Affiliation: International Medical Center of Japan
- [Tuberculosis and the human immunodeficiency virus infection]K Nakata
Department of Respiratory Diseases, International Medical Center of Japan
Nihon Hansenbyo Gakkai Zasshi 69:87-92. 2000..The promotion of HIV-1 production is not only due to activated translocation of a nuclear factor. NF-kB, but also due to reduced inhibitory factor, C/EBPb 16 kD which binds to HIV LTR and represses the transcription of HIV-1...
- [The mechanism of HIV replication at the site of inflammation coinfected with HIV and M. tuberculosis]Koh Nakata
Department of Respiratory Diseases, Research Institute, International Medical Center of Japan, 1 21 1, Toyama, Shinjuku ku, Tokyo 162 8655, Japan
Kekkaku 77:687-92. 2002..Contact between activated lymphocytes and macrophages is necessary to down-regulate inhibitory C/EBP beta, thereby derepressing the HIV-1 LTR. Lymphocyte derived soluble factor(s) activate NF-kappa B, further enhancing the HIV-LTR...
- Dihydroheptaprenyl and dihydrodecaprenyl monophosphates induce apoptosis mediated by activation of caspase-3-like proteaseE Yasugi
Division of Biochemistry and Nutrition, Research Institute, International Medical Center of Japan, Tokyo
Biochim Biophys Acta 1389:132-40. 1998..We interpret these results to mean that dihydroprenyl phosphates with more than seven isoprene units have apoptosis-inducing activity and that their signal is mediated by caspase-3-like activation...
- Mechanisms of polymorphonuclear neutrophil-mediated induction of HIV-1 replication in macrophages during pulmonary tuberculosisYoshihiko Hoshino
Division of Pulmonary and Critical Care Medicine, Department of Medicine, New York University School of Medicine, New York, NY 10016, USA
J Infect Dis 195:1303-10. 2007....
- Maximal HIV-1 replication in alveolar macrophages during tuberculosis requires both lymphocyte contact and cytokinesYoshihiko Hoshino
Division of Pulmonary and Critical Care Medicine, Department of Medicine, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA
J Exp Med 195:495-505. 2002..Contact between activated lymphocytes and macrophages is necessary to down-regulate inhibitory C/EBPbeta, thereby derepressing the HIV-1 LTR. Lymphocyte-derived cytokines activate NF-kappaB, further enhancing the HIV-1 LTR...
- Why does the autoantibody against granulocyte-macrophage colony-stimulating factor cause lesions only in the lung?Koh Nakata
Bioscience and Medical Research Center, Niigata University Medical and Dental Hospital, Asahimachi Dohri, Niigata, Japan
Respirology 11:S65-9. 2006..However, this finding posed the question as to why the autoantibody against GM-CSF caused lesions only in the lung...
- Granulocyte-macrophage colony-stimulating factor inhalation therapy for patients with idiopathic pulmonary alveolar proteinosis: a pilot study; and long-term treatment with aerosolized granulocyte-macrophage colony-stimulating factor: a case reportRyushi Tazawa
Respiratory Medicine and Translational Research Clinic, Tohoku University Hospital, Seiryomachi, Sendai, Japan
Respirology 11:S61-4. 2006..The results suggest that the efficacy of GM-CSF inhalation therapy might be related to the drug preparation mode, choice of nebulizer, and duration of treatment...
- Granulocyte-macrophage colony-stimulating factor and lung immunity in pulmonary alveolar proteinosisRyushi Tazawa
Institute of Development, Aging, and Cancer, Tohoku University Department of Hematology and Immunology, Tohoku University Hospital, Japan
Am J Respir Crit Care Med 171:1142-9. 2005..Our study shows that GM-CSF administration engenders a decrease in the neutralizing capacity against the protein in the lungs. Thereby, it facilitates restoration of the normal function of alveolar macrophages...
- [Molecular pathogenesis in tuberculosis complicated with AIDS]Koh Nakata
Bioscience Medical Research Center, Niigata Medical Dental Hospital, Niigata, Japan
Kekkaku 79:659-67. 2004..Contact between activated lymphocytes and macrophages is necessary to downregulate inhibitory C/EBP beta, thereby derepressing the HIV-1 LTR. Lymphocyte derived soluble factor(s) activate NF-kappaB, further enhancing the HIV-1 LTR...
- Pulmonary alveolar proteinosisJeffrey J Presneill
Intensive Care Unit, Royal Melbourne Hospital, Grattan Street, Parkville 3050, Victoria, Australia
Clin Chest Med 25:593-613, viii. 2004..The last decade has brought new advances in laboratory and clinical research that are lifting a veil not only on PAP but also on general aspects of pulmonary surfactant biology and innate immune defense...
- BCL-6 mutations in pulmonary lymphoproliferative disorders: demonstration of an aberrant immunological reaction in HIV-related lymphoid interstitial pneumoniaKatsushi Kurosu
Department of Respirology B2, Graduate School of Medicine, Chiba University, Chiba, Japan
J Immunol 172:7116-22. 2004....
- Pulmonary alveolar proteinosisBruce C Trapnell
Division of Pulmonary Biology, Children s Hospital Medical Center, Cincinnati, OH 45229, USA
N Engl J Med 349:2527-39. 2003
- High-affinity autoantibodies specifically eliminate granulocyte-macrophage colony-stimulating factor activity in the lungs of patients with idiopathic pulmonary alveolar proteinosisKanji Uchida
Department of Respiratory Diseases, Research Institute, International Medical Center of Japan, 1 21 1 Toyama, Shinjuku City, Tokyo 162 8655, Japan
Blood 103:1089-98. 2004..Our data strengthen the evidence associating anti-GM-CSF autoantibodies with the pathogenesis of this disease...
- Oligoclonal T cell expansions in pulmonary lymphoproliferative disorders: demonstration of the frequent occurrence of oligoclonal T cells in human immunodeficiency virus-related lymphoid interstitial pneumoniaKatsushi Kurosu
Department of Respirology, School of Medicine, Chiba University, Chiba, Japan
Am J Respir Crit Care Med 165:254-9. 2002....
- Expression of PU.1 and terminal differentiation of alveolar macrophages in newborn ratsHaruko Iwabuchi
Division of Cellular and Molecular Pathology, Department of Cellular Function, Niigata University Graduate School of Medical and Dental Sciences, Asahimachi 1 757, Niigata 951 8510, Japan
Cell Tissue Res 329:71-9. 2007..These results suggest that AMs are initially immature, and that their terminal differentiation starts after birth concomitantly with an increased expression of PU.1...