Murine NKT cells can recognize alpha-galactosylceramide (alpha-GalCer) in the context of a class Ib CD1d molecule. Here we show that alpha-GalCer can selectively activate freshly isolated human Valpha24(+)Vbeta11(+) cells, functionally defining the human NKT cells. The naive human NKT cell repertoire consisted of cells expressing an invariant Valpha24JalphaQ chain and a diverse array of beta chains derived from a single Vbeta11 gene segment. Stimulation with alpha-GalCer expanded a polyclonal subset of the human NKT cell repertoire carrying a novel complementarity-determining region (CDR) 3beta consensus motif that may directly interact with the sugar moiety of alpha-GalCer. Our data suggest that certain redundancy is allowed for CDR3beta of NKT antigen receptor to interact with the ligand and provide a first clue to understand the novel protein-carbohydrate interaction mechanisms.
We treated 2 intractable patients with pemphigoid by absorbent plasmapheresis using dextran sulfate conjugated cellulose columns with an automated regenerating unit. During a 2 week period, this plasmapheresis was performed 4 to 6 times for Cases 1 and 2, respectively. Clinical findings including skin eruptions were remarkably improved, and the titers of antibasement membrane zone antibodies were decreased after the treatment of 1.8 to 4.2 L of plasma. These results suggest that the absorbent column is effective for intractable pemphigoid.
To clarify the role of coronary spasm or dynamic coronary obstruction in the development of acute myocardial infarction (AMI) with spontaneous recanalization (SR), symptoms in 296 patients with AMI admitted within 24 h after the onset of chest pain were analyzed just before and after onset, and coronary angiograms were analyzed soon after onset. Patients were divided into 3 groups according to the initial angiographic findings in the infarct-related coronary artery (IRCA): group 1 comprised 172 patients with total occlusion (TIMI O); group 2 comprised 57 patients with subtotal occlusion (TIMI 1,2); and group 3 comprised 67 patients with SR (TIMI 3). The incidence of SR was 20.3% at 0-4 h after onset, 22.2% at 4-6 h, 19.7% at 6-12 h, 24.0% at 12-24 h, and 36.0% at 24 h or later. The incidence of SR did not increase significantly as time elapsed. The incidence of angina at rest and variable-threshold angina before the onset of infarction was only 16.2% in group 1, but was significantly higher in groups 2 (64.3%) and 3 (61.9%). The incidence of intermittent chest pain at onset in group 1 (8.4%) was significantly lower than in groups 2 (54.5%) and 3 (38.8%). Vasodilation of the proximal normal segment adjacent to the stenotic site of the IRCA induced by intracoronary nitroglycerin was significantly higher in groups 2 (11.7 +/- 1.2%) and 3 (20.7 +/- 2.6%) than in group 1 (4.0 +/- 0.6%). These results suggest that coronary spasm or dynamic obstruction may be involved in the pathogenesis of thrombus formation or coronary obstruction causing AMI in many Japanese patients.
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