Phagocytosis of enteropathogenic Escherichia coli and Candida albicans by lectin-like receptors

1. Ingestion of enteropathogenic Escherichia coli or Candida albicans by thioglycollate-elicited macrophages and polymorphonuclear leukocytes was investigated in vitro, 2. Goat antiserum against mannose receptors caused about 50% inhibition of E. coli phagocytosis and about 90% inhibition of C. albicans phagocytosis. 3. E. coli and C. albicans uptake was inhibited by about 60% and 98%, respectively, by plating the macrophages onto substrates coated with poly-L-lysine-mannan. Further addition of 50 mM mannose to the medium significantly increased the inhibition of phagocytosis of E. coli by macrophages from 60.7 +/- 1.5 to 79.8 +/- 13.1 and by polymorphonuclear cells from 58.9 +/- 3.7 to 88.7 +/- 4.9. 4. Preincubation of phagocytic cells with antiserum against substance A of human erythrocytes reduced E. coli ingestion by 95%, but this inhibition was not observed when the antiserum was incubated with N-acetylgalactosamine (50 mM) before being added to the phagocytes. The phagocytosis of C. albicans was not inhibited by anti-substance A antiserum. 5. The phagocytosis of E. coli was inhibited by about 25% by the addition of 7.8 micrograms/ml soluble mannan to the medium, and by about 50% by the addition of 50 mMN-acetylgalactosamine; when both substances were added to the medium, an additive inhibition of about 75% was observed. 6. These results indicate that mannose receptors on the surface of phagocytic cells mediate E. coli or Candida albicans uptake and that the binding of bacteria to N-acetylgalactosamine residues from the membrane of phagocytes is also involved in the phagocytosis of E. coli

Receptor de interleucina-2 (primera parte) / Receptor of interleukin-1 (first part)

Como todo factor de crecimiento, la interleucina-2 (IL-2) necesita unirse a un receptor específico, el IL-2 (IL-2R), para mediar su actividad. Este receptor se diferencia de los estudiados en endocrinología en que un factor no específico (IL-2) promueve una expansión clonal antígeno específica, sin inducir los IL-2R hasta que el receptor de antígeno es activado. El sistema se complica al descubrise dos tipos de receptores para el IL-2, los de alta y baja afinidad. La explicación molecular, genética e importancia biológica del IL-2R se describe en el presente artículo, así como la trascendencia del empleo de las técnicas de anticuerpos monoclonales y de recombinación genética en la caracterización del IL-2R. Y teniendo como base dicha caracterización explicar algunos de los mecanismos que se proponen para la transducción de la señal y que culminan con la inducción de nuevos receptores para IL-2 y una proliferación celular