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Biomedical subjects

M Uchijima

Publications and source records attributed to M Uchijima.

24 records · Page 2Linked to original sources
PubMed1995

Unimpaired clearance of Mycobacterium bovis BCG infection in selectively T-cell anergic TCR-V beta 8.2 transgenic mice.

The anergy induced in mice with staphylococcal enterotoxin B (SEB) has been shown to involve selective unresponsiveness in cytokine expression. While interleukin-2 (IL-2), IL-3 and IL-4 mRNA levels are substantially reduced in anergic T cells upon restimulation with SEB, mRNA for interferon-gamma (IFN-gamma) is expressed normally. On the other hand, infection with Nippostrongylus brasiliensis is known to break an established T-cell anergy. This knowledge prompted us to examine the effect of infection with an intracellular microbe, bacillus Calmett-Guérin (BCG), on the expression of anergy induced with SEB. We have demonstrated that while the SEB-induced anergy was not abrogated by BCG infection, the V beta 8.2 transgenic mice, in which almost all T cells were anergized with SEB, were capable of developing the effective acquired protective immunity, possibly through the preserved capacity to induce IFN-gamma leading to induction of nitric oxide synthase.

Animals↗
PubMed1994

Tax proteins of human T-cell leukemia virus type 1 and 2 induce expression of the gene encoding erythroid-potentiating activity (tissue inhibitor of metalloproteinases-1, TIMP-1).

A growth factor-like activity for erythroid cells (erythroid-potentiating activity) is produced by the T-cells infected with human T-cell leukemia virus type 2 (HTLV-2) (Gasson, J. C., Golde, D. W., Kaufman, S. E., Westbrook, C. A., Hewick, R. M., Kaufmann, R. J., Wong, G. G., Temple, P. A., Leary, A. C., Brown, E. L., Orr, E. C., and Clark, S. C. (1985) Nature 315, 768-771) and is reportedly identical with tissue inhibitors of matrix metalloproteinases-1 (TIMP-1) (Docherty, A. J. P., Lyons, A., Smith, B. J., Wright, E. M., Stephens, P. E., Harris, T. J. R., Murphy, G., and Reynolds, J. J. (1985) Nature 318, 66-69). We found that adult T-cell leukemia cell lines infected with HTLV-1 also express high levels of a TIMP-1 transcript. A viral transactivator of HTLV-1, Tax1, in a human T-cell line (Jurkat), was sufficient to stimulate transcription of the TIMP-1 gene. Deletion and mutation analysis of the TIMP-1 gene promoter showed that the AP-1 binding site in the 38-base pair sequence conserved between the human and mouse genes was essential for activation by Tax1. The transactivator of HTLV-2 also stimulated the promoter through the same cis-element. The reported growth-promoting activity of TIMP-1 against erythroid cells and potentially against HTLV-1-infected T-cells may modulate the clinical course of adult T-cell leukemia.

Animals↗
PubMed1994

IFN-gamma induces IL-12 mRNA expression by a murine macrophage cell line, J774.

Interleukin (IL)-12 is a logical candidate for participation in the differentiation of T helper (Th) 1 cells. IL-12 is produced by macrophages and B cells and induces the production of interferon (IFN)-gamma from Th1 cells and NK cells. In this study, we show that the IFN-gamma itself is capable of inducing IL-12 mRNA expression in murine macrophage cell line J774. The mRNA was apparent by 12h after IFN-gamma treatment, although maximal induction required 36 to 48h. Furthermore, we investigated the signal transduction mechanism responsible for the mRNA expression. The IFN-gamma-inducible IL-12 mRNA was blocked by two protein tyrosine kinase (PTK) inhibitors, genistein and herbimycin A, suggesting that PTK is involved in the IFN-gamma-inducible IL-12 mRNA expression.

Animals↗
PubMed1990

Clonal origin of mammalian hepatitis B virus-related hepatocellular carcinoma.

The clonal origins of 20 multifocal hepatocellular carcinomas (HCCs) in four woodchucks were analyzed by the Southern blot hybridization technique. The woodchucks were divided into two groups according to the morphological classification of multifocal tumors: 1) three woodchucks had multifocal tumors that were widely separated and similar in size, which suggests a multiclonal origin of the tumors; and 2) one woodchuck had ten small multifocal tumors surrounding two large main tumors, which indicated intrahepatic metastasis from an original tumor. Results from the first group demonstrated that the number of integrated woodchuck hepatitis virus (WHV) DNAs differed from tumor to tumor, and none of the bands were the same size. In the second group, eight of the ten small tumors surrounding the two large tumors showed the same pattern of WHV DNA integration. One demonstrated an additional band and also shared the same bands with the other tumors, and one small tumor had a different pattern of integration from the others. It was concluded that the clone dissimilarity demonstrated by hybridization patterns does not necessarily mean that HCCs originate independently from different clones, because genetic changes may occur after or at the time of metastasis.

Animals↗
PubMed1990

Hepadnavirus enhancer and its binding proteins.

In the hepadnavirus enhancer region, a 33 bp DNA sequence is strongly conserved among mammalian hepadnavirus genomes. To elucidate the role of the sequence, we tested enhancer activities and capability to form DNA-protein complex of several synthetic DNAs. Not only two tandem copies of a 46 bp DNA covering the sequence but also two tandem copies of a 23 bp in the sequence exhibit enhancer activity. Also the activity was augmented by treatment of a tumor promoter, TPA. DNA binding proteins complexes with the 23 bp DNA were augmented in extracts of HepG2 or HeLa cells stimulated with TPA. These results imply that the conserved sequence of hepadnavirus enhancer is a TPA-inducible enhancer which is transactivated by ubiquitous DNA-binding proteins. We presented results showing that DNA-protein complexes with a 23 bp DNA are similar to but distinct from those with a TPA-responsive element DNA, the recognition site for c-jun/fos products. We also presented results suggesting that hepadnavirus X protein may not directly or indirectly affect DNA-protein complex formation with the conserved sequence in the hepadnavirus enhancer.

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