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1.
Int Immunol ; 22(4): 217-26, 2010 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-20139175

RESUMEN

Japanese scientists were involved in pioneering work on therapeutic antisera and have made huge contributions to the characterization of the antibody molecules that are responsible for this and many other biological activities, as well as working back to understand the B cells that produce these Igs. This review emphasizes the role of Japanese immunologists in this field, starting with their work in developing antisera and studying the structure of Igs. It describes the molecular mechanisms that generate the enormous antibody repertoire and regulate B-cell development and signaling. It also details the importance of the germinal center in generating B-cell memory and the terminal differentiation of B cells as antibody-secreting plasma cells.


Asunto(s)
Anticuerpos/historia , Linfocitos B/inmunología , Animales , Anticuerpos/química , Anticuerpos/inmunología , Reordenamiento Génico de Linfocito B , Historia del Siglo XIX , Historia del Siglo XX , Historia del Siglo XXI , Humanos , Memoria Inmunológica , Japón , Células Plasmáticas/inmunología , Receptores Inmunológicos/historia , Receptores Inmunológicos/inmunología , Hipermutación Somática de Inmunoglobulina
4.
C R Acad Sci III ; 318(5): 609-18, 1995 May.
Artículo en Inglés | MEDLINE | ID: mdl-7671007

RESUMEN

A physiologically relevant thrombopoietin (TPO) must be a humoral regulator with lineage specificity for megakaryocytes and their precursors. It should be capable of stimulating platelet production in normal animals, and elevated levels of TPO should be detectable in the plasma following acute, severe thrombocytopenia. Acute thrombocytopenia provides a model system that is likely to predict the effects of TPO, since many of the effects on megakaryocytes and platelets observed after induction of acute thrombocytopenia would be mediated by TPO. Important questions remain to be answered. Do the currently available data for the c-Mpl ligand explain previously published data that describe elevated levels of Meg-CSF in the circulation following production of bone marrow aplasia? Does the c-Mpl ligand account for all of the megakaryocyte stimulatory factors that have been described? Is there another factor that accounts for at least some of the acute alterations in megakaryocytopoiesis that occur immediately following a decrease in platelet levels?


Asunto(s)
Receptores Inmunológicos/fisiología , Trombopoyetina/fisiología , Enfermedad Aguda , Animales , Recuento de Células , Historia del Siglo XX , Megacariocitos/citología , Megacariocitos/efectos de los fármacos , Megacariocitos/fisiología , Ratones , Recuento de Plaquetas , Receptores Inmunológicos/historia , Trombocitopenia/patología , Trombopoyetina/historia , Trombopoyetina/farmacología
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