100,541 research outputs found
The coincidence of glucose-6-phosphate dehydrogenase deficiency and hemoglobin s gene in çuxurova province, Turkey
No full textPubMedID: 3953546A total of 1,582 subjects from 10 villages of different ethnic populations were screened for glucose-6-phosphate dehydrogenase (G5PD deficiency (GdB-, Mediterranean variant) and hemoglobin S gene, and the coincidence of both abnormalities was determined. Although the prevalence of both abnormalities was found to be highest in an Eti-Turk group living in the Tarsus area, coincidence was not significant. In a single village of Adana Eti-Turks, however, coincidence was found to be significant, although neither the frequency of G5PD deficiency nor the existence of hemoglobin S gene was highest in that village. © 1986 by 1986 The Johns Hopkins University School of Hygiene and Public Health.Received for publication Match 19, 1985, and in final form August 8, 1985. Abbreviations: G»PD, glucose-6-phosphate dehydrogenase; Hb, hemoglobin. 1Cukurova University, Medical Faculty, Department of Hematology, Adana, Turkey. (Reprint requests to Dr. Tevfik Akoglu.) 'Cukurova University, Medical Faculty, Department of Nephrology, Adana, Turkey. This work was supported by Grant TAG-427 from the Scientific and Technical Research Council of Turkey
Letter, [Author unclear] to Paulina T. Merritt
No full textHandwritten letter to Paulina Merritt from an unknown author, October 1, 1876.
T and NK cell subset changes with microbial extracts and human HSP60-derived peptides in Behcet's disease
No full textObjective. Microorganisms such as streptococcus and autoantigens such as 60 kD heat-shock protein (HSP60) are implicated in the etiopathogenesis of Behcet's disease (BD). Methods. Peripheral blood mononuclear cells front patients with BD (n = 16) and health), controls (HC) (n = 11) were cultured for 5 days with extracts of S. sanguis-KTH-1 (SS), E. coli (EC) and a mixed peptide combination from human HSP60 (aa 136-50, 179-97, 224-58 (and 336-51) reported to be associated with BD. T and NK cell subset changes were determined by flow cytometry. Results. In unstimulated 5-day cultures gammadelta(+) (both CD4(+)gammadelta(+) and CD8(+)gammadelta(+)), CD8(+)alphabeta(+), CD4(+)CD56(+) and CD8(+)-CD11b(+) cells were increased in BD compared to HC. In antigen-stimulated cultures of BD patients CD3(+) and alphabeta(+) T cells responded to HSP60 peptides whereas EC stimulated only CD16/CD56(+) NK cells. In the control group, similar to BD, alphabeta(+) and CD4(+) T cells responded to HSP60 peptides, however SS and EC mainly activated cytotoxic T cell subsets (CD8(+)CD11b and CD4(+)-CD56(+) T cells). Conclusion. Significant increases in unstimulated T cell subsets suggest the presence of an in vivo T cell activation in BD. In both patients and controls similar patterns of responses were observed against different microorganisms, however the role of human. HSP60 peptides as immunodominant, cross-reactive antigens could not be demonstrated
T and NK cell subset changes with microbial extracts and human HSP60-derived peptides in Behçet's disease
No full textOBJECTIVE: Microorganisms such as streptococcus and autoantigens such as 60 kD heat-shock protein (HSP60) are implicated in the etiopathogenesis of Behçet's disease (BD). METHODS: Peripheral blood mononuclear cells from patients with BD (n = 16) and healthy controls (HC) (n = 11) were cultured for 5 days with extracts of S. sanguis-KTH-1 (SS), E. coli (EC) and a mixed peptide combination from human HSP60 (aa 136-50, 179-97, 224-58 and 336-51) reported to be associated with BD. T and NK cell subset changes were determined by flow cytometry. RESULTS: In unstimulated 5-day cultures gammadelta+ (both CD4+gammadelta+ and CD8+gammadelta+), CD8+alphabeta+, CD4+CD56+ and CD8+CD11b+ cells were increased in BD compared to HC. In antigen-stimulated cultures of BD patients CD3+ and alphabeta+ T cells responded to HSP60 peptides whereas EC stimulated only CD16/ CD56+ NK cells. In the control group, similar to BD, alphabeta+ and CD4+ T cells responded to HSP60 peptides, however SS and EC mainly activated cytotoxic T cell subsets (CD8+CD11b and CD4+CD56+ T cells). CONCLUSION: Significant increases in unstimulated T cell subsets suggest the presence of an in vivo T cell activation in BD. In both patients and controls similar patterns of responses were observed against different microorganisms, however the role of human HSP60 peptides as immunodominant, crossreactive antigens could not be demonstrated
Oligoclonal T cell expansions in patients with Behcet's disease
No full textBehcet's disease (BD) is a multisystem disorder with oral and genital ulcers, mucocutaneous, ocular, joint, vascular and central nervous system involvement. In this study, the peripheral T cell repertoire was analysed in patients with BD with MoAbs against T cell receptor (TCR) V beta gene products in CD4(+) and CD8(+) T cell compartments, and these were compared with rheumatoid arthritis (RA) patients and healthy controls (HC). In the CD4(+) T cell compartment, oligoclonal TCR V beta expression was observed in 56% of BD (10/18), 71% of RA (5/7) patients and 21% (3/14) of HC. In the CD8(+) T cell group 50% of BD (9/18), 57% of RA patients and 28% of HC (4/14) had an oligoclonal TCR repertoire. An increase of TCR V beta 5.1 subset was observed in five BD patients among CD8(+) T cells. Other elevations of TCR V beta subsets were heterogeneously distributed with one to three different V beta subsets. Our results suggest an antigen-driven oligoclonal increase of T cells in BD. There was no overall increase in any V beta group to suggest a superantigen effect. Analysis of the responsible antigens causing the increase in T cell subsets may give insights into the aetiopathogenesis of BD and immunomodulation of these T cells may lead to new treatments
Oligoclonal T cell expansions in patients with Behçet's disease
No full textBehçet's disease (BD) is a multisystem disorder with oral and genital ulcers, mucocutaneous, ocular, joint, vascular and central nervous system involvement. In this study, the peripheral T cell repertoire was analysed in patients with BD with MoAbs against T cell receptor (TCR) Vβ gene products in CD4+ and CD8+ T cell compartments, and these were compared with rheumatoid arthritis (RA) patients and healthy controls (HC). In the CD4+ T cell compartment, oligoclonal TCR Vβ expression was observed in 56% of BD (10/18), 71% of RA (5/7) patients and 21% (3/14) of HC. In the CD8+ T cell group 50% of BD (9/18), 57% of RA patients and 28% of HC (4/14) had an oligoclonal TCR repertoire. An increase of TCR Vβ5.1 subset was observed in five BD patients among CD8+ T cells. Other elevations of TCR Vβ subsets were heterogeneously distributed with one to three different Vβ subsets. Our results suggest an antigen-driven oligoclonal increase of T cells in BD. There was no overall increase in any Vβ group to suggest a superantigen effect. Analysis of the responsible antigens causing the increase in T cell subsets may give insights into the aetiopathogenesis of BD and immunomodulation of these T cells may lead to new treatments
T cell responses to 60/65 kDa heat shock protein derived peptides in Turkish patients with Behçet's disease
No full textOBJECTIVE: Sequence homology and cross reactivity between microbial and human heat shock proteins (HSP) led to the concept that HSP might be involved in the etiopathogenesis of Behçet's disease (BD). We investigated T cell responses to 8 synthetic peptides derived from the mycobacterial 65 kDa and homologous human 60 kDa HSP in patients with BD. METHODS: T cell proliferative responses to synthetic peptides were studied in 49 patients with BD and 46 disease (DC) and 34 healthy controls (HC) with 3H-thymidine uptake test. RESULTS: Positive T cell responses to one or more of the mycobacterial peptides were observed in 52% (12/23) of patients with BD compared with 17% (3/18) of DC (p = 0.02) and to homologous human peptides in 57% (13/23) of BD and 11% (2/18) of DC (p < 0.01). Responses to the mixtures of 4 mycobacterial peptides were also significantly higher in BD compared with controls (stimulation index in BD 4.7 +/- 3.5 vs DC 2.0 +/- 1.2, HC 1.6 +/- 0.4; BD vs DC and HC, p < 0.001). Similar elevated responses to the mixture of 4 human peptides was also observed in patients with BD (BD 3.4 +/- 2.3; DC 1.9 +/- 0.8; HC 1.4 +/- 0.6; BD vs DC, p < 0.01; BD vs HC, p < 0.001). CONCLUSION: These results suggest that cellular immunity against the 65 kDa mycobacterial and 60 kDa human HSP derived peptides is significantly increased in Turkish patients with BD compared to controls, as observed in the UK and Japan
T cell responses to 60/65 kDa heat shock protein derived peptides in Turkish patients with Behcet's disease
No full textObjective. Sequence homology and cross reactivity between microbial and human heal shuck proteins (HSP) led to the concept that HSP might be involved in the etiopathogenesis of Behcet's disease (BD). We investigated T cell responses to 8 synthetic peptides derived from the mycobacterial 65 kDa and homologous human 60 kDa HSP in patients with BD. Methods, T cell proliferative responses to synthetic peptides were studied in 49 patients with BD and 46 disease (DC) and 34 healthy controls (HC) with H-3-thymidine uptake test. Results, Positive T cell responses to one or more of the mycobacterial peptides were observed in 52% (12/23) of patients with BD compared with 17% (3/18) of DC (p = 0.02) and to homologous human peptides in 57% (13/23) of BD and 11% (2/18) of DC (p < 0.01). Responses to the mixtures of 4 mycobacterial peptides were also significantly higher in BD compared with controls (stimulation index in BD 4.7 +/- 3.5 vs DC 2.0 +/- 1.7, HC 16 +/- 0.4: BD vs DC and HC, p < 0.001). Similar elevated responses es to the mixture of 4 human peptides was also observed in patients with BD (BL) 3.4 +/- 2.3: DC 1.9 +/- 0.8; HC 1.4 +/- 0.6, BD vs DC, p < 0.01; BD vs HC, p < 0.001). Conclusion. These results suggest that cellular immunity against the 65 kDa mycobacterial and 60 kDa human HSP derived peptides is significantly increased in Turkish patients with RD compared to controls, as observed in the UK and Japan
Handwritten biographical information on Paulina T. McClung Merritt
No full textA handwritten biography of Paulina T. McClung Merritt by an unknown author, 1892.
Heterogeneous and tissue-specific regulation of effector T cell responses by IFN-gamma during Plasmodium berghei ANKA infection.
No full textIFN-γ and T cells are both required for the development of experimental cerebral malaria during Plasmodium berghei ANKA infection. Surprisingly, however, the role of IFN-γ in shaping the effector CD4(+) and CD8(+) T cell response during this infection has not been examined in detail. To address this, we have compared the effector T cell responses in wild-type and IFN-γ(-/-) mice during P. berghei ANKA infection. The expansion of splenic CD4(+) and CD8(+) T cells during P. berghei ANKA infection was unaffected by the absence of IFN-γ, but the contraction phase of the T cell response was significantly attenuated. Splenic T cell activation and effector function were essentially normal in IFN-γ(-/-) mice; however, the migration to, and accumulation of, effector CD4(+) and CD8(+) T cells in the lung, liver, and brain was altered in IFN-γ(-/-) mice. Interestingly, activation and accumulation of T cells in various nonlymphoid organs was differently affected by lack of IFN-γ, suggesting that IFN-γ influences T cell effector function to varying levels in different anatomical locations. Importantly, control of splenic T cell numbers during P. berghei ANKA infection depended on active IFN-γ-dependent environmental signals--leading to T cell apoptosis--rather than upon intrinsic alterations in T cell programming. To our knowledge, this is the first study to fully investigate the role of IFN-γ in modulating T cell function during P. berghei ANKA infection and reveals that IFN-γ is required for efficient contraction of the pool of activated T cells
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