RESUMO
Phagocytosis is a cellular process for ingesting and eliminating particles larger than 0.5 µm in diameter, including microorganisms, foreign substances, and apoptotic cells. Phagocytosis is found in many types of cells and it is, in consequence an essential process for tissue homeostasis. However, only specialized cells termed professional phagocytes accomplish phagocytosis with high efficiency. Macrophages, neutrophils, monocytes, dendritic cells, and osteoclasts are among these dedicated cells. These professional phagocytes express several phagocytic receptors that activate signaling pathways resulting in phagocytosis. The process of phagocytosis involves several phases: i) detection of the particle to be ingested, ii) activation of the internalization process, iii) formation of a specialized vacuole called phagosome, and iv) maturation of the phagosome to transform it into a phagolysosome. In this review, we present a general view of our current understanding on cells, phagocytic receptors and phases involved in phagocytosis.
Assuntos
Modelos Imunológicos , Fagocitose/imunologia , Apoptose/imunologia , Humanos , Moléculas com Motivos Associados a Patógenos/imunologia , Fagócitos/imunologia , Fagócitos/fisiologia , Fagocitose/fisiologia , Fagossomos/imunologia , Receptores de Complemento/imunologia , Receptores de IgG/imunologia , Receptores Imunológicos/imunologia , Receptores de Reconhecimento de Padrão/imunologia , Transdução de Sinais/imunologiaRESUMO
The G Immunoglobulin Fc Receptors (FcgammaR) belong to the TNFR5 receptors family, of the immunoglobulin superfamily and are widely expressed in the immune system; their function follows in importance after the complement receptors for immunocomplexes clearance. On the other hand, the systemic lupus erythematosus (SLE) is the prototype of the autoimmune diseases mediated by immunocomplexes and several studies have shown an impaired handle of these ones in part due to dysfunction of the FcgammaR. Among all types of Fcgamma receptors, the FcgammaRIIA, FcgammaRIIB, FcgammaRIIIA and FcgammaRIIIB have well characterized polymorphisms that produce an alteration in the receptor function. A number of studies have been done worldwide to probe an association between these polymorphism and SLE or some of its clinical features, among these the most important are two meta-analyses in which it is shown that the FcygammaRIIA-R131 polymorphism present a significant association with SLE susceptibility (OR: 1.3, 95% CI: 1.10-1.52), while the FcgammaRIIIA F176 polymorphism showed to be associated with lupic nephritis (OR: 1.47, 95% CI: 1.11-1.93, p = 0.006) but not with SLE susceptibility, the results in the rest of the polymorphisms studied are still contradictories.
Assuntos
Lúpus Eritematoso Sistêmico/genética , Polimorfismo Genético , Receptores de IgG/genética , Alelos , Autoanticorpos/imunologia , Autoimunidade , Predisposição Genética para Doença , Humanos , Imunoglobulina G/imunologia , Lúpus Eritematoso Sistêmico/imunologia , Nefrite Lúpica/genética , Nefrite Lúpica/imunologia , Macrófagos/imunologia , Metanálise como Assunto , Monócitos/imunologia , Isoformas de Proteínas/imunologia , Receptores de Complemento/imunologia , Receptores de IgG/imunologia , Relação Estrutura-AtividadeRESUMO
Tissue damage in autoimmune diseases involves excessive production of reactive oxygen species (ROS) triggered by immune complexes (IC) and neutrophil (PMN) interactions via receptors for the Fc portion of IgG (FcgammaR) and complement receptors (CR). Modulation of both the effector potential of these receptors and ROS generation may be relevant to the maintenance of body homeostasis. In the present study, the modulatory effect of four flavonols (myricetin, quercetin, kaempferol, galangin) on rabbit PMN oxidative metabolism, specifically stimulated via FcgammaR, CR or both classes of receptors, was evaluated by luminol- and lucigenin-dependent chemiluminescence assays. Results showed that flavonol inhibitory effect was not dependent on the cell membrane receptor class stimulated but related to the lipophilicity of the compounds (their apparent partition coefficient values were obtained by high-performance liquid chromatography), and was also inversely related to the number of hydroxyl groups in the flavonol B ring and the ROS-scavenger activity (assessed by the luminol--H2O2--horseradish peroxidase reaction). Under the experimental conditions the flavonols tested were not toxic to PMNs (evaluated by lactate dehydrogenase release and trypan blue exclusion) and did not interfere with IC-induced phagocytosis (evaluated by transmission electron microscopy). Our results suggested that inhibition of IC-stimulated PMNs effector functions by the flavonols tested herein was the result of cooperation of different cellular mechanisms.
Assuntos
Derivados de Benzeno/farmacologia , Flavonóis/farmacologia , Fatores Imunológicos/química , Neutrófilos/efeitos dos fármacos , Neutrófilos/metabolismo , Receptores de Complemento/metabolismo , Receptores Fc/metabolismo , Acridinas/química , Animais , Complexo Antígeno-Anticorpo/imunologia , Complexo Antígeno-Anticorpo/metabolismo , Derivados de Benzeno/química , Derivados de Benzeno/metabolismo , Proteínas do Sistema Complemento/metabolismo , Flavonoides/química , Flavonoides/metabolismo , Flavonoides/farmacologia , Flavonóis/química , Flavonóis/metabolismo , Sequestradores de Radicais Livres/química , Sequestradores de Radicais Livres/metabolismo , Sequestradores de Radicais Livres/farmacologia , Interações Hidrofóbicas e Hidrofílicas , Hidroxilação , Doenças do Complexo Imune/tratamento farmacológico , Doenças do Complexo Imune/metabolismo , Fatores Imunológicos/metabolismo , Quempferóis/química , Quempferóis/metabolismo , Quempferóis/farmacologia , Medições Luminescentes , Luminol/química , Estrutura Molecular , Neutrófilos/imunologia , Oxirredução/efeitos dos fármacos , Fagocitose/efeitos dos fármacos , Fagocitose/imunologia , Quercetina/química , Quercetina/metabolismo , Quercetina/farmacologia , Coelhos , Receptores de Complemento/imunologia , Receptores Fc/imunologia , Relação Estrutura-AtividadeRESUMO
We have investigated the individual role of FcgammaR and CR, as well as their cooperation, in mediating the oxidative burst and degranulation of neutrophils of Brazilian systemic lupus erythematosus (SLE) patients. Neutrophils were stimulated with the immune complexes (IC)-IgG or -F(ab')2, opsonized or not with normal or SLE human serum. The oxidative burst was decreased in neutrophils of active SLE patients compared to healthy controls when this response was mediated by FcgammaR and/or CR, while the degranulation was unaffected. The SLE hypocomplementemia did not affect the oxidative burst mediated only by CR. FcgammaRII and CR1 expression on neutrophils of active SLE patients was reduced, while the expression of FcgammaRIII and CR3 was unaffected. These results suggest that the different FcgammaR and CR may be involved or cooperate in different ways in the mediation of the oxidative burst and the degranulation. Moreover, the decreased oxidative burst of neutrophils of active SLE patients may not depend only on SLE hypocomplementemia for IC opsonization. These observations are directed at the understanding of how each of these immune system components (FcgammaR, CR and complement) influences the precise biological neutrophil responses both in physiological and pathological conditions. Since the Brazilian population comprises many races, these results are important because they are directed at a specific population of SLE patients.
Assuntos
Degranulação Celular , Lúpus Eritematoso Sistêmico/imunologia , Lúpus Eritematoso Sistêmico/patologia , Neutrófilos/imunologia , Neutrófilos/metabolismo , Receptores de Complemento/imunologia , Receptores de IgG/imunologia , Explosão Respiratória , Brasil , Feminino , Expressão Gênica , Hemólise , Humanos , Imunoglobulina G/imunologia , Medições Luminescentes , Masculino , Muramidase/metabolismo , Neutrófilos/citologia , Receptores de Complemento/genética , Receptores de IgG/genéticaRESUMO
Complement receptor type 1 (CR1) is a membrane glycoprotein that acts as a receptor for the C3b, iC3b and C4b fragments of complement. In primates, one function of erythrocytes is to promote safe clearance of immunocomplexes (IC) from the circulation through CR1. Theoretically, in diseases characterized by high levels of circulating IC, an erythrocyte CR1 (CR1/E) deficiency may favor IC deposition in tissues or facilitate inappropriate activation of leukocytes in the circulation. Depression of the cell immune response occurs in paracoccidioidomycosis (PCM), especially in the more severe cases, and is frequently associated with high serum IC levels. In the present study we quantified the number of CR1/E in patients with the acute and chronic forms of PCM before and after treatment and correlated it with serum IC levels and CD4+ and CD8+ T cell concentration in the peripheral blood of these patients. Patients with PCM, particularly those with active disease and who had received treatment for shorter periods of time, had low numbers of CR1/E. In addition, an increase in serum IC concentration and a reduction in the CD4+/CD8+ T cell ratio were observed. After treatment there was a significant increase in mean CR1/E number and a reduction in serum IC levels. In patients with the chronic form of the disease the CD4+/CD8+ T cell ratio tended to increase after treatment and was associated with increased CR1/E levels. These results suggest that the reduction in CR1/E observed in patients is a phenomenon acquired with the disease and that CR1 could play a role in the pathogenesis of PCM.
Assuntos
Eritrócitos/imunologia , Paracoccidioides/imunologia , Paracoccidioidomicose/imunologia , Receptores de Complemento/biossíntese , Complexo Antígeno-Anticorpo/biossíntese , Complexo Antígeno-Anticorpo/sangue , Proteína C-Reativa/metabolismo , Linfócitos T CD4-Positivos/imunologia , Linfócitos T CD8-Positivos/imunologia , Proteínas do Sistema Complemento/metabolismo , Eritrócitos/metabolismo , Citometria de Fluxo , Humanos , Imunoglobulinas/sangue , Paracoccidioidomicose/sangue , Receptores de Complemento/sangue , Receptores de Complemento/imunologiaRESUMO
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
Assuntos
Humanos , Proteínas do Sistema Complemento/fisiologia , Programas de Autoavaliação , Ativação do Complemento/imunologia , Inativadores do Complemento/imunologia , Complexo de Ataque à Membrana do Sistema Complemento/imunologia , Proteínas do Sistema Complemento/imunologia , Receptores de Complemento/imunologia , Via Alternativa do Complemento/imunologia , Via Clássica do Complemento/imunologiaRESUMO
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 (AU)
Assuntos
Humanos , Proteínas do Sistema Complemento/fisiologia , Programas de Autoavaliação , Proteínas do Sistema Complemento/imunologia , Via Clássica do Complemento/imunologia , Via Alternativa do Complemento/imunologia , Inativadores do Complemento/imunologia , Ativação do Complemento/imunologia , Receptores de Complemento/imunologia , Complexo de Ataque à Membrana do Sistema Complemento/imunologiaRESUMO
Immunoglobulin E (IgE) has been shown to play a critical role in the allergic late-phase reaction, which is marked by intense leukocyte infiltration and edema. In this study we assessed the allergic pleural inflammation triggered by intrapleural (i.pl.) challenge in sensitized rats. We examined pleural effluent from actively sensitized rats following anti-IgE monoclonal antibody (mAb) (MARE-1) provocation for protein exudation, neutrophil as well as eosinophil accumulation. Inflammatory changes triggered by antigen after passive sensitization with IgE mAb was also assessed for comparison. Total serum level of IgE was found to be about threefold increased 7-8 days post-active sensitization, remaining augmented for at least 30 days. Increased levels of peritoneal leukocyte-bound IgE and serum IgE with specificity to ovalbumin were also detected. Nevertheless, the anti-IgE challenge in 14-day actively sensitized was shown to be a weak stimulus of neutrophil and eosinophil accumulation, despite being able to cause intense protein extravasation. Similarly, antigen challenge of IgE-passively sensitized rats caused protein leakage that was comparable to that induced by anti-IgE mAb in actively sensitized rats but led to a much lower neutrophil/eosinophil infiltration. Also, blockade of complement with recombinant human soluble C receptor-1 (sCR1) treatment prevented actively sensitized rats from reacting to antigen with neutrophil and eosinophil recruitment without modifying protein extravasation. These data suggest that IgE and complement-mediated mechanisms probably account for the exudation and leukocyte infiltration that is characteristic of the pleural inflammatory response observed in actively sensitized rats.
Assuntos
Imunoglobulina E/imunologia , Pleurisia/imunologia , Proteínas/imunologia , Cloreto de Alumínio , Compostos de Alumínio , Animais , Anticorpos Monoclonais/imunologia , Cloretos , Eosinófilos/efeitos dos fármacos , Feminino , Imunoglobulina E/sangue , Contagem de Leucócitos/efeitos dos fármacos , Masculino , Neutrófilos/efeitos dos fármacos , Ovalbumina/imunologia , Proteínas/metabolismo , Ratos , Ratos Wistar , Receptores de Complemento/imunologiaRESUMO
The objective of this study was to compare the histopathological changes and expression of CR3 and CR4 in the liver and spleen of dogs naturally and experimentally infected with L. chagasi. The basic histopathological lesions observed mainly in naturally infected dogs were: epithelioid hepatic granulomas, hyperplasia and hypertrophy of Kupffer cells, Malpigui follicles and mononucleated cells of the red pulp of the spleen. Sections from the liver and spleen by immunocytochemistry technique showed the presence of CD11b, c/CD 18 antigens in the control and infected animals and no qualitative or quantitative differences in the liver. Nevertheless, CD18 was always increased in the spleen of naturally and experimentally infected dogs. These results indicate that there is a difference in the activation of CD18 in both experimental and natural cases of canine visceral leishmaniasis that should play an important role in the immunological response to Leishmania chagasi infection.
Assuntos
Antígenos de Protozoários/imunologia , Doenças do Cão/imunologia , Doenças do Cão/parasitologia , Leishmania/imunologia , Leishmaniose/veterinária , Fígado/imunologia , Receptores de Complemento/imunologia , Baço/imunologia , Animais , Antígenos CD18/imunologia , Cães , Feminino , Imuno-Histoquímica , Integrina alfaXbeta2/imunologia , Fígado/patologia , Antígeno de Macrófago 1/imunologia , Masculino , Baço/patologiaRESUMO
Peripheral blood monocytes (PBMs) from healthy individuals who had experienced distinctive clinical outcomes after natural infection with Leishmania (Viannia) were evaluated in vitro with respect to susceptibility to infection by stationary phase promastigotes of L. (V). panamensis. Concomitantly, the role of complement receptors (CR) CR1 and CR3 in the attachment and entry of L. (V). panamensis into human monocytes was analyzed using mAbs to CR1 (CD35) and CR3 (CD11b) to inhibit competitively these early events in the host-parasite interaction. Cell adherence to fibronectin was examined to determine how modulation of CR activity affected the attachment and uptake of this parasite species. The human monocyte cell line U-937 was also evaluated and found to provide a reproducible control for L. (V). panamensis infection in vitro. Opsonization with fresh AB+ serum markedly enhanced uptake by both PBMs and U-937 cells, and the fluid phase blocking of CR1 and CR3 resulted in partial inhibition of attachment and/or internalization. Uptake rather than attachment was abrogated by antireceptor antibodies in PBMs from previously infected individuals, whereas attachment was diminished in PBMs from unexposed controls. Adherence of PBMs to fibronectin resulted in decreased infection. PBMs from persons who had experienced chronic disease 5 to 8.4 yr before these studies were significantly more susceptible to in vitro infection by L. (V). panamensis than PBMs from asymptomatically infected or control individuals based on the percentage of cells infected, the number of parasites per cell, and viability of intracellular parasites at 48 h postinfection. Neither blocking of CR nor modulation by fibronectin altered the pattern of susceptibility of PBMs from the different clinical groups. These findings provide evidence for the participation of CR in the infection of human monocytes by L. (V). panamensis and demonstrate a correlation between clinical phenotype and in vitro infection of PBMs cultured in the presence of autologous plasma before experimental infection.
Assuntos
Leishmania guyanensis/imunologia , Leishmaniose Mucocutânea/imunologia , Monócitos/imunologia , Receptores de Complemento/imunologia , Animais , Adesão Celular/efeitos dos fármacos , Linhagem Celular , Fibronectinas/farmacologia , Humanos , Técnicas In Vitro , Leishmania guyanensis/citologia , Leishmania guyanensis/crescimento & desenvolvimento , Monócitos/citologia , Monócitos/parasitologia , Receptores de Complemento/metabolismoRESUMO
Previous studies of erythrocyte CR1 levels in systemic lupus erythematosus (SLE) and other diseases with in vivo complement activation have led to the conclusion that CR1 levels fall because of loss of CR1 from erythrocytes by proteolysis--predominantly in the liver. In order to measure the existence of proteolysed CR1 remnants on erythrocytes an antibody was raised to a peptide corresponding to the CR1 sequence between the proximal standard consensus repeat (SCR) and the transmembrane segment. This antipeptide antibody recognizes a neo-antigen found on trypsinized erythrocytes which has been demonstrated to represent the 'CR1-stump'. The anti-'CR1-stump' antiserum detects proteolysed CR1 on the ex vivo erythrocytes of a patient with cold haemolytic antibody disease (CHAD). However, higher affinity antibodies will be needed to make anti-CR1-stump a satisfactory diagnostic reagent.
Assuntos
Anticorpos/imunologia , Eritrócitos/imunologia , Peptídeos/imunologia , Receptores de Complemento/imunologia , Sequência de Aminoácidos , Animais , Epitopos/análise , Testes de Hemaglutinação , Humanos , Fragmentos Fab das Imunoglobulinas/imunologia , Dados de Sequência Molecular , Coelhos , Receptores de Complemento/análise , Receptores de Complemento 3b , Tripsina/farmacologiaAssuntos
Macrófagos/parasitologia , Trypanosoma cruzi/fisiologia , Adjuvantes Imunológicos/farmacologia , Animais , Interações Hospedeiro-Parasita , Fragmentos Fab das Imunoglobulinas/imunologia , Macrófagos/imunologia , Macrófagos/ultraestrutura , Receptores de Complemento/imunologia , Receptores Imunológicos/fisiologia , Trypanosoma cruzi/imunologia , Trypanosoma cruzi/ultraestruturaRESUMO
Incubation of Trypanosoma cruzi bloodstream trypomastigotes (Btrys) with C5-deficient blood in the presence of anti-T. cruzi immune mouse serum (IMS) or its IgG fraction resulted in an immediate formation of small clumps in which one could easily see platelets adhered to the parasites. After 4 h of incubation most of the clumps had disappeared and the number of the parasites was considerably reduced. Twenty-four hours later there were only a few remaining parasites. This same sequence of events was also observed when the parasites were incubated with isolated platelets in presence of IMS or its IgG fraction. When the parasites were incubated with plasma in the presence of IMS or its IgG fraction but in the absence of platelets there was strong agglutination of the parasites but no reduction in their number. Incubation of the parasites with platelets and IMS or its IgG fraction in C3-depleted plasma prevented adherence of the platelets to the parasites and their subsequent lysis. It is concluded that platelets are able to induce in-vitro lysis of the Btrys and that this phenomenon is dependent on the platelet' receptor for C3b.
Assuntos
Anticorpos Antiprotozoários/imunologia , Plaquetas/imunologia , Complemento C3b/imunologia , Receptores de Complemento/imunologia , Trypanosoma cruzi/imunologia , Aglutinação , Animais , Complemento C3/imunologia , Complemento C5/imunologia , Imunoglobulina G/imunologia , Camundongos , Receptores de Complemento 3bRESUMO
Blood neutrophils and their bone marrow cell progenitors have membrane receptors for C3 and for the Fc portion of IgG. To test possible changes in the expression of those receptors associated to diseases we studied: a) blood of 31 and bone marrow of 9 normal individuals; b) blasts of 29 patients with acute myeloblastic leukemia; c) bone marrow of 8 patients with severe bacterial infections. The receptors were evaluated by rosette techniques: Saccharomyces C3 and sheep erythrocyte specific IgG antibody. Dried droplet stained smears were used to count rosettes of cells at different stages of maturation. The studies disclosed the following: a) these receptors are detected in progressively increasing percentage of cells throughout the differentiation steps of the granulocytic series; receptor for C3 is depicted as starting in promyelocytes, and receptor for Fc in myelocytes; the percentage of bone marrow neutrophils expressing these receptors is lower than that of blood neutrophils; b) in acute myeloblastic leukemia, blasts frequently express receptors normally found at more mature levels of differentiation which is an expression of nucleocytoplasmic asynchronism; there is good correlation between the FAB classification and the expression of these receptors; c) in severe bacterial infections, the receptors are found at earlier stages and in a higher proportion of cells at early maturation steps, marking a shift to the left in the expression of receptors.
Assuntos
Infecções Bacterianas/sangue , Leucemia Mieloide Aguda/sangue , Receptores de Complemento/imunologia , Receptores Fc/imunologia , Células da Medula Óssea , Humanos , Neutrófilos/análise , Receptores de Complemento/análise , Receptores Fc/análise , Células-Tronco/análiseRESUMO
Los neutrófilos y sus progenitores medulares tienen receptores para C3 y para Fc de IgG. Con el objeto de estudiar las modificaciones de la expersión de estos receptores en patología se estudiaron: a) sangre de 31 y médula ósea de 9 individuos normales; b) blastos de 29 pacientes de leucemia mieloblástica aguda; c) médula ósea de 8 pacientes con infecciones bacterianas severas. Se trabajó con técnica de rosetas de Saccharomyces-C3 glóbulos rojos de carnero sensibilizados con IgG. Los resultados demuestran que: a) los receptores aparecen gradual y progresivamente en las etapas de diferenciación granulocítica; el receptor de C3 se evidencia en promielocitos y el de Fc en mielocitos; el porcentaje de neutrófilos de médula ósea que expresan estos receptores es inferior al de neutrófilos de la sangre; b) en leucemia mielobástica aguda, a pesar de los signos morfológicos de inmadurez, los blastos expresan frecuentemente receptores que normalmente aparecen en estadios más diferenciados, mostrando otra evidencia de asincronismo núcleocitoplasmático; se observa buena concordancia entre la expresión de receptores y la clasificación FAB; c) en infecciones bacterianas severas aparece desviación izquierda de la expresión de los receptores en la línea de diferenciación de la progenie granulocítica
Assuntos
Humanos , Infecções Bacterianas/imunologia , Leucemia Mieloide Aguda/imunologia , Receptores de Complemento/imunologia , Receptores Fc/imunologia , Células-Tronco/análise , Infecções Bacterianas/sangue , Leucemia Mieloide Aguda/sangue , Medula Óssea/citologia , Neutrófilos/análise , Receptores de Complemento/análise , Receptores Fc/análiseRESUMO
Los neutrófilos y sus progenitores medulares tienen receptores para C3 y para Fc de IgG. Con el objeto de estudiar las modificaciones de la expersión de estos receptores en patología se estudiaron: a) sangre de 31 y médula ósea de 9 individuos normales; b) blastos de 29 pacientes de leucemia mieloblástica aguda; c) médula ósea de 8 pacientes con infecciones bacterianas severas. Se trabajó con técnica de rosetas de Saccharomyces-C3 glóbulos rojos de carnero sensibilizados con IgG. Los resultados demuestran que: a) los receptores aparecen gradual y progresivamente en las etapas de diferenciación granulocítica; el receptor de C3 se evidencia en promielocitos y el de Fc en mielocitos; el porcentaje de neutrófilos de médula ósea que expresan estos receptores es inferior al de neutrófilos de la sangre; b) en leucemia mielobástica aguda, a pesar de los signos morfológicos de inmadurez, los blastos expresan frecuentemente receptores que normalmente aparecen en estadios más diferenciados, mostrando otra evidencia de asincronismo núcleocitoplasmático; se observa buena concordancia entre la expresión de receptores y la clasificación FAB; c) en infecciones bacterianas severas aparece desviación izquierda de la expresión de los receptores en la línea de diferenciación de la progenie granulocítica (AU)
Assuntos
Humanos , Leucemia Mieloide Aguda/imunologia , Infecções Bacterianas/imunologia , Receptores de Complemento/imunologia , Receptores Fc/imunologia , Leucemia Mieloide Aguda/sangue , Infecções Bacterianas/sangue , Receptores de Complemento/análise , Receptores Fc/análise , Medula Óssea/citologia , Células-Tronco/análise , Neutrófilos/análiseRESUMO
The role of mononuclear phagocytic cells in extraneural infection of the mouse with Junin virus (JV) was studied. Endpoint susceptibility (4 days of life) was evaluated by intraperitoneal (i.p.) inoculation of suckling mice. By means of immunofluorescence (IF) and C3 receptor assays, it was found that macrophages were permissive to viral replication in vivo and fostered the recruitment of inflammatory cells as evidenced by the absence of C3 marker. In support, in vitro infection failed to induce alterations of this receptor. Throughout, both in vivo and in vitro, there were no signs of C3-mediated phagocytosis. Silica treatment had no effect on either resistance or susceptibility, suggesting that the "macrophage-barrier" failed to hinder or favour the course of disease. Differences with other JV models are discussed.
Assuntos
Febre Hemorrágica Americana/imunologia , Macrófagos/imunologia , Fatores Etários , Animais , Arenavirus do Novo Mundo/imunologia , Técnicas In Vitro , Antígeno de Macrófago 1 , Camundongos , Camundongos Endogâmicos BALB C , Receptores de Complemento/imunologiaAssuntos
Complemento C3/imunologia , Pulmão/imunologia , Macrófagos/imunologia , Nippostrongylus/imunologia , Receptores de Complemento/imunologia , Animais , Brônquios/citologia , Brônquios/imunologia , Adesão Celular , Células Cultivadas , Larva/imunologia , Leucócitos/imunologia , Pulmão/citologia , Antígeno de Macrófago 1 , Alvéolos Pulmonares/citologia , Alvéolos Pulmonares/imunologia , RatosAssuntos
Complexo Antígeno-Anticorpo/análise , Complemento C1/imunologia , Técnicas Imunoenzimáticas , Nefropatias/imunologia , Lúpus Eritematoso Sistêmico/imunologia , Ativação do Complemento , Complemento C3/imunologia , Humanos , Fragmentos Fc das Imunoglobulinas/imunologia , Receptores de Complemento/imunologiaRESUMO
Serum circulating immune complexes (CIC) were measured in 27 patients with non insulin dependent diabetes (NIDD). This was done by measuring the degree of binding to human red blood cells by the C3b complement fraction. At the same time, the percentage of B lymphocytes in peripheral blood was evaluated by means of the direct immunofluorescence technique for surface IgG and EAC rosettes for cells with receptors to C3b complement fraction. Twenty normal control subjects were simultaneously studied by the same methodology. An increase in serum CIC was observed in NIDD patients, as compared to healthy subjects. Values were 35.8 +/- 3.2 and 25.6 +/- 2.1 micrograms/ml, respectively. The percentage of cells with surface IgG was 10.2 +/- 0.8 in diabetic patients; this value was significantly higher than that found in the control group (6.0 +/- 0.8). No significant quantitative difference in the percentage of EAC binding cells was found between NIDD patients and the control group. When NIDD patients were divided into two groups, those with and those without microvascular complications, neither differences in CIC levels nor in the percentage of B lymphocytes were found. Nor any correlation could be found between the highest individual CIC levels and the highest percentage of lymphocytes with surface IgG. These data show an increase of CIC levels and of cells with surface IgG in NIDD patients who had not received insulin at least not in a constant or prolonged therapy. This could allow us to suspect the existence of antigen-antibody complexes different to insulin-antiinsulin CIC found in insulin dependent diabetes.