Discriminación por Ganaspis pelleranoi (Hymenoptera: Figitidae) de larvas de Anastrepha fraterculus (Diptera: Tephritidae) previamente parasitoidizadas

La competencia inter e intraespecífica entre parasitoides en un programa de biocontrol puede mejorar o dificultar el impacto en la población de la plaga objetivo. Por lo tanto, la separación de nichos en parasitoides asociados a un mismo hospedero puede lograrse mediante el uso de especies competentes para la discriminación de hospederos. Se determinó la discriminación inter e intraespecífica, el súper y multiparasitoidismo por parte del figítido neotropical Ganaspis pelleranoi utilizando larvas de Anastrepha fraterculus de 9-10 días de edad en ensayos de elección, donde los tratamientos fueron combinaciones de: (1) larvas previamente parasitoidizadas por el exótico bracónido Diachasmimorpha longicaudata, (2) larvas previamente parasitoidizadas por el conespecífico G .pelleranoi y (3) larvas no parasitoidizadas. Los ensayos de elección involucraron hembras figitidas con y sin experiencia previa en oviposición. Cuando la hembra de G. pelleranoi podía elegir entre larvas no parasitoidizadas y parasitoidizadas no se produjo multiparasitoidismo. La discriminación del hospedero heteroespecífico mejoró con la experiencia de oviposición. Un número limitado de hembras experimentadas de G. pelleranoi ovipusieron, probaron o visitaron larvas hospedadoras previamente parasitoidizadas por D. longicaudata. Solo el 2% de los adultos de figítidos se recuperaron de las pupas resultantes de larvas previamente parasitoidizadas por D. longicaudata y expuestas a hembras, sin experiencia del figitido. No se recuperaron adultos figítidos en aquellos tratamientos que involucraron hembras experimentadas. Los datos de latencia y examen del hospedero, número de visitas, sondeo y oviposición mostraron que la hembra G. pelleranoi experimentada tiene una mayor propensión a elegir de larvas hospedero no parasitoidizadas en lugar de larvas previamente parasitoidizadas por hembras conespecíficas. El superparasitoidismo propio fue mayor que el superparasitoidismo conespecífico cuando las hembras figitidas tuvieron que elegir entre larvas no parasitoidizadas y parasitoidizadas por conespecíficos. La capacidad de las hembras de G. pelleranoi para discriminar larvas de A. fraterculus previamente parasitoidizadas sugiere niveles bajos de competencia heteroespecífica y conespecífica. Las liberaciones combinadas de D. longicaudata y G. pelleranoi en las regiones frutícolas argentinas podrían ser una alternativa más ventajosa que las liberaciones de especies individuales.Fil: Buonocore Biancheri, María Josefina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Planta Piloto de Procesos Industriales Microbiológicos; ArgentinaFil: Paz, José Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Planta Piloto de Procesos Industriales Microbiológicos; ArgentinaFil: Tomei, Carlos Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Planta Piloto de Procesos Industriales Microbiológicos; ArgentinaFil: Ibañez, Sofia Y.. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Planta Piloto de Procesos Industriales Microbiológicos; ArgentinaFil: Ponssa, Marcos Darío. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Planta Piloto de Procesos Industriales Microbiológicos; ArgentinaXI Congreso Argentino de Entomología; XII Congreso Latinoamericano de EntomologíaLa PlataArgentinaUniversidad Nacional de la PlataSociedad Entomológica Argentin

Oncostatin M drives intestinal inflammation and predicts response to tumor necrosis factor–neutralizing therapy in patients with inflammatory bowel disease

Inflammatory bowel diseases (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), are complex chronic inflammatory conditions of the gastrointestinal tract that are driven by perturbed cytokine pathways. Anti-tumor necrosis factor-α (TNF) antibodies are mainstay therapies for IBD. However, up to 40% of patients are nonresponsive to anti-TNF agents, which makes the identification of alternative therapeutic targets a priority. Here we show that, relative to healthy controls, inflamed intestinal tissues from patients with IBD express high amounts of the cytokine oncostatin M (OSM) and its receptor (OSMR), which correlate closely with histopathological disease severity. The OSMR is expressed in nonhematopoietic, nonepithelial intestinal stromal cells, which respond to OSM by producing various proinflammatory molecules, including interleukin (IL)-6, the leukocyte adhesion factor ICAM1, and chemokines that attract neutrophils, monocytes, and T cells. In an animal model of anti-TNF-resistant intestinal inflammation, genetic deletion or pharmacological blockade of OSM significantly attenuates colitis. Furthermore, according to an analysis of more than 200 patients with IBD, including two cohorts from phase 3 clinical trials of infliximab and golimumab, high pretreatment expression of OSM is strongly associated with failure of anti-TNF therapy. OSM is thus a potential biomarker and therapeutic target for IBD, and has particular relevance for anti-TNF-resistant patients

Influence de l'injection de cellules dendritiques immatures ou génétiquement modifiées sur le rejet d'allogreffe ;[Thèse annexe :L'IDO, une nouvelle molécule immunosuppressive]

Doctorat en sciences médicalesinfo:eu-repo/semantics/nonPublishe

Influence de l'injection de cellules dendritiques immatures ou génétiquement modifiées sur le rejet d'allogreffe ;[Thèse annexe :L'IDO, une nouvelle molécule immunosuppressive]

Doctorat en sciences médicalesinfo:eu-repo/semantics/nonPublishe

Unexpected effects of viral interleukin-10-secreting dendritic cells in vivo: preferential inhibition of TH2 responses.

Viral interleukin (IL)-10 (vIL-10) has been widely described as an immunoregulatory cytokine that does not possess the T-cell costimulatory activities of cellular IL-10; it was therefore believed to be a more potent tolerogenic mediator. The immunosuppressive properties of this cytokine are partly attributed to its capacity to render dendritic cells (DCs) unable to undergo full maturation and to activate T cells. We reported here that myeloid DCs retrovirally transduced with vIL-10 had an impaired production of IL-12 and a decreased expression of MHC class II molecules but had minor defects in costimulatory molecule expression and no alteration on CCR5 and CCR7 expression. In mixed leukocyte reaction, vIL-10-transduced C57BL/6 bm12 (MHC class II mismatch) DCs had a reduced capacity to stimulate C57BL/6 wild-type CD4+ T-cell proliferation. We show that bm12 vIL-10-transduced DC administration in CD8-/- C57BL/6 mice promoted IFN-gamma production, down-regulated TH2-type cytokine production, and did not induce skin graft tolerance. These findings suggest that vIL-10-transduced DC may surprisingly facilitate Th1-type inflammatory responses in vivo.Journal ArticleResearch Support, Non-U.S. Gov'tinfo:eu-repo/semantics/publishe

Unexpected effects of viral interleukin-10-transduced allogenic dendritic cells in vivo: preferential inhibition of Th2 responses

info:eu-repo/semantics/publishe

The role of neutrophils during allograft rejection

info:eu-repo/semantics/publishe

Le rôle des neutrophiles dans le rejet d'allogreffe.

Because rejection of allografts is primarily caused by T and B lymphocyte responses to allogeneic histocompatibility molecules, the role of innate immunity in organ transplant rejection is often overlooked. However, the very first damages to vascularized organ allografts are caused by ischemia-reperfusion, an inflammatory reaction involving activation of vascular endothelial cells and release of neutrophil chemoattractants. Herein, we review experimental observations suggesting that the early neutrophil influx in organ transplants favors T cell-mediated rejection.English AbstractJournal ArticleReviewinfo:eu-repo/semantics/publishe

Amplification of T-cell responses by neutrophils: relevance to allograft immunitys

Because rejection of allografts is primarily caused by T and B lymphocyte responses to allogenic histocompatibility molecules, the role of innate immunity in organ transplant rejection is often overlooked. However, the very first damages to vascularized organ allografts are caused by ischemia-reperfusion, an inflammatory reaction involving activation of vascular endothelial cells and release of neutrophil chemoattractants. Herein, we review experimental observations suggesting that the early neutrophil influx in organ transplants favors T cell-mediated rejection.Journal ArticleResearch Support, Non-U.S. Gov'tReviewinfo:eu-repo/semantics/publishe

Dendritic cells transduced with viral interleukin 10 or Fas ligand: no evidence for induction of allotolerance in vivo.

Dendritic cells (DC) are the most potent presenters of alloantigens and therefore are responsible for the induction of allograft rejection. Genetic modifications of DC allowing the expression of a tolerogenic molecule may render them immunosuppressive. We transduced bone marrow-derived DC with recombinant MFG retrovirus encoding either viral interleukin (vIL)-10 or Fas ligand (FasL) to induce transplantation tolerance. Up to 10 ng/ml of bioactive vIL-10 was produced by DC after transfer of the corresponding gene. Although the inhibitory properties of vIL-10-transduced DC were revealed in vitro in a mixed lymphocyte culture, no clear down-regulation of the allogeneic response was observed in vivo after single or multiple injections of those DC overexpressing vIL-10. When we transduced wild-type bone marrow-derived DC with recombinant MFG retrovirus encoding murine FasL, cells quickly died, probably because of suicidal or fratricidal Fas-dependent death. Indeed, only DC from Fas-deficient lpr mice survived to FasL gene transfer. Those FasL-transduced lpr DC exhibited a strong cytotoxic activity against Fas-positive targets in vitro. DC overexpressing FasL did not behave as immunosuppressive DC in vivo. The subcutaneous injection of FasL+ lpr DC in MHC class II-disparate mice hyperactivated the allospecific proliferation of T cells in the draining lymph nodes compared with mice treated with control-transduced DC. These results argue against the development of FasL+ DC or vIL-10-secreting DC as immunosuppressive tools in vivo. The alternative pathways of T-cell activation triggered by these genetically modified DC need to be investigated.Journal ArticleReviewinfo:eu-repo/semantics/publishe