15 research outputs found
Mycobacterial ESAT-6 and katG are Recognized by Sarcoidosis CD4+ T Cells When Presented by the American Sarcoidosis Susceptibility Allele, DRB1*1101
Criticizing and Evaluating the Translation of Mohammad Dashti from Nahj al-Balagha Based on the Model of Garcias (Case Study: Translation of the First Khotbeh and Hekamts One to Twenty)
Nahj al-Balaghah is one of the most important and authentic religious sources that has come to the fore of knowledge and bounty since its creation. Several translators have been devoted to explaining this valuable masterpiece by Amir al-Mu'minin (AS). But the question is, how far have these translations been able to introduce and transmit the miracle, power, and acceptance of the Amir's words to the Persian language community in the best way? The present study was conducted by descriptive-analytical method with the aim of evaluating the quality of translation from Nahj al-Balaghah by Mohammad Dashti. Among the various patterns of translation quality assessment, the Garcias model, which is relatively more comprehensive than the other proposed models, is considered as a research framework. This model includes four levels of lexical semantics, syntactic, cognitive, discursive-functional, and cognitive (practical) style. Each of these levels has subcategories and specific components whose translations are evaluated based on them. In this research, the translation of the first Khotbeh and the Hekamts one to twenty from the so-called translator are selected and evaluated for qualitative evaluation. After determining the abundance of each subgroup in the quadric levels according to the Garcias model, the results are plotted. The result of the evaluation based on the positive, negative and neutral techniques indicates that the translation of the plain has a criterion of acceptability and is of high quality
Cellular Recognition of Mycobacterium tuberculosis ESAT-6 and KatG Peptides in Systemic Sarcoidosis
Sarcoidosis is an enigmatic disease with a pathology similar to that of tuberculosis. We detected Th-1 immune responses to Mycobacterium tuberculosis ESAT-6 and KatG peptides from peripheral blood mononuclear cells from 15/26 sarcoidosis, 1/24 purified-protein-derivative-negative (PPD−) (P < 0.0001, Fisher's exact test), and 7/8 PPD-positive (PPD+) subjects (P = 0.21). This finding provides immunologic links between mycobacteria and systemic sarcoidosis
Cellular Responses to Mycobacterial Antigens Are Present in Bronchoalveolar Lavage Fluid Used in the Diagnosis of Sarcoidosisâ–¿ â€
Considerable evidence supports the concept that CD4+ T cells are important in sarcoidosis pathogenesis, but the antigens responsible for the observed Th1 immunophenotype remain elusive. The epidemiologic association with bioaerosols and the presence of granulomatous inflammation support consideration of mycobacterial antigens. To explore the role of mycobacterial antigens in sarcoidosis immunopathogenesis, we assessed the immune recognition of mycobacterial antigens, the 6-kDa early secreted antigenic protein (ESAT-6) and catalase-peroxidase (KatG), by T cells derived from bronchoalveolar lavage (BAL) fluid obtained during diagnostic bronchoscopy. We report the presence of antigen-specific recognition of ESAT-6 and KatG in T cells from BAL fluid of 32/44 sarcoidosis subjects, compared to 1/27 controls (P < 0.0001). CD4+ T cells were primarily responsible for immune recognition (32/44 sarcoidosis subjects), although CD8+ T-cell responses were observed (25/41 sarcoidosis subjects). Recognition was significantly absent from BAL fluid cells of patients with other lung diseases, including infectious granulomatous diseases. Blocking of Toll-like receptor 2 reduced the strength of the observed immune response. The presence of immune responses to mycobacterial antigens in cells from BAL fluid used for sarcoidosis diagnosis suggests a strong association between mycobacteria and sarcoidosis pathogenesis. Inhibition of immune recognition with monoclonal antibody against Toll-like receptor 2 suggests that induction of innate immunity by mycobacteria contributes to the polarized Th1 immune response
Superoxide dismutase A antigens derived from molecular analysis of sarcoidosis granulomas elicit systemic Th-1 immune responses-2
Ecognized sodA, recognition of more than one peptide was frequently observed. Peptides 36 and 38 were frequently immunogenic, although there was variation in the magnitude of the response generated by each subject. Numerous sodA peptides were recognized by PPD+ subjects. A representative analysis of the PPD+ subjects is included. The recognition of multiple sodA peptides by the sarcoidosis subjects suggests that the sarcoidosis Th-1 immune response may be elicited by multiple antigenic peptides rather than a single dominant antigen.<p><b>Copyright information:</b></p><p>Taken from "Superoxide dismutase A antigens derived from molecular analysis of sarcoidosis granulomas elicit systemic Th-1 immune responses"</p><p>http://respiratory-research.com/content/9/1/36</p><p>Respiratory Research 2008;9(1):36-36.</p><p>Published online 25 Apr 2008</p><p>PMCID:PMC2383887.</p><p></p
Superoxide dismutase A antigens derived from molecular analysis of sarcoidosis granulomas elicit systemic Th-1 immune responses-0
) among 10 of 12 sarcoidosis specimens, represented by Sarcoidosis 3. Region 4 of Sarcoid 2 contained the same nucleotide substitution as Sarcoid 15 (A302G), resulting in the amino acid substitution D101G (Figure 1A). The two sarcoidosis samples were processed three months apart. Phylogenetic analysis of the amplicons placed all the sequences as most consistent with members of MTB complex, but noted that the sequences detected in Sarcoid 2 and 15 were distinct from other members, including the 10 sarcoidosis samples (Figure 1B).<p><b>Copyright information:</b></p><p>Taken from "Superoxide dismutase A antigens derived from molecular analysis of sarcoidosis granulomas elicit systemic Th-1 immune responses"</p><p>http://respiratory-research.com/content/9/1/36</p><p>Respiratory Research 2008;9(1):36-36.</p><p>Published online 25 Apr 2008</p><p>PMCID:PMC2383887.</p><p></p