Реферат
Dentro de la respuesta inmune humoral se encuentran componentes que mantienen la homeostasis de los organismos a través del control de agentes patógenos por medio de la opsonización, quimiotaxis de células fagocíticas facilitando el proceso de eliminación de lo extraño o sin su acompañamiento, en el caso de la formación de poros en la membrana celular. A un grupo de este conjunto de componentes de origen molecular proteico se denominósistema del complemento, el cual posee tres vías de activación (Clásica, Alternativa y Lectinas), funciona comoanafilatoxinas, reguladores y receptores. La presente revisión tiene como objetivo discutir acerca de los diferentes componentes del sistema del complemento en la escala animal enfocándose principalmente en peces teleósteos y mamíferos, como organismos modelos en busca de elucidar sus diferencias, homologías y respuestas.
Within the humoral immune response can be found components that maintain an organisms homeostasis viacontrol of pathogenic agents using opsonization, chemotaxis of phagocytic cells which facilitates the processof elimination of foreign bodies, or in its absence, the formation of pores in the cellular membrane. One of these groups of components, of protein origin, is referred to as the complement system, which has 3 means of activation (Classic, Alternative, and Lectins) and functions as anaphylactic toxins, regulators and receptors. The aim of this review is to discuss the different components of the complement system in the animal kingdom, focusing principally on teleost fish and mammals, as model organisms in the search to elucidate their differences, homologies, and answers.
Dentro da resposta imune humoral encontram-se componentes que mantém a homeostase do organismo através docontrole de patógenos, por opsonização, quimiotaxia de células fagocíticas que facilita o processo de eliminaçãode corpos estranhos, ou na sua ausência, a formação de poros na membrana celular. Este conjunto de componentes moleculares de origem protéica são chamados de sistema complemento, que tem três vias de ativação (clássica, alternativa e lectinas), funciona como anafilatoxinas, reguladores e receptores. Esta revisão tem como objetivo discutir os vários componentes do sistema complemento na escala animal focando principalmente em peixes teleósteos e mamíferos como organismos modelos na busca de elucidar suas diferenças, homologias e respostas.
Тема - темы
Animals , Complement Activation/immunology , Fishes/immunology , Complement System Proteins/immunology , Complement Pathway, Alternative/immunology , Complement Pathway, Classical/immunology , Host-Pathogen Interactions/immunology , Serum/immunologyРеферат
In previous work, we proposed alternative protocols for following patients with treated Chagas disease and these are reviewed herein. Evidence was provided to support the following: (i) functional anti-trypomastigote antibodies are indicative of ongoing chronic Trypanosoma cruzi infections; (ii) specific antibodies detected by conventional serology (CS) with epimastigote extracts, fixed trypomastigotes or other parasite antigens may circulate years after parasite elimination; (iii) functional antibodies are evidenced by complement-mediated lysis of freshly isolated trypomastigotes, a test which is 100 percent specific, highly sensitive, and the first to revert after T. cruzi elimination and (iv) the parasite target for the lytic antibodies is a glycoprotein of high molecular weight (gp160) anchored at the parasite surface. The complement regulatory protein has been cloned, sequenced and produced as a recombinant protein by other groups and is useful for identifying functional anti-T. cruzi antibodies in ELISA tests, thus dispensing with the need for live trypomastigotes to manage treated patients. If used instead of CS to define cures for Chagas patients, ELISA will avoid unnecessary delays in finding anti-T. cruzi drugs. Other highly sensitive techniques for parasite DNA detection, such as PCR, need to be standardized and included in future protocols for the management of patients with drug-treated Chagas disease.
Тема - темы
Humans , Antibodies, Protozoan/immunology , Chagas Disease/immunology , Complement Activation/immunology , Trypanosoma cruzi/immunology , Acute Disease , Antibodies, Protozoan/blood , Chronic Disease , Chagas Disease/diagnosis , Chagas Disease/drug therapy , Enzyme-Linked Immunosorbent Assay , Trypanocidal Agents/therapeutic useРеферат
Since there are no studies evaluating the participation of the complement system (CS) in Jorge Lobo's disease and its activity on the fungus Lacazia loboi, we carried out the present investigation. Fungal cells with a viability index of 48 percent were obtained from the footpads of BALB/c mice and incubated with a pool of inactivated serum from patients with the mycosis or with sterile saline for 30 min at 37 °C. Next, the tubes were incubated for 2 h with a pool of noninactivated AB+ serum, inactivated serum, serum diluted in EGTA-MgCl2, and serum diluted in EDTA. The viability of L. loboi was evaluated and the fungal suspension was cytocentrifuged. The slides were submitted to immunofluorescence staining using human anti-C3 antibody. The results revealed that 98 percent of the fungi activated the CS by the alternative pathway and no significant difference in L. loboi viability was observed after CS activation. In parallel, frozen histological sections from 11 patients were analyzed regarding the presence of C3 and IgG by immunofluorescence staining. C3 and IgG deposits were observed in the fungal wall of 100 percent and 91 percent of the lesions evaluated, respectively. The results suggest that the CS and immunoglobulins may contribute to the defense mechanisms of the host against L. loboi.
Considerando que não existe nenhum estudo avaliando a participação do sistema complemento (SC) na doença de Jorge Lobo e sua atividade sobre o fungo Lacazia loboi, realizamos o presente trabalho. Os fungos foram obtidos dos coxins plantares de camundongos BALB/c com índice de viabilidade de 48 por cento e, em seguida, foram incubados com pool de soro inativado de pacientes ou com solução salina estéril (SSE) por 30 min, a 37 °C. Os tubos foram incubados, por 2 h, com pool de soro AB+ sem inativar, inativado, diluído em EGTA-MgCl2 e EDTA. A viabilidade do L. loboi foi avaliada e a suspensão fúngica foi citocentrifugada. As lâminas foram submetidas à técnica de imunofluorescência empregando o anticorpo anti-C3 humano. Os resultados revelaram que 98 por cento dos fungos ativaram o SC pela via alternativa e que não houve diferença significante na viabilidade do L. loboi após ativação do SC. Em paralelo, cortes histológicos congelados de 11 pacientes foram avaliados quanto à presença de C3 e IgG, pela técnica de imunofluorescência. Foram encontrados depósitos de C3 e de IgG na parede dos fungos em 100 por cento e 91 por cento das lesões avaliadas, respectivamente. Os resultados sugerem que o SC e as imunoglobulinas poderiam contribuir nos mecanismos de defesa do hospedeiro contra o L. loboi.
Тема - темы
Humans , Animals , Mice , Complement Activation/physiology , Complement System Proteins/physiology , Immunoglobulins/immunology , Paracoccidioides/physiology , Complement Activation/immunology , /immunology , /physiology , Complement System Proteins/immunology , Fluorescent Antibody Technique , Mice, Inbred BALB C , Paracoccidioides/immunologyРеферат
El Síndrome antifosfolípido (SAF) es una trombofilia adquirida, que se caracteriza por presentar eventos trombóticos recurrentes y complicaciones obstétricas en presencia de anticuerpos antifosfolípidos (aFL), los cuales son pesquisados por pruebas de laboratorio como anticoagulante lúpico y anticuerpos anticardiolipina. En esta revisión se muestran los aspectos más relevantes del SAF, destacando los avances en fisiopatología y criterios diagnósticos.
Тема - темы
Humans , Antiphospholipid Syndrome/diagnosis , Antiphospholipid Syndrome/physiopathology , Antiphospholipid Syndrome/immunology , Thrombosis/immunology , Complement Activation/immunology , Antibodies, Anticardiolipin/blood , Antibodies, Antiphospholipid/immunology , Pregnancy Complications/immunology , Endothelial Cells/immunology , Lupus Coagulation Inhibitor/blood , Antiphospholipid Syndrome/complications , Thrombosis/therapyРеферат
La inflamación es fundamental para que la respuesta inmune, tanto innata como adaptativa, pueda ser eficaz. La respuesta inflamatoria se origina cuando un agente nocivo de origen químico, físico o infeccioso compromete algún tejido vascularizado, desencadenando cambios vasculares y tisulares inducidos por moléculas provenientes de las células del sistema inmune (citoquinas) o de otros sistemas como la coagulación, las quininas y el complemento. El sistema del complemento se encarga de eliminar de un número importante de microorganismos patógenos, establecer una relación entre las respuestas innata y adaptativa y favorecer la eliminación de complejos inmunes y los productos del daño tisular. Una vez los anticuerpos se han unido al antígeno pueden inducir la activación del sistema del complemento, lo que conduce a una mayor respuesta inflamatoria
Тема - темы
Complement Activation/immunology , Antibodies , Inflammation/diagnosis , Inflammation/immunologyРеферат
We studied the relationship between the degree of complement activation in juvenile rheumatoid arthritis (JRA) with the levels of circulating IgM and IgA rheumatoid factors (RF). Forty children with JRA and 25 matched controls were included in the study. Levels of C3d (a degradation product of complement component C3), circulating immune complexes (CICs), IgM RF and IgA RF were measured by ELISA. Levels of C3d, CICs, IgM RF and IgA RF were elevated in patients with JRA as compared to controls. Levels of C3d had a linear relationship with levels of CICs (P < 0.05) but not with levels of circulating IgM RF and IgA RF. Thus, complement activation occurs in children with JRA and is associated with raised levels of CICs but not with levels of circulating IgM and IgA RF. Circulating IgM and IgA RF have little, if any, role in complement activation observed in patients with JRA.
Тема - темы
Adolescent , Adult , Antigen-Antibody Complex/blood , Arthritis, Juvenile/blood , Child , Child, Preschool , Complement Activation/immunology , Enzyme-Linked Immunosorbent Assay , Female , Humans , Immunoglobulin A/blood , Immunoglobulin M/blood , Male , Rheumatoid Factor/bloodТема - темы
Humans , Bacterial Infections/immunology , Antibody Formation/immunology , Parasitic Diseases/immunology , Virus Diseases/immunology , Complement Activation/immunology , Killer Cells, Natural/immunology , Cytokines/biosynthesis , Immunocompromised Host/immunology , Immunity, Cellular/immunology , Immunity, Innate/immunology , Interferon Type I/biosynthesis , Phagocytosis/immunology , Host-Parasite Interactions/immunologyРеферат
A un siglo de su descubrimiento por Bordet, se trata de poner un poco de orden en los mecanismos de activación del complemento a través de su hasta ahora conocidas rutas de activación clásica o de C1 y la vía alterna o de la properdina. Se hace además referencia a otras vías de activación descritas más recientemente como la activación iniciada por la lectina de unión a la manosa (MBL). Se destaca también la actividad de los componentes inhibidores o controladores, que frenan la actividad del sistema, evitando la producción de daños por la formación y liberación de péptidos con potente acción biológica derivados del mismo, tal el caso de las anafilatoxinas. Se hace además referencia a la presencia de receptores para el complemento, ubicados en la membrana de diversas células del sistema inmunológico, responsables de muchas de las principales actividades del sistema, como la fagocitosis de microorganismos a través de la unión de receptores para C3b (principal opsonina) sobre la membrana de las células fagocitarias
Тема - темы
Humans , Complement System Proteins/physiology , Self-Evaluation Programs , Complement Activation/immunology , Complement Inactivating Agents/immunology , Complement Membrane Attack Complex/immunology , Complement System Proteins/immunology , Receptors, Complement/immunology , Complement Pathway, Alternative/immunology , Complement Pathway, Classical/immunologyРеферат
La oncocercosis es una enfermedad parasitaria que tradicionalmente se ha considerado como un padecimiento que afecta exclusivamente a los tejifos oculares y cutáneos. Sin embargo, ya se ha demostrado que existen también otras alteraciones sistématicas, renales y neurológicas especialmente inducidas durante el tratamiento con microfilaricidas. En este artículo se hace una revisión de los aspectos renales de la oncocercosis que incluyen la presencia de microfilarias de onchocerca volvulus en orina (microfilaruria), así como de hematuria y proteinuria en pacientes infectados con esta filaria. Estas manifestaciones renales pueden observarse en oncocercosos que no se encuentran bajo tratamiento, pero su aparición es especialmente notable durante la quimioterapia tanto con microfilaricidas como con macrofilaricidas. No obstante que estas alteraciones pueden desaparecer o no después de finalizado el tratamiento, aparentemente tienen muy poca influencia en el cuadro clínico general de la oncocercosis. Se hace hincapié en los posibles mecanismos por los cuales las microfilarias de 0. volvulus pasan de los tejidos cutáneos hacia el torrente sanguíneo y, desde allí, hacia la orina. Asimismo, se comentan los mecanismos propuestos para explicar el lesión renal, mecanismos que al parecer tienen un origen inmunológico basado en el depósito de complejos inmunitarios en la membrana basal de glomérulo.
Тема - темы
Humans , Filaricides/adverse effects , Onchocerciasis/physiopathology , Kidney/parasitology , Urine/parasitology , Complement Activation/immunology , Onchocerciasis/drug therapy , Onchocerciasis/epidemiology , Kidney/immunologyРеферат
This paper presents a novel but entirely hypothetical concept on the pathogenesis of the shock syndrome (DSS) associated with dengue hemorrhagic fever (DHF). Antibody-dependent enhancement (ADE) is widely thought to be central to the development of these clinical entities. Current views on the mechanisms underlying ADE centre on two major lines of thought: 1) Non-neutralizing antibodies to dengue virus (DV) can enhance viral uptake and replication in target cells (monocytes). 2) DHF/DSS are the consequences of enhanced viral replication, paired with immunopathological processes that are evoked by monocyte dysfunction and detrimental reactions caused by activated T-lymphocytes. The present hypothesis proposes, by contrast, a central role for the following processes: 1) Secondary infection of an individual who has sub or non-neutralizing antibody titers against DV leads to a booster antibody response and a steep rise in antibody levels. 2) Antibodies against DV bind to and direct a selective attack of the complement system onto cells expressing viral antigens on their surface. DHF/DSS are the direct and indirect consequences of complement activation on these cells. The advanced hypothesis, which departs from the mainstream of "immune enhancement" concepts, can easily be tested by experimentation.