The immunopathological study on leukocyte adhesion molecule DNAM-1(CD226)

科学研究費助成事業(科学研究費補助金)研究成果報告書：基盤研究(A)2009-2011課題番号：2124902

CD34[+]造血前駆細胞からNK細胞への分化を誘導するリンフォカイン

Thesis (Ph.D. in Medical Sciences)--University of Tsukuba, (B), no. 1224, 1996.10.31Offprint. Originally published in: Blood, v. 85, no. 12, pp. 3538-3546, 1995Includes supplementary treatis

Upper crustal structure beneath the Ongul Island, East Antarctica

Two explosion seismic experiments were conducted in 1980 by the 21st Japanese Antarctic Research Expedition (JARE-21) to reveal the velocity structure beneath the Ongul Islands, East Antarctica. In one experiment eleven stations were established along a line of 5.2 km long at intervals of about 0.5 km on the outcrops on East and West Ongul Islands and two explosions of 100 and 80 kg were fired at the bottom of the sea. The other smaller-scale experiment was made on East Ongul Island to reveal the structure shallower than that obtained by the above-mentioned experiment. Five shots were fired and the seismic waves were observed at eight stations along two lines of 0.7 and 0.9 km long respectively. In both experiments direct waves were clearly recorded at all the stations as first arrivals. The mean apparent velocity and the mean average velocity of P-waves are 6.19±0.11 and 5.74±0.88 km/s, respectively. The obtained velocity in the ice-free area of the Ongul Islands is nearly the same as the velocities under the ice sheet in East Antarctica hitherto obtained by the research expeditions of the United States, USSR and Japan. The sedimentary layer with a velocity less than 5.5 km/s does not exist. Clear later arrivals with large amplitude were also detected at all the stations that ranged from 0.1 to 5.2 km from the shot point. The mean apparent velocity and the mean average velocity were 2.84±0.03 and 2.94±0.37 km/s, respectively. These later arrivals are presumably Rayleigh waves

Deep crustal structure along the profile between Syowa and Mizuho Stations, East Antarctica

Three big seismic explosion experiments were carried out by the 21st and 22nd Japanese Antarctic Research Expeditions in the vicinity of Syowa Station and in the northern Mizuho Plateau in East Antarctica. Twenty-seven temporal seismic observation stations were set up along a 300-km long profile from Syowa to Mizuho Stations. Explosives were fired near Syowa Station, near Mizuho Station and at the middle point of the profile. The apparent P-wave velocity in the upper crust varies from 6.0 to 6.4 km/s, suggesting a gradual increase of the P-wave velocity with depth. Apparent velocities of 6.9 km/s for P^* and 7.9 km/s for P_n were observed from the biggest shot near Syowa Station. From the analyses of travel times and an amplitude study by synthetic seismograms, the crustal structure of the northern Mizuho Plateau was determined. The depth of the Conrad and the Moho discontinuities was determined as about 30 km and 40 km, respectively. The P-wave velocity increases from 6.0 km/s on the surface to 6.4 km/s at a depth of 13 km. At the Conrad, there is no sharp velocity discontinuity. The thickness of the transition zone is 2.4 km. Comparing our results with those in Dronning Maud Land (in the vicinity of Novolazarevskaya Station of USSR), East Antarctica, velocity values are nearly the same, but the thickness of lower crust in the northern Mizuho Plateau is about a half of that in Dronning Maud Land

Selective loss of Purkinje cells in a patient with anti-gliadin-antibody-positive autoimmune cerebellar ataxia

The patient was an 84-year-old woman who had the onset of truncal ataxia at age 77 and a history of Basedow's disease. Her ataxic gait gradually deteriorated. She could not walk without support at age 81 and she was admitted to our hospital at age 83. Gaze-evoked nystagmus and dysarthria were observed. Mild ataxia was observed in all limbs. Her deep tendon reflex and sense of position were normal. IgA anti-gliadin antibody, IgG anti-gliadin antibody, anti-SS-A/Ro antibody, anti-SS-B/La antibody and anti-TPO antibody were positive. A conventional brain MRI did not show obvious cerebellar atrophy. However, MRI voxel based morphometry (VBM) and SPECT-eZIS revealed cortical cerebellar atrophy and reduced cerebellar blood flow. IVIg treatment was performed and was moderately effective. After her death at age 85, the patient was autopsied. Neuropathological findings were as follows: selective loss of Purkinje cells; no apparent degenerative change in the efferent pathways, such as the dentate nuclei or vestibular nuclei; no prominent inflammatory reaction. From these findings, we diagnosed this case as autoimmune cerebellar atrophy associated with gluten ataxia. All 3 autopsies previously reported on gluten ataxia have noted infiltration of inflammatory cells in the cerebellum

Selective DNAM-1 expression on small peritoneal macrophages contributes to CD4+ T cell costimulation

Mouse peritoneal macrophages consist of two subsets: large peritoneal macrophages (LPMs) and small peritoneal macrophages (SPMs), defined as CD11bhiF4/80hi and CD11b+F4/80lo cells, respectively. We reveal that SPMs, but not LPMs, have the ability to present antigens to naïve CD4+ T cells. Coculture of SPMs with naïve ovalbumin (OVA) specific CD4+ T cells (OT-II) in the presence of OVA peptide effectively induced CD4+ T cells priming. SPMs, but not LPMs, strongly express DNAM-1, an activating immunoreceptor. Although antigen uptake and processing were comparable between WT and DNAM-1-deficient SPMs, deficiency of DNAM-1 on SPMs or blockade of DNAM-1 and its ligand interaction impaired CD4+ T cells priming by SPMs. Furthermore, T and B cell responses in mediastinal lymph nodes of mice intraperitoneally immunized with trinitrophenyl (TNP)–OVA protein in Alum adjuvant were enhanced by intraperitoneally transferred wild-type, but not DNAM-1-deficient, SPMs. We propose that SPMs are functionally distinct from LPMs, and DNAM-1 plays a costimulatory role in antigen presentation by SPMs