PubMed Health⌕ Search

PubMed · 14101803

[THE LE-PHENOMENON].

Abstract

The source did not provide an abstract. Follow the original record for more information.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

A BOYUM. 1964-01-01. [THE LE-PHENOMENON].. https://pubmed.ncbi.nlm.nih.gov/14101803/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Regulation of metastasis-suppressive gene Nm23-H1 on glycosyl-transferases involved in the synthesis of sialyl Lewis antigens.

By using reverse transcriptase-polymerase chain reaction (RT-PCR), the mRNA expressions of three families of glycosyltransferases involved in the synthesis of sialyl Lewis antigens were determined in H7721 human hepatocarcinoma cell line before and after the transfection of metastasis-suppressive gene nm23-H1. These glycosyltransferases included alpha1,3fucosyltransferase (alpha1,3FucT)-III, -IV, -VI, -VII, and -IX, alpha2,3-sialyltransferase (ST3Gal)-I, -II, -III, and -IV as well as O-glycan core 2 beta1,6 N-acetylglucosaminyltransferase (C2GnT)-I and -II. In mock cells transfected with the vector, the expression-order of alpha1,3FucTs was IV>VI>III>VII>IX, that of ST3Gals was IV>I>II>III, and that of C2GnT was I>II. Nm23-H1 downregulated the mRNA expressions of all five subtypes of alpha1,3FucT and -I, -III, -IV subtypes of ST3Gal, but not ST3Gal-II and C2GnT-I, II. On the other hand, the expressions of cell surface sialyl Lewis X (SLe(x)) and alpha2,3 sialyl residues were decreased on nm23-H1 transfected cells as detected with monoclonal antibody of SLe(x) and enzyme-labeled lectins, respectively. Since SLe(x) was reported to be a metastasis-associated glycan structure, the reduced expressions of SLe(x) and some enzymes related to its synthesis may be one of the mechanisms to explain the metastasis-suppressive effect of nm23-H1.

Antigens↗

Impedimetric immunosensors based on the conjugated polymer PPV.

In the work reported here, we investigated the interaction between the semiconducting polymer MDMO-PPV and antibodies against the fluorescent dyes fluorescein isothiocyanate (FITC) and Cy5. The antibodies are adsorbed physically onto thin polymer films on gold electrodes, as seen in AFM images of these films. By tuning the antibody concentration, the contact angle of distilled water with the film can be made to vary between 95 degrees and 50 degrees, showing that different surface densities of antibody can be obtained. That these biosensor films specifically bind their antigenic fluorescent molecules from PBS buffer solution is demonstrated by confocal fluorescence microscopy. Specific antigen-antibody recognition is demonstrated by lack of cross-sensitivity between the two antibodies and their antigens. In a biosensor prototype based on differential impedance spectroscopy, these polymer films show a clear response to 1 ppb antigen solution, with a time constant of 2-3 min.

Antigens↗

T regulatory-1 cells induce IgG4 production by B cells: role of IL-10.

The study was aimed to find out whether T cells with a regulatory profile could regulate the secretion of IgG4. Using tetanus Ag we found that PBMC of healthy human donors responded to exogenous IL-10 by down-regulating IgG1 and increasing IgG4 secretion. IgE was not affected. To investigate the direct effect of IL-10-producing T cells on B cells, we generated T cell clones (TCC) with two different cytokine profiles: first, IL-10high, IL-2low, IL-4low TCC, and second, IL-10low, IL-2high, IL-4high. The T cell-dependent Ab secretion was measured by coculturing purified CD19+ B cells and the TCC. Interestingly, we found that IgG4 production in the coculture correlated with the TCC production of IL-10 (r2 = 0.352, p = 0.0001), but not with IL-2, IL-4, nor IFN-gamma. IgE showed only a trend with regard to IL-4. Further, there was decreased Ab secretion in the absence of T-B cell contact. IL-10 also induced IgG4 when added to a Th1 TCC-B cell coculture system. The present study thus shows that in T-B cell coculture, IL-10, if induced by the TCC or added to the system, down-regulates the immune response by inducing IgG4 secretion. This establishes a direct implication of IL-10 in humoral hyporesponsiveness, particularly in compartments where the T-B cell interplay determines the subsequent immune response. The correlation between IgG4 and IL-10 (r2 = 0.352) indicates that IL-10 is an important but not the only factor for IgG4 induction.

Antigens↗