Se han desarrollado híbridos comerciales de maíz (Zea mays L.) para la zona de transición de México (1900 a 2200 m de altitud), en los cuales se ha combinado germoplasma generado independientemente en las regiones del subtrópico y de los Valles Altos; sin embargo, no existe una estrategia combinada de mejoramiento genético que sea específica para la zona de transición. Los objetivos de esta investigación fueron: a) Presentar una estrategia de mejoramiento para integrar un patrón heterótico de maíz de grano amarillo para la zona de transición de México, y b) Describir la formación de poblaciones que conforman el patrón heterótico para esa zona. La estrategia para el primer objetivo incluye el método de mejoramiento y los tipos de híbridos a formar; para el segundo, en seis localidades de la región Centro-Occidente de México, se evaluaron cruzas dialélicas hechas entre poblaciones de origen tropical y templado de maíz de grano amarillo; se efectuó la conversión de progenitores de grano blanco a amarillo; y se establecieron ensayos de híbridos comerciales de grano amarillo y de familias de medios hermanos de grano amarillo con germoplasma de Valles Altos y de la zona de transición, en Tepatitlán, Jal. Se concluyó que la metodología propuesta para la integración de patrones heteróticos y de variedades mejoradas para la zona de transición de México, técnicamente presenta más ventajas que el enfoque actual del Programa de Maíz del INIFAP. Se confirmó que el germoplasma templado puede hacer contribuciones importantes en el rendimiento de grano y precocidad para esa zona, por lo que ese germoplasma se utilizó como fuente en la conversión de la línea de grano blanco a amarillo “LPC1A-9R-1-1”. Las familias que integraron la población INIFAP Amarillo Dentado-3 tuvieron mayor tolerancia al acame y más sanidad de mazorca, con un ciclo de madurez similar al Criollo Amarillo Zamorano, el mejor criollo amarillo de la región.
BALB/c mice injected at birth with 10 8 semi-allogeneic (C57BL/6 x BALB.IgH b )F, spleen cells develop a lupus-like syndrome In which autoantibodles bear exclusively the donor allotype. We have analyzed the evolution of donor B cell chlmerlsm and the autoimmune manifestations during the first year of life in these mice. Antl-DNA, -histone, and -cardlollpln IgG antibodies as well as circulating immune complexes appeared in the second week of life, reached the highest values around the sixth week, and then progressively dropped to normal values after the sixth month in most mice. The kinetics of the evolution of the autoimmune manifestations, as well as the kinetics of serum donor Ig allotype, were parallel to the kinetics of donor B cell chlmerism, which was particularly prominent in the spleens in early weeks of life, and progressively decreased after remission of the autoimmune syndrome. Membrane-proliferative glomerulonephritls, which was followed as the more representative hlstological abnormality in this model, was particularly evident after 10 weeks of life, but disappeared by the end of the follow-up. Interestingly, when mice with a self-limited disease were re-injected with 10 8 F, spleen cells i.v., a flare in the serologlcal manifestations was observed. In these re-injected mice a predominance of anti-DNA, lgG1 antibodies bearing exclusively the donor allotype was also observed, as in the early weeks of life. These results emphasize the central role of donor B cell chimerism in the development and in the self-limitation of the autoimmune disease in parental mice neonatally injected with F, cells and Indicate that the capacity to react with F, cells, to generate a renewed burst of symptoms, persists in these mice after the disappearance of autoimmune findings.
Neonatal injection of semiallogeneic spleen cells induces a state of specific tolerance to the parental alloantigens, but also the development of an autoimmune syndrome known as host-versus-graft disease (HVGD). The autoimmune features are a consequence of the allogeneic cooperation between persisting alloreactive host T helper type 2 (TH2) cells and donor semiallogeneic B cells. It has been established that I-A alloantigens play a central role in the triggering of this HVGD. Here it was investigated if I-E antigens, which have shown functional differences, regarding autoimmunity and alloreactivity, with respect to I-A antigens, are also able to trigger this autoimmune syndrome. The injection of spleen cells from [B10.A(4R) x B10.A(2R)]F1 (I-E+) hybrid mice into newborn B10.A(4R) (I-E-) mice was accompanied by the establishment of chimerism and also by the development of a characteristic, but moderated, HVGD. The weak intensity of this HVGD is likely due to the moderation of the alloreactive responses induced against I-E molecules. Moreover, the marked increase in the levels of IgE and in the titers of anti-DNA IgG1 antibodies strongly suggest that alloreactive TH2 cells play also a main role in the autoimmune syndrome following tolerization to I-E antigens. Therefore, it is concluded that the I-E and I-A isotypes are functionally similar with respect to the allogeneic cellular interactions that account for the HVGD.
Babesiosis is a tick-borne disease of cattle caused by Babesia bigemina and Babesia bovis and is transmitted by the tick vector Boophilus microplus. In this study, we investigate B. bigemina infection regarding the clinical infection, T cell distribution, and cytokine profile during the acute phase of an experimental infection in pregnant cows.
The presence of naturally occurring anti-Galalpha1-3Gal (antialphaGal) Ab in human serum is believed to be a major factor in the pathogenesis of hyperacute rejection of discordant organ xenografts such as the pig-to-human combination. Galalpha1-3Gal epitopes are expressed on pig tissues and the binding of anti-Galalpha1-3Gal leads to endothelial cell activation and complement-mediated hyperacute graft rejection. Several strategies have been suggested in donor animals or in the xenograft recipient to overcome the anti-alphaGal barrier. Protein-A immunoadsorption (PAIA) was developed for the in vivo removal of circulating Ab and it has been shown to be effective in cases where pathogenic auto or alloAb are present. The aim of our study was to analyze the effect of PAIA on total and xenoreactive serum anti-alphaGal immunoglobulin levels in a group of patients treated with this technique for different diseases. After three consecutive sessions of PAIA, total and xenoreactive IgG and IgM immunoglobulin levels were decreased by more than 50% of pre-treatment levels. So we conclude that PAIA is an effective method to significantly reduce circulating Ab, including xenogeneic IgM and IgG Ab. This mode of therapy might be considered as a tool to overcome hyperacute xenograft rejection. PAIA combined with other therapeutic approaches may well protect the xenograft.
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