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1.
Rev. Fac. Med. Hum ; 21(1): 124-129, Ene.-Mar. 2021.
Artigo em Inglês, Espanhol | LILACS-Express | LILACS | ID: biblio-1147289

RESUMO

La diabetes es una enfermedad crónica que aparece cuando el páncreas no produce insulina suficiente o cuando el organismo no utiliza eficazmente la insulina que produce. La insulina es una hormona que regula el azúcar en la sangre. El efecto de la diabetes no controlada es la hiperglucemia (aumento del azúcar en la sangre), que con el tiempo daña gravemente muchos órganos y sistemas, especialmente los nervios y los vasos sanguíneos.


Diabetes is a chronic disease that appears when the pancreas does not produce enough insulin or when the body does not use the insulin it produces effectively. Insulin is a hormone that regulates blood sugar. The effect of uncontrolled diabetes is hyperglycemia (increased blood sugar), which over time severely damages many organs and systems, especially nerves and blood vessels.

2.
Transpl Immunol ; 9(2-4): 101-10, 2002 May.
Artigo em Inglês | MEDLINE | ID: mdl-12180815

RESUMO

Our previous results showed that TAP1 mutant mice rejected heart and skin grafts from donors with no H-2 disparity that express normal density of MHC class I molecules at the cell surface. During rejection, CD4 cells were predominant and essentially, no CD8 cells were found infiltrating the grafts. We hypothesized that TAP1 mutant mice, which developed and matured in an MHC class I-deficient environment, may have selected a repertoire of T cells with distinct reactivity to self class I molecules. The rejection of grafts with no H-2 disparity could be mediated by CD4+ T cells reactive to wild type H-2b class I molecules, or derived peptides, in the context of self-APC. Accordingly, we observed that transplanted TAP1 mutant mice presented a significant amplification of the proliferative T cell response to H-2Kb peptides, indicating that the stimulus with the graft was sufficient to induce peripheral expansion of these T cell repertoires. Therefore, the response to H-2Kb molecules could be a relevant pathway of activating T cells and triggering rejection of grafts expressing normal levels of these class I molecules. To test our hypothesis, we investigate the effect of pre-transplantation H-2Kb peptide-immunization on TAP1 mutant, which were then transplanted with C57BL/6 skin grafts (H-2b). Mice were immunized with a pool of five peptides derived from the polymorphic region of Kb alpha chain, before tail skin grafting. To study the role of CD4+ T cells in the rejection of C57BL/6 skin grafts, mice were in vivo depleted with an anti-CD4 monoclonal antibody GK1.5, and transplant evolution was observed. Sensitization of TAP1 mutant mice with H-2Kb peptides accelerated the rejection of skin grafts. Immunized mice rejected grafts with a MST of 13 days, compared to 16 days for the non-immunized mice (P=0.0089). The significant acceleration of graft rejection, induced by immunization with H-2Kb peptides, indicates that these peptides are capable of mobilizing effector T-cells that participate in rejection. These results support our hypothesis that class I molecules may be a target in the rejection of grafts with no MHC disparity. Depletion of CD4 T-cells resulted in a significant delay in rejection compared with the untreated control group. The MST of skin grafts in the controls was 16 days, whereas CD4-depleted recipients rejected skin grafts with a MST of 41 days (P=0.025). Moreover, some animals did not show macroscopic signs of rejection up to > 100 days posttransplantation. The contribution of CD4+ T cells to skin graft rejection, in our model, may reflect the occurrence of the presentation of H-2b peptides during graft rejection, in the context of self-APC. In conclusion, our results demonstrate an important role for H-2b molecules and CD4 T cells in the rejection of C57BL/6 grafts by TAP1 mutant mice. The low expression of MHC-I molecules on TAP1-/- mice may be determinant in the selection of a T cell repertoire strongly reactive to self MHC class I molecules which probably escapes the control of peripheral regulatory mechanisms.


Assuntos
Transportadores de Cassetes de Ligação de ATP/fisiologia , Linfócitos T CD4-Positivos/imunologia , Rejeição de Enxerto/imunologia , Antígenos H-2/imunologia , Membro 2 da Subfamília B de Transportadores de Cassetes de Ligação de ATP , Sequência de Aminoácidos , Animais , Citocinas/biossíntese , Imuno-Histoquímica , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Dados de Sequência Molecular , Transplante de Pele/imunologia
3.
Rev. Fac. Med. (Caracas) ; 17(2): 143-8, jul.-dic. 1994. ilus
Artigo em Espanhol | LILACS | ID: lil-151542

RESUMO

Los anticuerpos anticardiolipina son autoanticuerpos clínicamente asociados con eventos trombóticos arteriales y venosos, muerte fetal recurrente y trombocitopenia. El presente trabajo describe el desarrollo de un sistema indirecto de ELISA para la detección de anticuerpos anticardiolipina. Las placas fueron fijadas con cardiolipina a una concentración de 25 µg/ml por evaporación al vacio. Las uniones inespecificas fueron eliminadas por bloqueo de las placas con albúmina bovina al 4 por ciento en PBS. El suero a una dilución de 1:50 fue incubado en la placa por 1h. Se utilizó un conjugado anti-IgG humana marcado con peroxidasa y obtenido en conejos a una dilución 1:1000. Se estudiaron 150 sueros de donantes voluntarios para establecer los valores límites que fueron fijados en la X más 3DS. Se estudiaron 17 pacientes con Lupus Eritematoso Sistémico encontrando correlación significativa entre los niveles elevados de anticuerpos anticardiolipinas y la presencia de trombosis venosa y/o arterial, trobocitopenia y muerte fetal y/o abortos espontáneos


Assuntos
Humanos , Anticorpos/imunologia , Cardiolipinas/imunologia , Técnicas Imunoenzimáticas
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