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Search results for: Rabbit Anti-MC3 Receptor Polyclonal Antibody, FITC conjugated,Isotype: IgG

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Immunological and parasitological studies of Cryptosporidium muris, Tyzzer (1907).

Oocysts of C. muris and the events of excystation using 0.5% sodium hypochlorite as excystation medium were described with light microscope. The response of the immunocompetent BALB/c mice against infection was studied using sera of orally infected mice at different periods postinoculation by indirect immunofluorescence antibody test using 1:150 FITC conjugated rabbit serum antimouse polyclonal IgG. From the patterns of IFAT, it was suggested that the dominant antigen in C. muris was restricted to the apical complex of the sporozoites. Such antigen may play a role in the invasion of the host cell. Future analysis of such receptor molecules might constitute prime candidates as immunogens for a vaccine, the efficiency of which might cause inhibition of parasite invasion.
N M Abdel-Maksoud, A K Dyab, M A Shatat

2618 related Products with: Immunological and parasitological studies of Cryptosporidium muris, Tyzzer (1907).

50 mg100 ug25 mg0.1ml (1mg/ml)96T100ul10 mg1000 1000 tests100 100ug500 mg

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Expression of Fc mu receptors on human natural killer cells.

Fc receptors for IgG (CD16) have been described as the only type of immunoglobulin receptor on large granular lymphocytes (LGL). However, the ability of natural killer (NK) cells to mediate antibody-dependent cellular cytotoxicity (ADCC) in the presence of monoclonal or polyclonal IgM and the inhibition of NK activity by highly purified IgM could not be explained on the basis of FcR for IgG. In order to directly assess the expression of Fc receptors for IgM (Fc mu R), NK cells were treated with human polyclonal IgM, and its binding was visualized by a direct anti-globulin rosette assay with identification of rosette-forming LGL on Giemsa-stained smears. The data indicated that a high proportion of LGL (up to 68%) were Fc mu R-positive cells. However, this percentage varied depending on the IgM preparation (polyclonal or monoclonal), the indicator reagent used for the rosette assays, and the cell preparations studied. Two-color flow cytometry of human nonadherent lymphocyte preparations confirmed the presence of CD56+IgM+ cells, which represented from 43 to 78% of CD56+ cells. Flow cytometry was also performed using highly enriched preparations of human NK cells (the mean percentage of CD3-CD56+ cells was 84%). Up to 88% of purified NK cells bound FITC-labeled monoclonal IgM at a saturating concentration. By indirect immunofluorescence, from 34 to 62% of NK cells purified from the peripheral blood of normal donors were able to bind polyclonal IgM. Similar results were obtained with LGL from a patient with NK lymphoproliferative disease. Thus the presence of Fc mu R on a majority of human NK cells was demonstrated by different techniques, using unseparated peripheral blood mononuclear leukocytes, purified normal NK cells, and also LGL from a patient with NK lymphoproliferative disease.
L Pricop, C Galatiuc, M Manciulea, A DeLeo, A Sulica, R B Herberman, T L Whiteside

1462 related Products with: Expression of Fc mu receptors on human natural killer cells.

200 50 11.00 flask16 Arrays/Slide1.00 flask25 100 μg1mg1.00 flask0.5mg

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Comparative studies on FcR (FcRII, FcRIII, and FcR alpha) functions of murine B cells.

Distribution of FcR II, FcRIII, and FcR alpha on murine splenic B cells was examined by using FITC-labeled heat-aggregated IgG of each subclass and IgA. Almost 60 to 80% of B cells expressed both FcRII and FcRIII. However, FcR alpha was expressed on only a small proportion (6%) of B cells that co-expressed FcRII. By inhibition assays with the use of cold IgG of each subclass and IgA in addition to anti-FcRII mAb (2.4G2), it was found that IgG1, IgG2a, and IgG2b utilized the same receptor (FcRII), whereas IgG3 and IgA bound only to their unique receptors, FcRIII and FcR alpha, respectively. Immune complexes IC prepared by IgG1, IgG2a, IgG2b, and IgA anti-TNP mAb with TNP-coupled SRBC inhibited the polyclonal Ig secretion and proliferative responses of B cells stimulated with either IL-4 or LPS. The inhibition of B cell activation was associated with the blockade of the membrane depolarization. Moreover, IC prepared by these antibodies caused production of suppressive B cell factor (SBF) as is the case with rabbit IgG antibody to SRBC, and SBF thus prepared regulated antibody responses in an isotype-nonspecific manner. In contrast, no inhibition for these responses or production of SBF was attained by the IC of IgG3 antibody. We concluded that FcRII and FcR alpha mediates a suppressive signal for B cells by acting on the initial step of activation, whereas FcRIII lacks this activity.
K Tsujimura, Y H Park, M Miyama-Inaba, T Meguro, T Ohno, M Ueda, T Masuda

2252 related Products with: Comparative studies on FcR (FcRII, FcRIII, and FcR alpha) functions of murine B cells.

5 G50mlOne 96-Well Strip Micropl25ml100ug Lyophilized0.25 mg100 MG100ug50 1,000 tests100 μg100ul

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Infection enhancement of influenza A H1 subtype viruses in macrophage-like P388D1 cells by cross-reactive antibodies.

The contribution of cross-reactive hemagglutination inhibition (HI) antibodies to infection enhancement of influenza A H1 subtype NWS virus and two antigenic drift strains was investigated in a macrophage-like cell line P388D1. When P388D1 cells, previously treated with neuraminidase (NA) to remove the viral receptors, were infected with NWS virus exposed to rabbit antiviral immunoglobulin (IgG) showing various levels of cross-HI titers, virus yields were enhanced in the presence of a subneutralizing antibody, depending on their cross-HI titers. By flow cytometric analysis using a fluorescein isothiocyanate (FITC)-labeled NWS virus, the efficiency of attachment of virus-rabbit IgG complexes to Fc receptors on NA-treated cells showed close correlation with its cross-HI titer. These data suggest that cross-reactive HI antibodies could contribute to infection enhancement through the formation of potent infectious immune complexes with drift strains to mediate virus infection via Fc receptor uptake. Two monoclonal antibodies (mAB) in mouse IgG subclasses IgG1 and IgG2a showing strain-specific or cross-reactive HI activity were tested for their infection enhancement characteristics. A strain-specific mAB enhanced infection of homologous NWS virus, but not that of two other drift strains in either antibody dilution. In contrast, a cross-reactive mAB caused infection enhancement of all three virus strains in the presence of the subneutralizing antibody. This indicates that cross-reactivity, but not the IgG subclass, acts as an enhancing factor to this phenomenon. The antibody, with the same specificity as cross-reactive mAB, was detected semiquantitatively by competitive enzyme-linked immunosorbent assay (ELISA) with results almost consistent with cross-HI titers of polyclonal rabbit antiviral IgGs. These data suggest that the antibody detected by this assay might be one of the potent antibodies governing cross-HI activity as a whole antibody and causing infection enhancement of drift strains.
H Ochiai, M Kurokawa, Y Kuroki, S Niwayama

2539 related Products with: Infection enhancement of influenza A H1 subtype viruses in macrophage-like P388D1 cells by cross-reactive antibodies.

1 mL51mg50101 ml1 mL1001 ml151 ml1 mg

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Deposits of immunoglobulins, complement, and immune complexes in inflamed human gingiva.

Gingival biopsy specimens from 20 patients with moderate to advanced periodontitis were obtained from inflamed sites with pockets of 5 mm or more. Sections were studied by an immunofluorescence technique, using polyclonal rabbit or goat anti-IgG, anti-IgM, anti-C1q, anti-C3a, and anti-C3c and mouse monoclonal anti-C9. Prewashed ethanol-fixed and nonwashed ethanol-fixed or frozen specimens showed many plasma cells staining for IgG or C3a, suggesting the possible occurrence of a receptor for C3a in plasma cells. Plasma cells containing IgM were also seen. Deposits of IgG and IgM with C1q, C3a, and C3c, suggesting immune complexes, were demonstrated by a double staining technique, combining fluorescein (FITC) or rhodamine (TRITC)-labeled anti-immunoglobulins with TRITC- or FITC-conjugated antibody to C3a, C3c, and C1q. The complexes were located mainly within or around vessel walls. Deposits of C3a and C1q were found in vessel walls, in the basement membrane zone of oral gingival epithelium, or diffusely distributed in the tissues. Deposits of C3c were found to a lesser extent and only in vessel walls. Mouse monoclonal anti-C9, visualized with FITC-labeled rabbit anti-mouse and swine anti-rabbit antiserum, showed granular deposits of C9, mainly in the basement membrane zone of oral gingival epithelium. The study indicates the involvement of immune complex vasculitis in inflammatory periodontal lesions. Also, our observations of the occurrence of deposits of complement factors support the hypothesis that complement factors play an important role in the immunopathology of the periodontal lesion.
A A Nikolopoulou-Papaconstantinou, A C Johannessen, T Kristoffersen

2986 related Products with: Deposits of immunoglobulins, complement, and immune complexes in inflamed human gingiva.

100 μg1 kit(96 Wells)100 μg100 μg10ug100 μg100 μg10 100 μg1000 0.1 mg100 μg

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