Publications by authors named "Enriquez-Rincon F"

Extracellular matrix metalloproteases and the fibrinolytic system are important protease systems interacting with each other in charge of remodeling and recycling of tissues. Their role in tumor invasion and metastasis is often discussed. In this study several metalloproteases such as MMP-1, MMP-3, MMP-9, and TIMP-1 together with molecules from the fibrinolytic system like uPA, its receptor uPAR, and its inhibitor, PAI-1, were studied by immune-histochemistry to establish a comparison with and without metastasis.

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Objective: To investigate whether the HlyA-induced vacuolating effect is produced by V. cholerae O1 ElTor strains isolated from different geographic origins, including Mexico.

Material And Methods: Supernatant-induced haemolysis, vacuolating activity and cytotoxicity in Vero cells were recorded.

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As part of the innate immune response NK cells destroy infected, transformed, or otherwise stressed cells within hours of activation. In contrast, CD4(+) T lymphocytes require a sustained increase in their metabolism in order to cope with the biogenesis of cell components, in a process of proliferation and differentiation into effector cells. Recently, mitochondria have been implied in T lymphocyte immune synapse function but little is known on the role of mitochondria in the NK cell interaction with tumour cells.

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Non-O1 strains of Vibrio cholerae implicated in gastroenteritis and diarrhea generally lack virulence determinants such as cholera toxin that are characteristic of epidemic strains; the factors that contribute to their virulence are not understood. Here we report that at least one-third of diarrhea-associated nonepidemic V. cholerae strains from Mexico cause vacuolation of cultured Vero cells.

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Background: Cancer-associated, major histocompatibility complex (MHC)-restricted peptide antigens have been elucidated in human melanomas and ovarian, breast, and renal carcinomas; but relatively little is known about lung cancer antigens.

Methods: To work toward delineation of lung cancer-associated antigens, we developed tumor infiltrating lymphocytes (TILs), peripheral blood mononuclear cell-derived cytolytic T cell lines (CTL), autologous lung cancer cell lines, and normal lung cell lines from 17 patients undergoing lung cancer resections. The TILs and CTL lines were subsequently evaluated for markers of activation and specific lysis of autologous or allogeneic lung cancer cell lines or both.

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We have investigated the role of IgE in the local immunity of intestinal amebiasis, a parasitic infection known to induce specific antibody-forming cells (AFC) and IgA antibodies in rodents and humans. We found that intragastric immunization of rats with glutaraldehyde-fixed Entamoeba histolytica trophozoites significantly increased antiameba AFC in the Peyer's patches and spleen and that the lamina propria of the cecum from immunized animals was infiltrated by eosinophils armed with IgE antibodies. Morphometric analysis showed that IgE-containing cells and eosinophils were nearly three times more abundant in the cecum of immunized rats.

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It has not been established whether seric antiamebic antibodies are produced after local presence of amebas, or only after they invade the tissues. Therefore, the purpose of this work was to determine if mucosal immunization with glutaraldehyde-fixed trophozoites (GFT) could induce seric anti-amebic antibody responses in mice. We determined by ELISA the quality and quantity of anti-E.

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We performed an immunoblot analysis of the main E. histolytica proteins recognized by immune sera and intestinal fluids of Balb/c mice immunized with glutaraldehyde fixed trophozoites (GFT) by intragastric, rectal and intraperitoneal routes, to determine if there were differences in the amebic antigens immunodominantly recognized at mucosal and systemic levels. The antigen patterns recognized by mice immunized via intraperitoneal and rectal routes were complex and similar suggesting that the immunization route (systemic or local), does not influence the recognition pattern elicited at mucosal or systemic levels.

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The purpose of this work was to determine if anti-amebic antibody producing cell responses could be elicited in Peyer's patches and spleen in mice locally or systemically immunized with glutaraldehyde-fixed trophozoites of Entamoeba histolytica (GFT). The animals were inoculated with either a single or four doses of GFT via intragastric, rectal, and intraperitoneal routes. The anti-amebic antibody producing cell responses were analyzed by a spot forming cell assay (ELISPOT).

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The local induction of humoral immune response to Entamoeba histolytica trophozoites in the gut has not been studied. This work reports some of our recent studies aimed to induce optimal immune responses against E. histolytica in mice and to describe a novel approach for monitoring mucosal immune responses induced in the gastrointestinal tract and expressed locally and systemically.

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The kinetics of the anti-amebic antibody producing cell (APC) response was analyzed by a spot forming cell (SFC) assay, after a single dose of glutaraldehyde fixed amebas (GFA) by intragastric, rectal and intraperitoneal routes. It was found that mice elicited both local and systemic immune responses in Peyer's patches and spleen, by either local or systemic stimulation. The analysis of the isotype of the anti-amebic APC in mice given four times the GFA by the mentioned routes revealed that mice produced anti-amebic APC of the three major isotypes in both spleen and Peyer's patches.

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The antibody responses against Entamoeba histolytica in Peyer's patches and spleen after rectal, intraperitoneal and intragastric immunization with glutaraldehyde-fixed amebas (GFA) was compared between male and female mice by the use of a spot forming cell (SFC) assay. We found that female mice elicit significant higher anti-amebic SFC responses than male mice, in both spleen and Peyer's patches after rectal and intraperitoneal stimulation, whereas by intragastric route females show higher responses than males in spleen but not in Peyer's patches.

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Mice were treated from birth with either goat anti-mouse IgM or with a monoclonal anti-IgD antibody. When they were 8 weeks old, cohorts of these mice were given 125I-labelled antigen, either by itself, or in an antigen-antibody complex. Anti-IgM-treated mice, which did not develop follicular structures in their spleens, failed to retain immune complexes on follicular dendritic cells in the characteristic pattern.

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This study compares the effects of passive administration of monoclonal anti-hapten (DNP) antibodies on primary plaque-forming cell (PFC) responses in mice to either soluble (DNP-keyhole limpet haemocyanin [KLH] ) or particulate (TNP-erythrocyte) antigens. IgM, IgG1, IgG2a and IgG2b antibodies at doses up to 500 micrograms induced at best a modest suppression of the IgM response, and reproducibly enhanced the IgG response to DNP-KLH by up to 30-fold. In contrast, with the particulate antigen only the IgM antibody enhanced IgG PFC; IgG2 antibodies, and one out of two IgG1 antibodies caused marked suppression of the primary response to TNP-RBC.

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In this study we followed the in vivo fate and distribution of hapten-coupled sheep red blood cells (TNP-SRBC) coated with 125I-labelled anti-hapten antibody in mice. The majority of these complexes was rapidly taken up by the liver, and by macrophages in the marginal zone of the spleen. Within a few hours, however, marginal zone labelling diminished and label appeared in the corona of lymphoid follicles.

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