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Multiple isoforms of UDP-GalNAc:polypeptide N-acetylgalactosaminyl-
transferase (ppGaNTase) have been cloned and expressed from a variety of
organisms. In general, these isoforms display different patterns of
tissue-specific expression, but exhibit overlapping substrate
specificities, in vitro . A peptide substrate, derived from the sequence of
the V3 loop of the HIV gp120 protein (HIV peptide), has previously been
shown to be glycosylated in vitro exclusively by the ppGaNTase-T3 (Bennett
et al. , 1996). To determine if this isoform- specificity is maintained in
vivo , we have examined the glycosylation of this substrate when it is
expressed as a reporter peptide (rHIV) in a cell background (COS7 cells)
which lacks detectable levels of the ppGaNTase-T3. Glycosylation of rHIV
was greatly increased by coexpression of a recombinant ppGaNTase-T3.
Overexpression of ppGaNTase- T1 yielded only partial glycosylation of the
reporter. We have also determined that the introduction of a proline
residue at the +3 position flanking the potential glycosylation site
eliminated ppGaNTase- T3 selectivity toward rHIV observed both in vivo and
in vitro .
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Batchelder JM Burns JM Cigel FK Lieberg H Manning DD Pepper BJ Yañez DM van der Heyde H Weidanz WP 《Experimental parasitology》2003,105(2):159-166
Cell-mediated immunity (CMI) may be important in immunity against blood-stage malaria. Accordingly, we examined the role of type 1 cytokines in the resolution of Plasmodium chabaudi adami malaria in mice genetically modified to have type 1 cytokine gene defects. Parasitemia was prolonged in double knockout (IL-2(-/-), IFNgamma(-/-)) mice compared to control mice. Despite deficiencies in gammadelta T cell and B cell subsets, these mice produced anti-malarial antibodies and eventually cured their infections, possibly by antibody-mediated immunity. However, because acute P. c. adami parasitemia may also be suppressed by CMI, the requirements for IL-2 and IFNgamma were evaluated in mice lacking B cells and functional IL-2 or IFNgamma genes. Acute malaria in J(H)(-/-), IL-2(-/-) mice was prolonged, but eventually cured. In contrast, J(H)(-/-), IFNgamma(-/-) mice developed unremitting parasitemia. These data strongly suggest that IFNgamma, but not IL-2, plays an essential role in the expression of CMI against P. c. adami infections. This finding may prove useful in developing malarial vaccines aimed at inducing CMI. 相似文献
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W P Weidanz J R Kemp J M Batchelder F K Cigel M Sandor H C Heyde 《Journal of immunology (Baltimore, Md. : 1950)》1999,162(12):7383-7388
gammadelta T cells have a crucial role in cell-mediated immunity (CMI) against P. chabaudi malaria, but delta-chain knockout (KO) (deltao/o) mice and mice depleted of gammadelta T cells with mAb cure this infection. To address the question of why mice deficient in gammadelta T cells resolve P. chabaudi infections, we immunized deltao/o mice by infection with viable blood-stage parasites. Sera from infection-immunized mice were tested for their ability to protect JHo/o, deltao/o double KO mice passively against P. chabaudi challenge infection. The onset of parasitemia was significantly delayed in mice receiving immune sera, compared with saline or uninfected serum controls. Immune sera were then fractionated into Ig-rich and Ig-depleted fractions by HPLC on a protein G column. Double KO mice were passively immunized with either fraction and challenged with P. chabaudi. The onset of parasitemia was significantly delayed in recipients of the Ig-rich fraction compared with recipients of the Ig-poor fraction of immune sera. We conclude that deltao/o mice, which are unable to activate CMI against the parasite, suppress P. chabaudi infection by a redundant Ab-mediated process. 相似文献
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