrupted developed a RA-like joint disease with increased production of Th1-type cytokines and immunoglobulins of the IgG2a and IgG2b classes [78]. | |||||||||||||||
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However, antigen-specific IgG2c ASCs were also present in the lymph nodes of mice immunized with NP-Ficoll + poly(I:C) and were virtually absent in mice immunized with antigen alone (Fig. 3 B). | |||||||||||||||
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For granulocyte depletion studies, GR-1 or control antibody (IgG2b) at 300 µg/mouse (Biolegend, San Diego, CA) was administered intraperitoneally two days prior to B16-BL6 melanoma implantation in PPAR? | |||||||||||||||
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RIII-deficient DBA/1 mice were almost completely protected from arthritogenic IgG1, IgG2a or IgG2b antibodies, indicating that activating Fc? | |||||||||||||||
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The plasma levels of IgM, IgG1, IgG2a, IgG2b, IgG3, and IgA were determined simultaneously in the same sample using a bead-based assay with monoclonal anti-mouse antibodies conjugated to beads of different color regions (Biorad, USA), and acquired on a Bioplex reader (Biorad). | |||||||||||||||
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General Comments
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