La cultura homérica en la Escenografía del Seiscientos: "Il Greco in Troia" y "La caduta del regno dell´Amazzoni"

Sería imposible hacer una enumeración de festejos, espectáculos y representaciones teatrales, que a lo largo de la época moderna, tuvieron como argumento las historias narradas por la literatura homérica. Incontables, pero todas ellas buscaban el don de la elocuencia que tenían desde que en la Antigüedad empezaron a reeditarse. Apenas un iglo después de la recopilación de relatos orales que quedaron hilvanados bajo los títulos de la Iliada y la Odisea –si se acepta la autoría de ese personaje mítico que fue Homero en torno al siglo VIII antes de Cristo–, tiranos y oligarcas atisbaron de forma visionaria las posibilidades que aportaban las tramas en las que se vieron envueltos dioses y héroes. La mitología olímpica no sólo sirvió al propósito de la unificación panhelénica de la nación de naciones que era Grecia, en torno a un mundo de creencias común en el marco de los grandes santuario, sino que además, las vicisitudes de los principales personajes, como Paris, Aquiles, Héctor, Ulises, Pentesilea, Eneas, Agamenón, Andrómaca, Casandra y Helena, proporcionaron un repertorio de modelos de conducta y un protocolo ceremonial en sociedad extremadamente útil. Piedad, fidelidad, excelencia, belleza, sumisión, virtudes morales que habían de “adornar” por igual a gobernantes y a ciudadanos, garantizaban un nuevo orden en la Hélade, constituyendo asimismo las notas distintivas con respecto a los anquilosados y monolíticos Imperios hegemónicos en la zona de Oriente Próximo, Egipcio y Babilónico o Persa, respectivamente. Se propone el análisis de la incidencia iconológica de tales asuntos a partir de la revisión escenográfica de dos libretos para dos representaciones teatrales italianas de finales del Seicento, de los que se encuentran sendos ejemplares en la Biblioteca Nacional de Madrid: Il Greco in Troia y La caduta del regno dell´amazzone.

CCL11 blocks IL-4 and GM-CSF signaling in hematopoietic cells and hinders dendritic cell differentiation via suppressor of cytokine signaling expression

The chemokine eotaxin/CCL11 is an important mediator of leukocyte migration, but its effect on inflammatory cytokine signaling has not been explored. In this study, we find that CCL11 induces suppressor of cytokine signaling (SOCS) 1 and SOCS3 expression in murine macrophages, human monocytes, and dendritic cells (DCs). We also discover that CCL11 inhibits GM-CSF-mediated STAT5 activation and IL-4-induced STAT6 activation in a range of hematopoietic cells. This blockade of cytokine signaling by CCL11 results in reduced differentiation and endocytic ability of DCs, implicating CCL11-induced SOCS as mediators of chemotactic inflammatory control. These findings demonstrate cross-talk between chemokine and cytokine responses, suggesting that myeloid cells tracking to the inflammatory site do not differentiate in the presence of this chemokine, revealing another role for SOCS in inflammatory regulation. J. Leukoc. Biol. 85: 289-297; 2009.

Adult neural stem cells expressing IL-10 confer potent immunomodulation and remyelination in experimental autoimmune encephalitis

Adult neural stem cells (aNSCs) derived from the subventricular zone of the brain show therapeutic effects in EAE, an animal model of the chronic inflammatory neurodegenerative disease MS; however, the beneficial effects are modest. One critical weakness of aNSC therapy may be an insufficient antiinflammatory effect. Here, we demonstrate that i.v. or i.c.v. injection of aNSCs engineered to secrete IL-10 (IL-10–aNSCs), a potent immunoregulatory cytokine, induced more profound functional and pathological recovery from ongoing EAE than that with control aNSCs. IL-10–aNSCs exhibited enhanced antiinflammatory effects in the periphery and inflammatory foci in the CNS compared with control aNSCs, more effectively reducing myelin damage, a hallmark of MS. When compared with mice treated with control aNSCs, those treated with IL-10–aNSCs demonstrated differentiation of transplanted cells into greater numbers of oligodendrocytes and neurons but fewer astrocytes, thus enhancing exogenous remyelination and neuron/axonal growth. Finally, IL-10–aNSCs converted a hostile environment to one supportive of neurons/oligodendrocytes, thereby promoting endogenous remyelination. Thus, aNSCs engineered to express IL-10 show enhanced ability to induce immune suppression, remyelination, and neuronal repair and may represent a novel approach that can substantially improve the efficacy of neural stem cell–based therapy in EAE/MS.

IL-12R2 promotes the development of CD4+CD25+ regulatory T cells

We have previously shown that mice lacking the IL-12-specific receptor subunit ß2 (IL-12Rß2) develop more severe experimental autoimmune encephalomyelitis than wild-type (WT) mice. The mechanism underlying this phenomenon is not known; nor is it known whether deficiency of IL-12Rß2 impacts other autoimmune disorders similarly. In the present study we demonstrate that IL-12Rß2-/- mice develop earlier onset and more severe disease in the streptozotocin-induced model of diabetes, indicating predisposition of IL-12Rß2-deficient mice to autoimmune diseases. T cells from IL-12Rß2-/- mice exhibited significantly higher proliferative responses upon TCR stimulation. The numbers of naturally occurring CD25+CD4+ regulatory T cells (Tregs) in the thymus and spleen of IL-12Rß2-/- mice were comparable to those of WT mice. However, IL-12Rß2-/- mice exhibited a significantly reduced capacity to develop Tregs upon stimulation with TGF-ß, as shown by significantly lower numbers of CD25+CD4+ T cells that expressed Foxp3. Functionally, CD25+CD4+ Tregs derived from IL-12Rß2-/- mice were less efficient than those from WT mice in suppressing effector T cells. The role of IL-12Rß2 in the induction of Tregs was confirmed using small interfering RNA. These findings suggest that signaling via IL-12Rß2 regulates both the number and functional maturity of Treg cells, which indicates a novel mechanism underlying the regulation of autoimmune diseases by the IL-12 pathway. Copyright © 2008 by The American Association of Immunologists, Inc.