Navegando por Palavras-chave "lymphocyte"
Agora exibindo 1 - 4 de 4
Resultados por página
Opções de Ordenação
- ItemSomente MetadadadosCell cycle distribution of CD4(+) lymphocytes in HIV-1-infected subjects(Wiley-Blackwell, 2004-11-01) Sauer, Mariana Melillo [UNIFESP]; Kallas, Esper Georges [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Background: Apoptosis is one of the possible explanations for the progressive loss of CD4(+) T lymphocytes in infection with the human immunodeficiency virus (HIV), which may interfere with cell cycle distribution. This study evaluated the cell cycle of CD4(+) and CD8(+) lymphocytes in HIV-infected subjects and controls.Methods: Two methods to identify lymphocytes for cell cycle analysis were evaluated, magnetic beads and concurrent staining, and both were followed by propidium iodide DNA labeling. the chosen method was used to evaluate the cell cycle of lymphocytes in HIV-1-infected subjects and controls.Results: There was no significant difference between the two methods, although a higher variability was observed with the magnetic bead cell separation method. A higher proportion of cells in the S phase was observed in HIV-1 patients (2.69% vs. 1.19%, P = 0.016), coupled with a decrease in G, (96.11% vs. 98.10%, P = 0.005) in CD4(+) lymphocytes, a phenomenon not observed in CD8(+) lymphocytes. No correlation was detected between the different cell cycle phases and T-lymphocyte counts or viral load.Conclusions: the present work developed a new approach to evaluate lymphocyte cell cycle distribution, applied in the setting of HIV-1 infection. It may contribute to the understanding of the CD4(+) T-Iymphocytes depletion seen in these patients. (C) 2004 Wiley-Liss, Inc.
- ItemSomente MetadadadosImmunophenotypic characterization of peripheral T lymphocytes in Mycobacterium tuberculosis infection and disease(Blackwell Publishing Ltd, 2002-04-01) Rodrigues, Denise do Socorro da Silva [UNIFESP]; Medeiros, Eduardo Alexandrino Servolo de [UNIFESP]; Weckx, Lily Yin [UNIFESP]; Bonnez, W.; Salomão, Reinaldo [UNIFESP]; Kallas, Esper Georges [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ RochesterThe cellular immune response probably plays a pivotal role in determining the clinical outcome after exposure to Mycobacterium tuberculosis. We used multi-parameter flow-cytometry to evaluate the distribution of T-lymphocyte subsets during infection and disease caused by M. tuberculosis. Samples were obtained from 71 volunteers to identify the T CD4(+) and CD8(+) lymphocyte numbers, and the activation plus memory/naive phenotypes, as defined by CD38, HLA-DR, CD45RA and CD27 markers. Subjects were divided into 18 healthy volunteers without detectable reaction to purified protein derivative (PPD-), 18 health care workers with a recent conversion to PPD, 20 patients with active pulmonary tuberculosis (TBC) and 15 patients with treated TBC at 6 months of therapy. By multiple-comparison analyses, the T CD4(+) lymphocyte number of the TBC group was lower than the PPD- group (P < 0.05). Ibis difference was apparently lost after treatment. the higher and the lower number of naive T CD4(+) cells was observed in the PPD- and TB C group, respectively. CD8(+) T lymphocytes were also statistically different among the four groups (P = 0.0002), lower in the TBC group (P < 0.05). CD8(+) T lymphocyte activation was evaluated by the CD38 and HLA-DR surface expression. the percentage distribution of these markers was statistically different between the four groups (P = 0.0055). TBC patients had a higher percentage of CD38(+) cells and mean fluorescence index, suggesting an overall increase of cell activation. These results suggest that peripheral T lymphocytes reflect cellular activation during TBC, along with possible redistribution of naive, memory/effector and late differentiated memory/effector phenotypes in the peripheral blood after infection and disease caused by M. tuberculosis.
- ItemSomente MetadadadosMouse B-1 cell-derived mononuclear phagocyte, a novel cellular component of acute non-specific inflammatory exudate(Oxford Univ Press, 2001-09-01) Almeida, Sandro Rogério de [UNIFESP]; Aroeira, L. S.; Frymuller, E. [UNIFESP]; Dias, Maria Ângela Amorim [UNIFESP]; Bogsan, Cristina Stewart Bittencourt [UNIFESP]; Lopes, José Daniel [UNIFESP]; Mariano, Mario [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Inst Nucl & Energet ResAt least three B cell subsets, B-1a, B-1b and B-2, or conventional B cells are present in the mouse periphery. Here we demonstrate that B-1 cells spontaneously proliferate in stationary cultures of normal adherent mouse peritoneal cells. B-1 cells were characterized by morphology, immunohistochemistry and flow cytometry. IgM was detected in the supernatants of these cultures. We demonstrated that the major cell population analyzed expresses the B-1b phenotype. When these cells were transferred to a new culture, a large proportion of them adhere to the plastic surface, and spread as bipolar cells endowed with the capacity to phagocytose via Fe and mannose receptors. Flow cytometry analysis of these adherent cells demonstrated that the great majority of them share both B-220 and Mac-1 antigens. Nevertheless, 45% of them were exclusively Mac-1(+). Finally, when they were labeled in vitro with [H-3]thymidine and transferred to the peritoneal cavity of naive mice, they migrate to a non-specific inflammatory focus induced by a foreign-body implant. These data demonstrate that B-1 cells, mainly B-1b cells, not only proliferate and differentiate into a mononuclear phagocyte in vitro, but also that they exit the peritoneal cavity and migrate to a non-specific inflammatory milieu.
- ItemAcesso aberto (Open Access)Profound peripheral T-lymphocyte depletion and activation in disseminated tuberculosis(Brazilian Society of Infectious Diseases, 2006-02-01) Rodrigues, Denise do Socorro da Silva [UNIFESP]; Salomão, Reinaldo [UNIFESP]; Kallas, Esper Georges [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Three HIV-1-seronegative patients with disseminated tuberculosis presented significant depletion of T-cell counts, in CD4+ and/or CD8+ cells, associated with increased expression of activation marker CD38 on CD8+ T-lymphocytes. This finding raises the question of potential mechanisms involved in the activation or loss of T-cells in disseminated tuberculosis.