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Afonso, Luis Carlos Crocco
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Id: lil-361997
Autor: Souza-Neto, Sebastião Martins de; Carneiro, Cláudia Martins; Vieira, Leda Quercia; Afonso, Luís Carlos Crocco.
Título: Leishmania braziliensis: partial control of experimental infection by interleukin-12 p40 deficient mice
Fonte: Mem. Inst. Oswaldo Cruz;99(3):289-294, May 2004. graf.
Idioma: en.
Resumo: Resistance to infection by Leishmania major has been associated with the development of a Th1 type response that is dependent on the presence of interleukin 12 (IL-12). In this work the involvement of this cytokine in the response to infection by L. braziliensis, a less virulent species in the mouse model, was evaluated. Our results show that while interferon (IFN-gamma) deficient (-/-) mice inoculated L. braziliensis develop severe uncontrolled lesions, chronic lesions that remained under control up to 12 weeks of infection were observed in IL-12p40 -/- mice. IL 12p40 -/- mice had fewer parasites in their lesions than IFN-gamma-/- mice. Lymph node cells from IL-12p40 -/- were capable of producing low but consistent levels of IFN-gamma suggestive of its involvement in parasite control. Furthermore, as opposed to previous reports on L. major-infected animals, no switch to a Th2 response was observed in IL-12p40 -/- infected with L. braziliensis.
Descritores: Interferon gama
Interleucina-12
Leishmania braziliensis
Leishmaniose Cutânea
-Interferon gama
Interleucina-12
Camundongos Endogâmicos C57BL
Fatores de Tempo
Limites: Animais
Masculino
Camundongos
Responsável: BR1.1 - BIREME


  2 / 11 LILACS  
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Costa, R. S
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Id: lil-356626
Autor: Chiossi, M. P. V; Costa, R. S; Roselino, A. M. F.
Título: Dermal dendritic cell number correlates with serum autoantibody titers in Brazilian pemphigus foliaceus patients
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;37(3):337-341, Mar. 2004. graf.
Idioma: en.
Conferência: Apresentado em: American Autoimmune Related Disease Association International Meeting: Pemphigus as a Model of Organ-Specific Humoral Autoimmune Diseases, Bethesda, Apr. 20-21, 2001.
Resumo: Pemphigus foliaceus (PF) is an autoimmune bullous disease endemic in Brazil. Since serum IL-12 is increased in patients with PF and Langerhans cells (LC) produce IL-12, we titrated serum autoantibodies by indirect immunofluorescence, and quantified epidermal dendritic cells, known as LC, and dermal dendritic cells (DC). Biopsies of blistering lesions were obtained from 22 patients, 13 of whom were submitted to biopsy of both injured and of apparently healthy skin. The control groups consisted of skin from 8 cadavers and from 12 women submitted to breast plastic surgery. LC and DC were identified with anti-CD1a antibody and quantified by morphometric analysis. LC number in the lesion and in apparently healthy skin from PF patients was similar to that of both control groups. DC number in the injured skin (median = 0.94 DC/mm basement membrane) was higher than that of the cadaver group (median = 0.13 DC/mm basement membrane). In the 13 patients with biopsies of both injured and apparently healthy skin, LC and DC were present in larger numbers in the lesion. There was a direct correlation between DC number in the lesion of the PF group and serum autoantibody titers. This correlation was not observed for LC number. The increased number of DC in the lesion, as well as its direct correlation with serum autoantibody titers suggest the participation of DC in the pathogenesis of PF. The relationship between increased DC number and IL-12 in PF needs to be clarified.
Descritores: Autoanticorpos
Células Dendríticas
Interleucina-12
Células de Langerhans
Pênfigo
-Biomarcadores
Biópsia
Estudos de Casos e Controles
Contagem de Células
Técnica Indireta de Fluorescência para Anticorpo
Imuno-Histoquímica
Pênfigo
Limites: Humanos
Masculino
Feminino
Responsável: BR1.1 - BIREME


  3 / 11 LILACS  
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Texto completo SciELO Cuba
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Id: lil-322856
Autor: Sánchez de la Rosa, Rainel; Sánchez de la Rosa, Ernesto; Rodríguez Hernández, Néstor.
Título: Interleucina-12 VS. Enfermedades infecciosas / Interleukin 12 vs infectious diseases
Fonte: Rev. cuba. med;40(2):118-121, abr.-jun. 2001.
Idioma: es.
Resumo: Se conoce que uno de los mayores retos de la inmunología en el presente es desarrollar vacunas e inmunoterapias que protejan al paciente contra la infección o que modulen los efectos de la respuesta inmune inducida por los agentes patógenos. Los estudios que definen la función de las diferentes citokinas contribuyen al progreso de estas nuevas estrategias en la manipulación de la respuesta inmune. Estudios recientes demuestran que la interleucina 12 (IL-12) es una clave promotora de la inmunidad celular y de la resistencia inicial a las infecciones, un potente estimulador de la defensa del huésped contra una variedad de patógenos, es una gran promesa su uso terapéutico. Se afirma que, los antagonistas de la IL-12 protegen al huésped de la inmunopatología y la muerte causada por el exceso de la respuesta celular inmune que puede ocurrir durante infecciones microbianas agudas
Descritores: Doenças Transmissíveis
Imunidade Celular
Interleucina-12
Responsável: CU1.1 - Biblioteca Médica Nacional


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Texto completo SciELO Chile
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Id: lil-317353
Autor: Arenillas P., Silvana; Godoy F., Alex; Einisman F., Helly; García P., Daniela; Harris Diez, Paul.
Título: Regulación de la respuesta inmune frente a la infección por helicobacter pylori / Regulation of the immune response against infection caused by helicobacter pylori
Fonte: Rev. chil. pediatr;73(2):108-115, mar.-abr. 2002. ilus.
Idioma: es.
Resumo: Frente a una infección por Helicobacter pylori (H. pylori), el huésped desarrolla una respuesta inmune que es inefectiva en eliminar la bacteria. El sistema inmune innato, juega un rol central procesando y presentando antígenos de H. pylori. La presencia de citoquinas reguladoras (IL-10 o IL-12) podrían modular una respuesta linfocitica (Th) tipo 1 estableciendo una gastritis crónica, o una respuesta Th2 con producción de anticuerpos y la erradicación de la bacteria. IFN-Ý (respuesta Th1) podría mediar la inducción y la expresión de proteínas que pertenecen al complejo de histocompatibilidad tipo II (HLA-II) en células epiteliales, aumentando la adherencia de H. pylori al epitelio gástrico e induciendo apoptosis. IL-4 (respuesta Th2) podría aumentar la expresión del HLA-II, la producción de IgG e IgE, el crecimiento de células T. Finalmente estudios recientes se han focalizado en la inducción de apoptosis celular como un mecanismo de proliferación celular balanceada y como método de defensa del huésped frente a la infección por H. pylori
Descritores: Infecções por Helicobacter
Helicobacter pylori
-Apoptose
Citocinas
Imunidade nas Mucosas
Inflamação/imunologia
Interleucina-10
Interleucina-12
Interleucina-18
Interleucina-4
Limites: Humanos
Tipo de Publ: Revisão
Responsável: CL1.1 - Biblioteca Central


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Id: lil-296179
Autor: Díaz Amor, Patricia.
Título: Citoquinas: la internet biológica ¿futura terapia en el asma bronquial? / Cytokines: the biological internet, the future therapy of bronchial asthma?
Fonte: Rev. chil. enferm. respir;17(1):32-42, ene.-mar. 2001. tab.
Idioma: es.
Projeto: FONDECYT.
Resumo: Las citoquinas son polipéptidos producidos por variadas células nucleadas que actúan como intercomunicadores celulares. Participan en funciones de defensa y reparación del adño del organismo y restablecimiento de la homeostasis. En los últimos años y gracias al desarrollo de la biología molecular, ha sido posible identificar y producir en el laboratorio numerosas citoquinas disponibles en el tratamiento de diversas enfermedades. En el asma bronquial existe un desbalance de algunas citoquinas con predominio de la producción de las interleuquinas (ILs) dependientes de los linfocitos tipo Th-2, como IL-4 e IL-5, las cuales inducen la producción de IgE y la eosinofilia, respectivamente. Actualmente están en marcha estudios clínicos tendientes a bloquear o impedir la acción de la IL-4 e IL-5 mediante anticuerpos monoclonales anti-IL o mediante la acción inhibidora sobre estas citoquinas que ejerce la IL-12. En esta revisión bibliográfica se analiza el estado actual de esta nueva futura terapia del asma
Descritores: Asma/tratamento farmacológico
Citocinas/farmacologia
Imunidade Celular
-Asma/etiologia
Citocinas/biossíntese
Citocinas/imunologia
Homeostase/fisiologia
Interferon gama/farmacologia
Interleucina-12/farmacologia
Interleucina-13/farmacologia
Interleucina-4/imunologia
Interleucina-4/farmacologia
Interleucina-5/farmacologia
Receptores de Interleucina-4/uso terapêutico
Limites: Humanos
Tipo de Publ: Revisão
Responsável: CL1.1 - Biblioteca Central


  6 / 11 LILACS  
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Id: lil-242240
Autor: Cardoni, Rita L; Antunez, Maria Ines; Abrami, Analia A.
Título: Respuesta TH1 en la infeccion experimental con Trypanosoma cruzi / TH1 response in the experimental infection with Trypanosoma cruzi
Fonte: Medicina (B.Aires);59(supl.2):84-90, 1999. ilus, graf.
Idioma: es.
Conferência: Apresentado em: Simposio Internaciona: Problematica de la Enfermedad de Chagas, Buenos Aires, 19-20 abr. 1999.
Resumo: En el huésped infectado con Trypanosoma cruzi, la respuesta inmune protectora involucra principalmente la producción de anticuerpos específicos y la activación de células fagocíticas por interferon-gamma (IFN-gamma). El efecto central del IFN-gamma in vivo sería la activación de la sintetasa inducible de óxido nítrico de macrófagos (iNOS) y la generación de óxido nítrico (NO§) que participa en la destrucción intracelular de los parásitos. En la infección aguda, la inducción de la respuesta TH1 sería llevada a cabo por la interleuquemia 12 (IL-12), que estimula la producción de IFN-gamma en células NK. En la liberación de IFN-gamma también intervienen otros tipos de células, como los linfocitos Thy-1 +CD4-CD4-CD8-, CD4+ y CD8+. El control de la respuesta TH1, podría ser, en parte, el resultado de la menor activación de macrófagos, por la disminución de la carga parasitaria, y de la producción de IL-10 y del factor de trasnformación del crecimiento beta (TGF-beta). La respuesta protectora TH1 también estaría implicada en el daño tisular y en las alteraciones de la respuesta inmune observadas durante la infección. Nosotros estudiamos la cinética de la actividad NK y de la producción de IL-12 e IFN-gamma por células de bazo, así como los niveles séricos de estas citoquinas centrales de la respuesta TH1, en ratones BALB/c y C3H infectados con T. cruzi, cepa Tulahuén. Inmediatamente después de la infección encontramos que, en las células de bazo, incrementó tanto la producción de IL-12 como la actividad NK, y este efecto fue mayor en ratones C3H que en BALB/c. En los C3H, el IFN-gamma aumentó simultáneamente, a diferencia de los BALB/c en los que la citoquina incrementó más tardíamente en la fase aguda. Em ambas cepas, la infección indujo muy rápidamente altos niveles séricos de IL-12 que se mantuvieron elevados durante toda la fase aguda. Por otro lado, el IFN-gamma sérico incrementó unos días antes del pico de parasitemia y alcanzó mayor concentración, y más tempranamente, en los ratones BALB/c que en los C3H. Para nuestra sorpresa, en la fase crónica de la infección, la producción de IL-12 seguía alta en ambas cepas, a pesar de ello, el IFN-gamma sólo continuó elevado en los ratones BALB/c. Aunque en la fase aguda la respuesta global fue predominantemente TH1 en las dos cepas de ratones, los BALB/c tienen una mayor susceptibilidad que los C3H...
Descritores: Doença de Chagas/imunologia
Interferon gama
Interleucina-12
Células Matadoras Naturais/imunologia
Óxido Nítrico/sangue
Células Th1/imunologia
Trypanosoma cruzi/imunologia
Trypanosoma cruzi/patogenicidade
-Doença Crônica
Interferon gama/sangue
Interleucina-12/sangue
Camundongos Endogâmicos BALB C
Baço/citologia
Baço/imunologia
Limites: Animais
Camundongos
Responsável: BR1.1 - BIREME


  7 / 11 LILACS  
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Id: lil-212552
Autor: Netto, M. Barral; Brodskyn, C; Carvalho, E. M; Barral, A.
Título: Human_Leishmaniasis@cytokines.bahia.br
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;31(1):149-55, Jan. 1998. tab, graf.
Idioma: en.
Conferência: Apresentado em: International Meeting on Cytokines, Angra dos Reis, Nov. 24-28 1996.
Projeto: NIH; . CNPq.
Resumo: The cell-mediated immune response is critical in the resistance to and recovery from leishmaniasis. Cytokines are central elements in mounting an immune response and have received a great deal of attention in both human and experimental leishmaniasis. IFN-gamma is responsible for macrophage activation leading to leishmanicidal mechanisms. Understanding the balance of cytokines that lead to enhanced production of or synergize with IFN-gamma, and those cytokines that counterbalance its effects is fundamental for developing rational immunotherapeutic or immunoprophylactic approaches to leishmaniasis. Here we focus on the cytokine balance in human leishmaniasis, particularly IL-10 as an IFN-gamma opposing cytokine, and IL-12 as an IFN-gama inducer. The effects of these cytokines were evaluated in terms of several parameters of the human immune response. IL-10 reduced lymphocyte proliferation, IFN-gamma production and cytotoxic activity of responsive human peripheral blood mononuclear cells. Neutralization of IL-10 led to partial restoration of lymphoproliferation, IFN-gamma production and cytotoxic activity in unresponsive visceral leishmaniasis patients. IL-12 also restored the responses of peripheral blood mononuclear cells from visceral leishmaniasis patients. The responses obtained with IL-12 are higher than those obtained with anti-IL-10, even when anti-IL-10 is combined with anti-IL-4.
Descritores: Citocinas/fisiologia
Leishmaniose/imunologia
Leishmaniose/fisiopatologia
-Brasil
Interleucina-10
Interleucina-12
Limites: Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  8 / 11 LILACS  
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Texto completo
Id: lil-212546
Autor: Abrahamsohn, I. A.
Título: Cytokines in innate and acquired immunity to Trypanosoma cruzi infection
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;31(1):117-21, Jan. 1998.
Idioma: en.
Conferência: Apresentado em: International Meeting on Cytokines, Angra dos Reis, Nov. 24-28 1996.
Resumo: Reistance to Trypanosoma cruzi infections is critically dependent on cytokine-mediated activation of cell-mediated immune effector mechanisms. This review focuses on the role of IL-10, TNF-alpha, IFN-gamma and IL-12 in controlling T. cruzi replication by the innate and specific immune systems of the vertebrate host. A study performed on mice with disrupted recombinase-activating genes (RAG/KO), which lack T and B lymphocytes, revealed the importance of IL-12, IFN-gamma and TNF-alpha in the resistance against T. cruzi mediated by the innate immune system. In addition, data from experiments using IL-10 KO, RAG/KO and double RAG/IL-10 KO mice indicating an in vivo regulatory role of IL-10 in innate and T. cruzi-specific immunity are discussed.
Descritores: Citocinas/fisiologia
Imunidade Inata/fisiologia
Imunidade/fisiologia
Trypanosoma cruzi/patogenicidade
Tripanossomíase/imunologia
Tripanossomíase/fisiopatologia
-Interferon gama
Interleucina-10
Interleucina-12
Camundongos Knockout
Fator de Necrose Tumoral alfa
Limites: Camundongos
Animais
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  9 / 11 LILACS  
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Texto completo
Id: lil-212545
Autor: Silva, J. S; Aliberti, J. C. S; Martins, G. A; Souza, M. A; Souto, J. T; Pádua, M. A.
Título: The role of IL-12 in experimental Trypanosoma cruzi infection
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;31(1):111-5, Jan. 1998.
Idioma: en.
Conferência: Apresentado em: International Meeting on Cytokines, Angra dos Reis, Nov. 24-28 1996.
Resumo: Host resistance to Trypanosoma cruzi infection in dependent on both natural and acquired immune responses. During the early acute phase of infection in mice, natural killer (NK) cell-derived IFN-gamma is involved in controlling intracellular parasite replication, mainly through the induction of nitric oxide biosynthesis by activate macrophages. We have shown that IL-12, a powerful inducer of IFN-gamma production by NK cells, is synthesized soon after trypomastigote-macrophage interaction. The role of IL-12 in the control of T. cruzi infection in vivo was determined by treating infected mice with anti-IL-12 monoclonal antibody (mAb) and analyzing both parasitemia and mortality during the acute phase of infection. The anti-IL-12 mAb-treated mice had higher levels of parasitemia and mortality compared to control mice. Also, treatment of infected mice with mAb spectific for IFN-gamma or TNF-alpha inhibited the protective effect of exogenous IL-12. On the other hand, TGF-beta and IL-10 produced by infected macrophages inhibited the induction and effects of IL-12. Therefore, while IL-12, TNF-alpha and IFN-gamma correlate with resistance to T. cruzi infection, TGF-beta and IL-10 promote susceptibility. These results provide support for a role of innate immunity in the control of T. cruzi infection. In addition to its protective role, IL-12 may also be involved in the modulation of T. cruzi-induced myocarditis, since treatment of infected mice with IL-12 or anti-IL-12 mAb leads to an enhanced or decreased inflammatory infiltrate in the heart, respectively. Understanding the role of the cytokine produced during the acute phase of T. cruzi infection and their involvement in protection and pathogenesis would be essential to devise new vaccines or therapies.
Descritores: Modelos Animais de Doenças
Interleucina-12/fisiologia
Trypanosoma cruzi/patogenicidade
Tripanossomíase/imunologia
Tripanossomíase/fisiopatologia
-Imunidade Inata
Limites: Camundongos
Animais
Responsável: BR1.1 - BIREME


  10 / 11 LILACS  
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Texto completo
Id: lil-202020
Autor: Wynn, Thomas A.
Título: The debate over the effector function of eosinophils in helminth infection: new evidence from studies on the regulation of vaccine immunity by IL-12
Fonte: Mem. Inst. Oswaldo Cruz;92(supl.2):105-8, Dec. 1997.
Idioma: en.
Conferência: Apresentado em: New perspectives in eosinophils, Rio de Janeiro, 1996.
Resumo: The production of Th1-type cytokines is associated with strong cell-mediated immunity while Th2-type cytokines are typically involved in the generation of humoral immune responses. In mice vaccinated a single time (1x) with attenuated cercariae of Schistosoma mansoni, the immunity induced is highly dependent on CD4+ T cells and IFN-gamma. In contrast, mice vaccinated multiple times (3x) have decreased IFN-gamma expression, develop a more dominant Th2-type cytokine response as well as protective antibodies which can passively transfer immunity to naive recipients. Previously, we demonstrated the ability of IL-12, a potent IFN-gamma-inducing cytokine to enhance (1x) schistosome cell-mediated immunity when administered during the period of immunization. More recently, we asked what effects IL-12 would have on the development humoral-based immunity. While multiply-immunized/saline-treated mice demonstrated a 70-80 per cent reduction in parasite burden, 3x/IL-12-vaccinated animals displayed an even more striking >90 per cent reduction in challenge infection, which many mice in the later group demonstrating complete protection. Analysis of pulmonary cytokine mRNA responses demonstrated that control challenged mice elicited a dominant Th2-type response, 3x/saline-vaccinated produced a mixed Th1/Th2-type cytokine response, while 3x/saline-vaccinated produced a mixed Th1/Th2-type cytokine response, while 3x/IL-12 immunized animals displayed a dominant Th1-type response. The IL-12-treated group also showed a marked reduction in total serum IgE and tissue eosinophilia while SWAP-specific IgG2a and IgG2b Abs elevated. Interestingly, animals vaccinated with IL-12 also showed a highly significant increase in total Ig titers specific for IrV-5, a known protective antigen. More importantly, 3x/IL-12 serum alone, when transferred to naive mice reduced worm burdens by over 60 per cent while 3x/saline serum transferred significantly less protection. Nevertheless, animals vaccinated in the presence of IL-12 also develop macrophages with enhanced nitric oxide dependent killing activity against the parasites. Together, these observations suggest that IL-12, initially described as an adjuvant for cell-mediated immunity, may also be used as an adjuvant for promoting both humoral and cell-mediated protective responses.
Descritores: Eosinófilos/fisiologia
Helmintíase
Interleucina-12/imunologia
Schistosoma mansoni/imunologia
Vacinas
-Formação de Anticorpos
Células Th1/parasitologia
/parasitologia
CELULAS THTEMEFOS/parasitologia
Citocinas
Limites: Animais
Camundongos
Responsável: BR15.1 - Biblioteca de Ciências Biomédicas



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