ABSTRACT
Objective To investigate the phenotypes and the HIV-1-specific T cell responses of KIR3DL1 positive CD8 cells in patients with early HIV-1 infection. Methods Fifty-six HIV-1 antibody negative individuals and thirty-two patients with early HIV-1 infection were enrolled in the study. Fluores-cence-activated cell sorting (FACS) was performed to detect the phenotypes of KIR3DL1 receptor expressed on the surface of CD8 cells. The levels of IFN-γwere measured by intracellular cytokine staining assay after the PBMCs were stimulated with an HIV-1 Gag peptide pool. Results The percentages of KIR3DL1+CD8 T cells in HIV-1 negative individuals and patients with early HIV-1 infection were 1. 45% (0. 12%-8. 4%) and 0. 82% (0. 14%-6. 14%), respectively, and there was no significant difference between them. The percentages of KIR3DL1+CD8 Temra cells in HIV-1 negative individuals and patients with early HIV-1 infec-tion were (4. 55±3. 84)% and (6. 71±8. 50)%, respectively, which were significantly higher than the per-centages of KIR3DL1+CD8 Tem cells, which were (0. 50±0. 59)% and (1. 18±1. 39)%, respectively (all P<0. 01). Moreover, the percentages of KIR3DL1+CD8 Tem cells in patients with early HIV-1 infection were higher than those in HIV-1 negative individuals (P=0. 001 2). The percentage of KIR3DL1+CD8 Temra cells was positively correlated with the HIV-1 viral load in patients with early HIV-1 infection ( rs=0. 576,P=0. 000 9). The percentages of KIR3DL1+CD8 Temra cells in HIV-1 patients, whose viral loads were larger than 4. 0log, were much higher than those in HIV-1 patients with viral loads less than 4. 0 log (P=0. 002). Additionally, the levels of IFN-γsecreted by KIR3DL1 positive CD8 cells were much lesser than those secreted by KIR3DL1 negative CD8 cells (P<0. 000 1). Conclusion The receptor of KIR3DL1 was mainly expressed on CD8 Temra cells in both HIV-1 negative subjects and patients with early HIV-1 infec-tion. High HIV-1 viremia was associated with the high percentage of KIR3DL1+CD8 Temra cells. The KIR3DL1 positive CD8 cells induced lower HIV-1-specific T cell responses.
ABSTRACT
Tuberculosis is the most prevalent infectious disease in the world. Granuloma formation and caseous necrosis are hallmarks of M. tuberculosis infection and they represent the protective and inflammatory reactions in the infected tissues. The molecular mechanisms that mediate granuloma necrosis are still not well understood. Objectives: To immunolocalize and correlate the amounts of CD68+ macrophages and CD8+ lymphocytes to caseous necrosis extension in granulomas of tuberculous pleurisy. Methods: The study is a retrospective analysis of 30 pleural biopsies with histopathological diagnosis of chronic granulomatous pleurisy with caseous necrosis. These biopsies were classified according to necrosis intensity as minimal (N1), moderate (N2) and intense (N3). The number of granulomas was also observed and categorized as G1 (1 to 4 granulomas per section), G2 (5 to 8 granulomas per section), and G3 (more than 8 granulomas per section). Results: The means of CD68+ cells counts per mm² in N1, N2 and N3 categories of necrosis were 1,287 +/- 254, 1086 +/- 181 and 930 +/- 115 respectively. The means for CD8+ cells were 483.7 +/- 396, 366.3 +/- 43 and 558 +/- 53 cells per mm² in N1, N2 and N3 respectively. Conclusions: There were no significant statistical correlations between necrosis extension and cell counts. In analyzed biopsies, the number of CD68+ cells was significantly higher than the number of CD8+ cells.
La tuberculosis es una de las enfermedades más prevalentes en el mundo. La formación del granuloma junto con la necrosis caseosa son características propias de la infección por M. tuberculosis y representan reacciones inflamatorias y protectoras en los tejidos infectados. No se conocen bien los mecanismos moleculares que median la necrosis en el granuloma. Los objetivos fueron inmunolocalizar y correlacionar la cantidad de macrófagos CD68+ y linfocitos CD8+ con la extensión de la necrosis caseosa, en los granulomas de tuberculosis pleural. Análisis retrospectivo que incluyeron 30 biópsias con diagnóstico histopatológico de tuberculosis pleural granulomatosa crónica con necrosis caseosa. Estas biópsias fueron clasificadas según la intensidad de necrosis como mínima (N1), moderada (N2) e intensa (N3). También se determinó el número de granulomas, que fueron clasificados como G1 (1 a4 granulomas por sección), G2 (5 a 8 granulomas por sección), y G3 (más de 8 granulomas por sección). La cuantificación de células CD68+ por mm² en las categorías N1, N2 y N3 de necrosis fue de 1,287 +/- 254; 1086 +/-181 y 930 +/- 115, respectivamente. La cuantificación de las células CD68+ fue de 483,7 +/- 396; 366,3 +/- 43 y 558 +/- 53 células por mm² para N1, N2 y N3, respectivamente. No hubo correlación estadísticamente significativa entre la extensión de la necrosis y la cuantificación celular. El número de células CD68+ fue significativamente mayor que el número de células CD8+ en las biópsias analizadas.
Subject(s)
Humans , Tuberculosis, Pleural/physiopathology , Tuberculosis, Pleural , Tuberculosis, Pleural/blood , Biopsy, Needle , /cytology , /ultrastructure , Macrophages, Alveolar/cytology , Macrophages, Alveolar/ultrastructure , Retrospective StudiesABSTRACT
AIM: To investigate the effect of CD_8+ cells from aplastic anemia (AA) patients and its histamine type II (H_2) receptors on the growth of normal CFU-Mk. METHODS: The effects of CD_8+ cells and/or cimetidine, on normal human CFU-Mk growth were studied by using CFU-Mk assay. RESULTS: The CD_8+ cells from the perpheral blood of AA patients significantly suppressed the growth of normal allogeneic CFU-Mk. This inhibitory effect was blocked by cimetidine at concentration of 1.0?10~-5 mol/L. 1.0?10~-5 mol/L cimitidine alone didn't inhibit the growth of normal CFU-Mk. CONCLUSION: H_2 receptor antagonist cimitidine abolishes the suppressive effect of AA patients CD_8+ cells on the growth of normal CFU-Mk.