Regulatory and effector T-cells are differentially modulated by Dexamethasone.

It is assumed that the ratio between effector T cells (Teff) and regulatory T cells (Tregs) controls the immune reactivity within the T-cell compartment. The purpose of this study was to investigate if Dexamethasone (Dex) affects Teff and Tregs subsets. Dex induced on Tregs a dose and time-dependent apoptosis which resulted in a relative increase of Teff. After TCR activation, Dex induced a strong proliferative inhibition of Teff, but a weaker proliferative inhibition on Tregs. These effects were modulated by IL-2, which not only restored the proliferative response, but also prevented Dex-induced apoptosis. The highest dose of IL-2 prevented apoptosis on all FOXP3+CD4+ T cells. Meanwhile, the lowest dose only rescued activated Tregs (aTregs), probably related to their CD25 higher expression. Because Dex did not affect the suppressor capacity of aTregs either, our results support the notion that under Dex treatment, the regulatory T-cell compartment maintains its homeostasis.

Participación de la prolactina en la respuesta inmune / Role of prolactin in the immune response

Existen evidencias de la relación entre el sistema inmune y el endocrino vía múltiples factores de comunicación, como citocinas, neuropéptidos, neurotransmisores y hormonas. Se ha demostrado la participación de la hormona prolactina en la respuesta inmune innata y adaptativa. Además de ser producida por la glándula pituitaria, también es producida y secretada por las células del sistema inmunológico. El objetivo de esta revisión fue puntualizar acerca de la participación de la prolactina secretada por estas células en la respuesta inmune.

Evidence exists about the relationship between the immune and the endocrine systems through communication of multiple factors such as cytokines, neuropeptides, neurotransmitters and hormones. Among the hormones, prolactin (PRL) has been shown to participate in the innate and adaptive immune response. In addition to being produced by the pituitary gland, PRL is also produced and secreted by cells of the immune system. The aim of this review is to update information about the involvement of PRL secreted by immune system cells in the immune response.

Interleukin (IL)-35 is raising our expectations / Las expectativas futuras de la interleukina (IL)-35

Purpose: To elucidate and discuss the role of IL-35 in immunity to parasitic and bacterial infections as well as in autoimmunity in terms of its anti-infammatory properties, we highlight significant findings on this novel member of the IL-12 family. Methods: Studies using genetically defcient mice have greatly enhanced our understanding of the biology of IL-35. On the basis of data derived from the analysis of these genetically deficient mice published by NIH, we focus on the key features of this heterodimeric cytokine, especially its relation to the other IL-12 family members, and discuss its potential relevance to the clinical usage. Principal fndings: IL-35 is required for the CD4+CD25+ Treg cells-mediated immune regulation, the alleviation of some inflammatory responses, as well as the expansion of CD4+CD25- Teff cells simultaneously. Moreover, administration or augmentation of IL-35 suppresses some diseases of autoimmune or allergic origin like collagen-induced arthritis or Helicobacter- induced colitis in animal models, demonstrating its potential in therapy of diseases mediated by inflammatory cytokines. However, some questions involving it are still unclear, including the composition of IL-35 receptor, IL-35-related cell signaling pathway, the different expression patterns of IL-35 between human and murine T cells, etc. Conclusion: As our understanding of the IL-35 is rapidly growing and changing, it will bring us more therapeutic strategies towards some intractable immune diseases such as Lupus Erythematosus.

Esta es una revisión acerca del rol de IL-35, un nuevo miembro de la familia IL-12, en la respuesta inmunitaria contra infecciones parasitarias y bacterianas y de su rol benefcioso en reacciones auto inmunes, debido sus propiedades antiinfamatorias. Basándose en estudios de ratones genéticamente defcientes se ha determinado que se requiere IL-35 para la acción inmunoreguladora de las células T reguladoras CD4+CD25+, para mitigar algunos procesos inflamatorios y para expandir simultáneamente los clones de células T efectoras CD4+CD25-. Mas aún, la administración o estimulación de la acción de IL-35 en modelos animales, suprime algunas enfermedades de origen alérgico o autoinmune tales como la colitis colágena y la colitis inducida por Helicobacter. Estos experimentos demuestran el potencial terapéutico de IL-35 en enfermedades mediadas por citokinas inflamatorias. Sin embargo, algunos aspectos de la citokina aún no han sido dilucidados, tales como la composición del receptor de IL-35, la vía de señalización celular asociada a IL-35 y los diversos patrones de expresión de la citokina en células humanas y de ratones. En la medida que aumente el conocimiento acerca de las acciones de IL-35, nos podrá proveer tratamientos para algunas enfermedades auto inmunes actualmente limitadas en su tratamiento, como el lupus eritematoso.