Relevant bibliographies by topics / T-Lymphocyte Epitopes

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Academic literature on the topic 'T-Lymphocyte Epitopes'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 February 2022

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Journal articles on the topic "T-Lymphocyte Epitopes"

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Manuel, Edwin R., William A. Charini, Pritha Sen, Fred W. Peyerl, Marcelo J. Kuroda, Jörn E. Schmitz, Patrick Autissier, Dennis A. Sheeter, Bruce E. Torbett, and Norman L. Letvin. "Contribution of T-Cell Receptor Repertoire Breadth to the Dominance of Epitope-Specific CD8+ T-Lymphocyte Responses." Journal of Virology 80, no. 24 (October 11, 2006): 12032–40. http://dx.doi.org/10.1128/jvi.01479-06.

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ABSTRACT Dominant epitope-specific CD8+ T-lymphocyte responses play a central role in controlling viral spread. We explored the basis for the development of this focused immune response in simian immunodeficiency virus (SIV)- and simian-human immunodeficiency virus (SHIV)-infected rhesus monkeys through the use of two dominant (p11C and p199RY) and two subdominant (p68A and p56A) epitopes. Using real-time PCR to quantitate T-cell receptor (TCR) variable region beta (Vβ) family usage, we show that CD8+ T-lymphocyte populations specific for dominant epitopes are characterized by a diverse Vβ repertoire, whereas those specific for subdominant epitopes employ a dramatically more focused Vβ repertoire. We also demonstrate that dominant epitope-specific CD8+ T lymphocytes employ TCRs with multiple CDR3 lengths, whereas subdominant epitope-specific cells employ TCRs with a more restricted CDR3 length. Thus, the relative dominance of an epitope-specific CD8+ T-lymphocyte response reflects the clonal diversity of that response. These findings suggest that the limited clonal repertoire of subdominant epitope-specific CD8+ T-lymphocyte populations may limit the ability of these epitope-specific T-lymphocyte populations to expand and therefore limit the ability of these cell populations to contribute to the control of viral replication.
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Liu, Jinyan, Bonnie A. Ewald, Diana M. Lynch, Anjali Nanda, Shawn M. Sumida, and Dan H. Barouch. "Modulation of DNA Vaccine-Elicited CD8+ T-Lymphocyte Epitope Immunodominance Hierarchies." Journal of Virology 80, no. 24 (September 27, 2006): 11991–97. http://dx.doi.org/10.1128/jvi.01348-06.

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ABSTRACT Generating broad cellular immune responses against a diversity of viral epitopes is a major goal of current vaccine strategies for human immunodeficiency virus type 1 (HIV-1) and other pathogens. Virus-specific CD8+ T-lymphocyte responses, however, are often highly focused on a very limited number of immunodominant epitopes. For an HIV-1 vaccine, the breadth of CD8+ T-lymphocyte responses may prove to be critical as a result of the need to cover a wide diversity of viral isolates in the population and to limit viral escape from dominant epitope-specific T lymphocytes. Here we show that epitope modification strategies can alter CD8+ T-lymphocyte epitope immunodominance hierarchies elicited by a DNA vaccine in mice. Mice immunized with a DNA vaccine expressing simian immunodeficiency virus Gag lacking the dominant Db-restricted AL11 epitope generated a marked and durable augmentation of responses specific for the subdominant Db-restricted KV9 epitope. Moreover, anatomic separation strategies and heterologous prime-boost regimens generated codominant responses against both epitopes. These data demonstrate that dominant epitopes can dramatically suppress the immunogenicity of subdominant epitopes in the context of gene-based vaccines and that epitope modification strategies can be utilized to enhance responses to subdominant epitopes.
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Spencer, Juliet V., and Thomas J. Braciale. "Incomplete Cd8+ T Lymphocyte Differentiation as a Mechanism for Subdominant Cytotoxic T Lymphocyte Responses to a Viral Antigen." Journal of Experimental Medicine 191, no. 10 (May 15, 2000): 1687–98. http://dx.doi.org/10.1084/jem.191.10.1687.

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CD8+ cytotoxic T lymphocytes (CTLs) recognize antigen in the context of major histocompatibility complex (MHC) class I molecules. Class I epitopes have been classified as dominant or subdominant depending on the magnitude of the CTL response to the epitope. In this report, we have examined the in vitro memory CTL response of H-2d haplotype murine CD8+ T lymphocytes specific for a dominant and subdominant epitope of influenza hemagglutinin using activation marker expression and staining with soluble tetrameric MHC–peptide complexes. Immune CD8+ T lymphocytes specific for the dominant HA204-210 epitope give rise to CTL effectors that display activation markers, stain with the HA204 tetramer, and exhibit effector functions (i.e., cytolytic activity and cytokine synthesis). In contrast, stimulation of memory CD8+ T lymphocytes directed to the subdominant HA210-219 epitope results in the generation of a large population of activated CD8+ T cells that exhibit weak cytolytic activity and fail to stain with the HA210 tetramer. After additional rounds of restimulation with antigen, the HA210-219–specific subdominant CD8+ T lymphocytes give rise to daughter cells that acquire antigen-specific CTL effector activity and transition from a HA210 tetramer–negative to a tetramer-positive phenotype. These results suggest a novel mechanism to account for weak CD8+ CTL responses to subdominant epitopes at the level of CD8+ T lymphocyte differentiation into effector CTL. The implications of these findings for CD8+ T lymphocyte activation are discussed.
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Harcourt, Gillian C., Sarah Garrard, Miles P. Davenport, Anne Edwards, and Rodney E. Phillips. "HIV-1 Variation Diminishes CD4 T Lymphocyte Recognition." Journal of Experimental Medicine 188, no. 10 (November 16, 1998): 1785–93. http://dx.doi.org/10.1084/jem.188.10.1785.

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Effective long-term antiviral immunity requires specific cytotoxic T lymphocytes and CD4+ T lymphocyte help. Failure of these helper responses can be a principle cause of viral persistence. We sought evidence that variation in HIV-1 CD4+ T helper epitopes might contribute to this phenomenon. To determine this, we assayed fresh peripheral blood mononuclear cells from 43 asymptomatic HIV-1+ patients for proliferative responses to HIV-1 antigens. 12 (28%) showed a positive response, and we went on to map dominant epitopes in two individuals, to p24 Gag restricted by human histocompatibility leukocyte antigen (HLA)-DR1 and to p17 Gag restricted by HLA-DRB52c. Nine naturally occurring variants of the p24 Gag epitope were found in the proviral DNA of the individual in whom this response was detected. All variants bound to HLA-DR1, but three of these peptides failed to stimulate a CD4+ T lymphocyte line which recognized the index sequence. Antigenic variation was also detected in the p17 Gag epitope; a dominant viral variant present in the patient was well recognized by a specific CD4+ T lymphocyte line, whereas several natural mutants were not. Importantly, variants detected at both epitopes also failed to stimulate fresh uncultured cells while index peptide stimulated successfully. These results demonstrate that variant antigens arise in HIV-1+ patients which fail to stimulate the T cell antigen receptor of HLA class II–restricted lymphocytes, although the peptide epitopes are capable of being presented on the cell surface. In HIV-1 infection, naturally occurring HLA class II–restricted altered peptide ligands that fail to stimulate the circulating T lymphocyte repertoire may curtail helper responses at sites where variant viruses predominate.
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Loffredo, John T., Eva G. Rakasz, Juan Pablo Giraldo, Sean P. Spencer, Kelly K. Grafton, Sarah R. Martin, Gnankang Napoé, Levi J. Yant, Nancy A. Wilson, and David I. Watkins. "Tat28-35SL8-Specific CD8+ T Lymphocytes Are More Effective than Gag181-189CM9-Specific CD8+ T Lymphocytes at Suppressing Simian Immunodeficiency Virus Replication in a Functional In Vitro Assay." Journal of Virology 79, no. 23 (December 15, 2005): 14986–91. http://dx.doi.org/10.1128/jvi.79.23.14986-14991.2005.

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ABSTRACT Epitope-specific CD8+ T lymphocytes may play an important role in controlling human immunodeficiency virus (HIV)/simian immunodeficiency virus replication. Unfortunately, standard cellular assays do not measure the antiviral efficacy (the ability to suppress virus replication) of CD8+ T lymphocytes. Certain epitope-specific CD8+ T lymphocytes may be better than others at suppressing viral replication. We compared the antiviral efficacy of two immunodominant CD8+ T lymphocyte responses—Tat28-35SL8 and Gag181-189CM9—by using a functional in vitro assay. Viral suppression by Tat-specific CD8+ T lymphocytes was consistently greater than that of Gag-specific CD8+ T lymphocytes. Such differences in antigen-specific CD8+-T-lymphocyte efficacy may be important for selecting CD8+ T lymphocyte epitopes for inclusion in future HIV vaccines.
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LALVANI, Ajit, and Adrian V. S. HILL. "Cytotoxic T-lymphocytes against malaria and tuberculosis: from natural immunity to vaccine design*." Clinical Science 95, no. 5 (November 1, 1998): 531–38. http://dx.doi.org/10.1042/cs0950531.

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1. Mycobacterium tuberculosis and the liver stage of Plasmodium falciparum are intracellular pathogens which are potentially susceptible to cytotoxic T-lymphocytes, a crucial component of the protective immune response to viral infections. Evidence from animal models points to a protective role for cytotoxic T-lymphocytes against M. tuberculosis and P. falciparum, but cytotoxic T-lymphocytes specific for these pathogens have been difficult to identify in man. 2.Using a reverse immunogenetic approach, candidate epitopes from selected antigens of P. falciparum and M. tuberculosis were used to detect peptide-specific cytotoxic T-lymphocyte responses in individuals exposed to these pathogens. Cytotoxic T-lymphocyte activity was detected by the 51Cr release cytotoxicity assay and a sensitive ELISPOT assay for single-cell interferon-γ release. 3.In naturally exposed, partially immune Africans in The Gambia, eight largely conserved cytotoxic T-lymphocyte epitopes in P. falciparum, restricted by several different HLA class I alleles, were identified. Several epitopes were also recognized in Tanzanians and cytotoxic T-lymphocytes recognized endogenously processed antigen. 4.In tuberculosis patients with HLA-B52, a CD8+ cytotoxic T-lymphocyte epitope was identified in ESAT-6, a secreted antigen specific for M. tuberculosis complex but absent in BCG. Cytotoxic T-lymphocytes exhibited HLA-B52-restricted peptide-specific interferon-γ release and lytic activity and recognized endogenously processed antigen. 5.These studies demonstrate that CD8+ cytotoxic T-lymphocytes specific for mycobacterial and protozoal antigens are induced during natural infections in humans. The identification of these T-cells endorses current strategies to develop cytotoxic T-lymphocyte-inducing vaccines against P. falciparum and M. tuberculosis and highlights candidate antigens for inclusion in subunit vaccines.
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Mylin, Lawrence M., Todd D. Schell, Debra Roberts, Melanie Epler, Alina Boesteanu, Edward J. Collins, Jeffrey A. Frelinger, Sebastian Joyce, and Satvir S. Tevethia. "Quantitation of CD8+ T-Lymphocyte Responses to Multiple Epitopes from Simian Virus 40 (SV40) Large T Antigen in C57BL/6 Mice Immunized with SV40, SV40 T-Antigen-Transformed Cells, or Vaccinia Virus Recombinants Expressing Full-Length T Antigen or Epitope Minigenes." Journal of Virology 74, no. 15 (August 1, 2000): 6922–34. http://dx.doi.org/10.1128/jvi.74.15.6922-6934.2000.

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ABSTRACT The cytotoxic T-lymphocyte response to wild-type simian virus 40 large tumor antigen (Tag) in C57BL/6 (H2b ) mice is directed against three H2-Db -restricted epitopes, I, II/III, and V, and oneH2-Kb -restricted epitope, IV. Epitopes I, II/III, and IV are immunodominant, while epitope V is immunorecessive. We investigated whether this hierarchical response was established in vivo or was due to differential expansion in vitro by using direct enumeration of CD8+ T lymphocytes with Tag epitope/major histocompatibility complex class I tetramers and intracellular gamma interferon staining. The results demonstrate that epitope IV-specific CD8+ T cells dominated the Tag-specific response in vivo following immunization with full-length Tag while CD8+ T cells specific for epitopes I and II/III were detected at less than one-third of this level. The immunorecessive nature of epitope V was apparent in vivo, since epitope V-specific CD8+ T cells were undetectable following immunization with full-length Tag. In contrast, high levels of epitope V-specific CD8+ T lymphocytes were recruited in vivo following immunization and boosting with a Tag variant in which epitopes I, II/III, and IV had been inactivated. In addition, analysis of the T-cell receptor β (TCRβ) repertoire of Tag epitope-specific CD8+ cells revealed that multiple TCRβ variable regions were utilized for each epitope except Tag epitope II/III, which was limited to TCRβ10 usage. These results indicate that the hierarchy of Tag epitope-specific CD8+T-cell responses is established in vivo.
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Lucchiari-Hartz, Maria, Peter M. van Endert, Grégoire Lauvau, Reinhard Maier, Andreas Meyerhans, Derek Mann, Klaus Eichmann, and Gabriele Niedermann. "Cytotoxic T Lymphocyte Epitopes of HIV-1 Nef." Journal of Experimental Medicine 191, no. 2 (January 17, 2000): 239–52. http://dx.doi.org/10.1084/jem.191.2.239.

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Although a pivotal role of proteasomes in the proteolytic generation of epitopes for major histocompatibility complex (MHC) class I presentation is undisputed, their precise function is currently the subject of an active debate: do proteasomes generate many epitopes in definitive form, or do they merely generate the COOH termini, whereas the definitive NH2 termini are cleaved by aminopeptidases? We determined five naturally processed MHC class I ligands derived from HIV-1 Nef. Unexpectedly, the five ligands correspond to only three cytotoxic T lymphocyte (CTL) epitopes, two of which occur in two COOH-terminal length variants. Parallel analyses of proteasomal digests of a Nef fragment encompassing the epitopes revealed that all five ligands are direct products of proteasomes. Moreover, in four of the five ligands, the NH2 termini correspond to major proteasome cleavage sites, and putative NH2-terminally extended precursor fragments were detected for only one of the five ligands. All ligands are transported by the transporter associated with antigen processing (TAP). The combined results from these five ligands provide strong evidence that many definitive MHC class I ligands are precisely cleaved at both ends by proteasomes. Additional evidence supporting this conclusion is discussed, along with contrasting results of others who propose a strong role for NH2-terminal trimming with direct proteasomal epitope generation being a rare event.
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Vijh, Sujata, Ingrid M. Pilip, and Eric G. Pamer. "Noncompetitive Expansion of Cytotoxic T Lymphocytes Specific for Different Antigens during Bacterial Infection." Infection and Immunity 67, no. 3 (March 1, 1999): 1303–9. http://dx.doi.org/10.1128/iai.67.3.1303-1309.1999.

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ABSTRACT Listeria monocytogenes is an intracellular bacterium that elicits complex cytotoxic T-lymphocyte (CTL) responses in infected mice. The responses of CTL populations that differ in antigen specificity range in magnitude from large, dominant responses to small, subdominant responses. To test the hypothesis that dominant T-cell responses inhibit subdominant responses, we eliminated the two dominant epitopes of L. monocytogenes by anchor residue mutagenesis and measured the T-cell responses to the remaining subdominant epitopes. Surprisingly, the loss of dominant T-cell responses did not enhance subdominant responses. While mice immunized with bacteria lacking dominant epitopes developed L. monocytogenes-specific immunity, their ability to respond to dominant epitopes upon rechallenge with wild-type bacteria was markedly diminished. Recall responses in mice immunized with wild-type or epitope-deficient L. monocytogenes showed that antigen presentation during recall infection is sufficient for activating memory cells yet insufficient for optimal priming of naive T lymphocytes. Our findings suggest that T-cell priming to different epitopes during L. monocytogenes infection is not competitive. Rather, T-cell populations specific for different antigens but the same pathogen expand independently.
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Friedrich, Thomas C., Adrian B. McDermott, Matthew R. Reynolds, Shari Piaskowski, Sarah Fuenger, Ivna P. de Souza, Richard Rudersdorf, et al. "Consequences of Cytotoxic T-Lymphocyte Escape: Common Escape Mutations in Simian Immunodeficiency Virus Are Poorly Recognized in Naïve Hosts." Journal of Virology 78, no. 18 (September 15, 2004): 10064–73. http://dx.doi.org/10.1128/jvi.78.18.10064-10073.2004.

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ABSTRACT Cytotoxic T lymphocytes (CTL) are associated with control of immunodeficiency virus infection but also select for variants that escape immune recognition. Declining frequencies of epitope-specific CTL frequencies have been correlated with viral escape in individual hosts. However, escape mutations may give rise to new epitopes that could be recognized by CTL expressing appropriate T-cell receptors and thus still be immunogenic when escape variants are passed to individuals expressing the appropriate major histocompatibility complex class I molecules. To determine whether peptide ligands that have been altered through escape can be immunogenic in new hosts, we challenged naïve, immunocompetent macaques with a molecularly cloned simian immunodeficiency virus (SIV) bearing common escape mutations in three immunodominant CTL epitopes. Responses to the altered peptides were barely detectable in fresh samples at any time after infection. Surprisingly, CTL specific for two of three escaped epitopes could be expanded by in vitro stimulation with synthetic peptides. Our results suggest that some escape variant epitopes evolving in infected individuals do not efficiently stimulate new populations of CTL, either in that individual or upon passage to new hosts. Nevertheless, escape variation may not completely abolish an epitope's immunogenicity. Moreover, since the mutant epitope sequences did not revert to wild type during the study period, it is possible that low-frequency CTL exerted enough selective pressure to preserve epitope mutations in viruses replicating in vivo.
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Dissertations / Theses on the topic "T-Lymphocyte Epitopes"

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DeMille, Janet. "Mapping the cytotoxic T-lymphocyte epitopes of Pichinde virus." Thesis, University of Ottawa (Canada), 1994. http://hdl.handle.net/10393/6495.

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One of the aims of this study was to determine whether the glycoproteins of Pichinde virus harbour any cytotoxic T-lymphocyte (CTL) epitopes on the murine haplotypes, H-2$\sp{\rm b}$ and H-2$\sp{\rm d}$ since, on neither of these MHC backgrounds are there any CTL epitopes on the nucleoprotein of this virus. Using a vaccinia virus recombinant, vvGPC, which expresses the full-length glycoprotein precursor (GPC) of Pichinde virus, standard chromium release CTL assays were performed. Three independent assays are shown for each of the haplotypes. In each of these assays for both of the haplotypes, it was observed that CTL derived against Pichinde virus did not recognize vvGPC-infected target cells nor did CTL derived against vvGPc recognize Pichinde-infected target cells. This indicates that no CTL were generated with either virus that might recognize the glycoproteins of Pichinde virus and, therefore, that the glycoproteins do not contain CTL epitopes on these murine MHC backgrounds. A second aim of this work was to compare the CTL epitopes of Pichinde wild-type virus with two temperature sensitive mutants derived from it. Both these mutants have been shown to be defective in their glycoprotein processing. The H-2$\sp{\rm d}$-restricted epitopes appear to be disrupted in TS13 as it is not recognized by Pichinde-specific CTL derived on this background. TS908 is not recognized by Pichinde-specific CTL on either haplotype suggesting that the wild-type virus' epitopes were probably disrupted during the derivation of this mutant. (Abstract shortened by UMI.)
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Petersson, Max. "Immunity and immunosuppression in the tumor-host interaction /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3931-4/.

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Borgo, Adriana Coutinho. "Caracterização fenotípica e funcional de linfócitos T de memória de indivíduos infectados pelo HIV reativos a epitopos T CD4+ derivados de sequências do consenso B do HIV-1." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/5/5146/tde-28042010-171033/.

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A persistência de células T de memória funcionais é importante para garantir uma imunidade protetora na infecção pelo Vírus da Imunodeficiência Humana (HIV). As células T de memória têm sido subdivididas em memória central (TCM), memória efetora (TEM) e memória efetora altamente diferenciada (TEMRA) com base na expressão de moléculas de superfície como CCR7 e CD45RA, e na capacidade de produzir citocinas e proliferar. Recentemente, identificamos 18 peptídeos derivados de seqüências do consenso B do HIV-1, ligadores de múltiplas moléculas HLA-DR e amplamente reconhecidos por linfócitos T de sangue periférico de pacientes infectados pelo HIV. Diante disso e considerando a importância das células T de memória na manutenção da resposta imune específica, nosso objetivo foi caracterizar fenotípica e funcionalmente as subpopulações de células T de memória de indivíduos infectados pelo HIV envolvidas no reconhecimento in vitro desses epitopos. Foram incluídos 14 indivíduos controles sadios e 61 pacientes HIV+ com contagem de linfócitos T CD4+ maior que 250 células/mm3. Os pacientes HIV+ foram divididos em seis diferentes grupos clínicos de acordo com o estágio da infecção, carga viral (CV) plasmática e uso de terapia anti-retroviral (ART): não progressores por longo tempo (LTNP), avirêmicos em uso de ART (AV-ART), virêmicos em uso de ART (VI-ART), virêmicos sem uso de ART (VI sem ART), virêmicos recéminfectados sem uso de ART (VI-RI) e controladores. Células mononucleares do sangue periférico dos indivíduos do estudo foram estimuladas com o conjunto de peptídeos do HIV-1 e com um conjunto de peptídeos do Citomegalovírus (CMV). A freqüência de células de memória produtoras de IFN- e IL-2 e a proliferação celular antígeno-específica foram detectadas por citometria de fluxo de multiparâmetros. Nossos resultados mostraram que o conjunto de peptídeos do HIV-1 foi capaz de ativar subpopulações funcionais de memória TCM, TEM e TEMRA secretoras de IFN- e IL-2 em 100% dos pacientes HIV+ dos diferentes grupos clínicos. O conjunto de peptídeos do HIV-1 também induziu proliferação das subpopulações de linfócitos T de memória. As freqüências de TEMRA CD4+IFN-+, TEMRA CD4+IFN-+ total, TCM CD8+IFN-+, TCM CD8+IFN-+ total, TEM CD8+IFN-+, TEM CD8+IFN-+ total e TEMRA CD8+IFN-+ correlacionaram-se negativamente com a carga viral do HIV em pacientes virêmicos. Esses dados sugerem que essas subpopulações de memória funcionais são importantes no controle da viremia. Comparando as respostas HIV e CMVespecíficas observamos freqüências mais elevadas de células T de memória produtoras de IL-2, IFN-/IL-2 e IFN- em respostas ao pool de peptídeos do HIV. Esses dados sugerem que esse conjunto de peptídeos derivados de seqüências do HIV-1 ativa respostas polifuncionais de subpopulações de linfócitos T de memória. Nossos resultados mostraram que o conjunto de peptídeos do HIV-1 foi capaz de estimular diferentes subpopulações distintas de linfócitos T de memória produtores de IFN-, IFN-,/IL-2 e IL-2 de indivíduos em diferentes estágios da infecção pelo HIV e sugerem o envolvimento de subpopulações de memória funcionais no controle da viremia. Estes achados fortalecem a possibilidade de uso desses peptídeos em uma formulação vacinal bem-sucedida em humanos
The persistence of functional memory T cell is important to ensure a protective immunity to Human Immunodeficiency Virus (HIV) infection. Memory T cells have been subdivided into central memory (TCM), effector memory (TEM) and highly differentiated effector memory (TEMRA) based on the expression of surface molecules such as CCR7 and CD45RA, and the ability to produce cytokines and proliferate. Recently, we identified 18 peptides derived from B consensus sequences of HIV-1 that bind to multiple HLA-DR molecules and are widely recognized by peripheral blood T lymphocytes from HIV-infected patients. Given this and considering the importance of memory T cells in the maintenance of specific immune response, our objective was to characterize phenotypic and functionally memory T cell subsets from HIV-infected individuals involved in the recognition of these epitopes in vitro. The study included 14 healthy control subjects and 61 HIV+ patients with CD4+ lymphocytes counts higher than 250 cells/mm3. The HIV+ patients were divided into six different clinical groups according to the stage of infection, plasma viral load (VL) and antiretroviral therapy use (ART): long-term non-progressors (LTNP), aviremic under ART (AV-ART), viremic under ART (VI-ART), viremic without using ART (VI without ART), recently infected viremic without using ART (VI-RI) and controllers. Peripheral blood mononuclear cells from study subjects were stimulated with HIV-1 peptide pool and with a cytomegalovirus (CMV) peptide pool. The frequencies of IFN- and IL-2 producing memory cells and antigenspecific cell proliferation were detected by multiparametric flow cytometry. Our results showed that the HIV-1 set of peptides was able to activate TCM, TEM and TEMRA functional memory subsets that secrete IFN- and IL-2 in 100% of the HIV patients from the different clinical groups. The HIV-1 set of peptides also induced memory T lymphocyte subsets proliferation. TEMRA CD4+IFN-+, total TEMRA CD4+IFN-+, TCM CD8+IFN-+, total TCM CD8+IFN-+, total TEM CD8+IFN-+, TEM CD8+IFN-+ and TEMRA CD8+IFN- + frequencies negatively correlated with HIV viral load in viremic patients. These data suggest that these functional memory subsets are important to control the viremia. When comparing the HIV and CMV-specific responses we observed higher frequencies of IL-2, IFN-/IL-2 and IFN- producing memory T cells in response to HIV peptide pool. These data suggest that this set of HIV sequence derived peptides activates polyfunctional response of memory T lymphocyte subsets. Our results showed that the HIV-1 peptide set was able to stimulate different IFN-, IFN-/IL-2 e IL-2 producing memory T lymphocytes from individuals in different stages of HIV infection and suggest the involvement of functional memory subsets in the control of viremia. These findings strengthen the possibility of using these peptides in a successful vaccine formulation in humans
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Novak, Erik Joseph. "Tracking antigen-specific immune responses in human infection and disease /." Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/5084.

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Wipke, Brian Todd. "Epitope immunodominance and the murine cytotoxic T lymphocyte response to Listeria monocytogenes /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/8345.

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McMahan, Rachel H. "Relating TCR-peptide-MHC affinity to immunogenicity for the design of tumor vaccines /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2007.

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Thesis (Ph.D. in Immunology) -- University of Colorado Denver, 2007.
Typescript. Includes bibliographical references (leaves 133-156). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;
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Yin, Liusong. "Studies of HLA-DM in Antigen Presentation and CD4+ T Cell Epitope Selection: A Dissertation." eScholarship@UMMS, 2014. http://escholarship.umassmed.edu/gsbs_diss/700.

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Antigen presented to CD4+ T cells by major histocompatibility complex class II molecules (MHCII) plays a key role in adaptive immunity. Antigen presentation is initiated by the proteolytic cleavage of pathogenic or self proteins and loading of resultant peptides to MHCII. The loading and exchange of peptides to MHCII is catalyzed by a nonclassical MHCII molecule, HLA-DM (DM). It is well established that DM promotes peptide exchange in vitro and in vivo. However, the mechanism of DM-catalyzed peptide association and dissociation, and how this would affect epitope selection in human responses to infectious disease remain unclear. The work presented in this thesis was directed towards the understanding of mechanism of DM-mediated peptide exchange and its role in epitope selection. In Chapter II, I measured the binding affinity, intrinsic dissociation half-life and DM-mediated dissociation half-life for a large set of peptides derived from vaccinia virus and compared these properties to the peptide-specific CD4+ T cell responses. These data indicated that DM shapes the peptide repertoire during epitope selection by favoring the presentation of peptides with greater DM-mediated kinetic stability, and DM-susceptibility is a strong and independent factor governing peptide immunogenicity. In Chapter III, I computationally simulated peptide binding competition reactions and found that DM influences the IC50 (50% inhibition concentration) of peptides based on their susceptibility to DM, which was confirmed by experimental data. Therefore, I developed a novel fluorescence polarization-based method to measure DM-susceptibility, reported as a IC50 (change in IC50 in the absence and presence of DM). Traditional assays to measure DM-susceptibility based on differential peptide dissociation rates are cumbersome because each test peptide has to be individually labeled and multiple time point samples have to be collected. However, in this method developed here only single probe peptide has to be labeled and only single reading have to be done, which allows for fast and high throughput measure of DM-susceptibility for a large set of peptides. In Chapter IV, we generated a series of peptide and MHCII mutants, and investigated their interactions with DM. We found that peptides with non-optimal P1 pocket residues exhibit low MHCII affinity, low kinetic stability and high DM-susceptibility. These changes were accompanied with conformational alterations detected by surface plasmon resonance, gel filtration, dynamic light scattering, small-angle X-ray light scattering, antibody-binding, and nuclear magnetic resonance assays. Surprisingly, all these kinetic and conformational changes could be reversed by reconstitution with a more optimal P9 pocket residue. Taken together, our data demonstrated that conformation of MHCII-peptide complex constrained by interactions throughout the peptide binding groove is a key determinant of DM-susceptibility. B cells recognizing cognate antigen on the virion can internalize and process the whole virion for antigen presentation to CD4+ T cells specific for an epitope from any of the virion proteins. In turn, the epitope-specific CD4+ T cells provide intermolecular (also known as noncognate or heterotypic) help to B cells to generate antibody responses against any protein from the whole virion. This viral intermolecular help model in which CD4+ T cells provide help to B cells with different protein specificities was established in small size influenza virus, hepatitis B virus and viral particle systems. For large and complex pathogens such as vaccinia virus and bacteria, the CD4+ T cell-B cell interaction model may be complicated because B cells might not be able to internalize the large whole pathogen. Recently, a study in mice observed that CD4+ T cell help is preferentially provided to B cells with the same protein specificity to generate antibody responses against vaccinia virus. However, for larger pathogens such as vaccinia virus and bacteria the CD4+ T cell-B cell interaction model has yet to be tested in humans. In Chapter V, I measured in 90 recently vaccinated and 7 long-term vaccinia-immunized human donors the CD4+ T cell responses and antibody responses against four vaccinia viral proteins (A27L, A33R, B5R and L1R) known to be strongly targeted by cellular and humoral responses. We found that there is no direct linkage between antibody and CD4+ T cell responses against each protein. However, the presence of immune responses against these four proteins is linked together within donors. Taken together, our data indicated that individual viral proteins are not the primary recognition unit and CD4+ T cells provide intermolecular help to B cells to generate robust antibody responses against large and complicated vaccinia virus in humans.
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Smidt, Werner. "In silico discovery of novel cytotoxic T-lymphocyte epitopes in the HIV-1 Pol region in response to antiretroviral resistance mutations." Thesis, University of Pretoria, 2014. http://hdl.handle.net/2263/46185.

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The Acquired Immunode ciency Syndrome pandemic continues to have a large social impact. Many advances in the treatment of infection by the causative agent, Human Immunode ciency Virus, have been made in the last three decades. However, this treatment often means a life-long rigorous adherence to treatment and acquisition of resistance mutations to antiretrovirals. Thus far, the e cacy of promising vaccines has been disappointing. In the last decade, interest has grown concerning the interaction between mutations conferring resistance to antiretrovirals and the e ect this has on epitopes recognized by cytotoxic-T-lymphocytes (CTL). Investigating this is a di cult task, owing to both the extreme polymorphism of HIV and the polymorphism of the Human Leukocyte Antigen (HLA) molecules that present peptides to the CTLs. A large amount of HLA-associated CTL escape mutations have been discovered. Together with this, computational approaches in CTL epitope discovery is becoming increasingly accurate. Here, a method of imputing HLA type from patients together with predicting the in uence of anitretroviral mutations was used to discover potential epitopes for the HLA B*15 and B*48 types in the HIV-1 Subtype B pol region.
Thesis (PhD)--University of Pretoria, 2014.
tm2015
Biochemistry
PhD
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Yaciuk, Jane Cherie. "Mechanisms of T cell tolerance to the RNA-binding nuclear autoantigen human La/SS-B." Oklahoma City : [s.n.], 2008.

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Townsley, Elizabeth. "CD8+ T Cell and NK Responses to a Novel Dengue Epitope: A Possible Role for KIR3DL1 in Dengue Pathogenesis: A Dissertation." eScholarship@UMMS, 2004. http://escholarship.umassmed.edu/gsbs_diss/709.

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Variation in the sequence of T cell epitopes between dengue virus (DENV) serotypes is believed to alter memory T cell responses during second heterologous infections contributing to pathology following DENV infection. We identified a highly conserved, novel, HLA-B57-restricted epitope on the DENV NS1 protein, NS126-34. We predicted higher frequencies of NS126-34-specific CD8+ T cells in PBMC from individuals undergoing secondary, rather than primary, DENV infection due to the expansion of memory CD8+T cells. We generated a tetramer against this epitope (B57-NS126-34TET) and used it to assess the frequencies and phenotype of antigen-specific T cells in samples from a clinical cohort of children with acute DENV infection established in Bangkok, Thailand. High tetramer-positive T cell frequencies during acute infection were seen in only 1 of 9 subjects with secondary infection. B57-NS126-34-specific, other DENV epitope-specific CD8+ T cells, as well as total CD8+ T cells, expressed an activated phenotype (CD69+ and/or CD38+) during acute infection. In contrast, expression of CD71 was largely limited to DENV-specific CD8+ T cells. In vitro stimulation of CD8+ T cell lines, generated against three different DENV epitopes, indicated that CD71 expression was differentially sensitive to stimulation by homologous and heterologous variant peptides with substantial upregulation of CD71 detected to peptides which also elicited strong functional responses. CD71 may therefore represent a useful marker of antigenspecific T cell activation. During the course of our analysis we found substantial binding of B57-NS126-34 TET to CD8- cells. We demonstrated that the B57-NS126-34 TET bound KIR3DL1, an inhibitory receptor on natural killer (NK) cells. NK sensitive target cells presenting the NS126-34 peptide in the context of HLA-B57 were able to dampen functional responses of only KIR3DL1+ NK cells. Analysis of the activation of an NK enriched population in our Thai cohort revealed peak activation during the critical time phase in patients with severe dengue illness, dengue hemorrhagic fever, compared to people with mild illness. Our data identified CD71 as biologically useful marker to study DENV-specific CD8+ T cell responses and highlighted the role of viral peptides in modulating NK cell activation through KIR-MHC class I interactions during DENV infection.
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Books on the topic "T-Lymphocyte Epitopes"

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Korber, Bette. HIV molecular immunology 2006/2007. Edited by Los Alamos National Laboratory. Theoretical Biology and Biophysics Group T-10. Los Alamos, N.M: Los Alamos National Laboratory, Theoretical Biology and Biophysics Group T-10, 2006.

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Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0074_update_001.

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Individuals appear to be predisposed to antiglomerular basement membrane (anti-GBM) disease by carrying a predisposing human leucocyte antigen type, DRB1*1501 being identified as the highest risk factor, and there are likely to be other predisposing genes or influences on top of which a relatively rare ‘second hit’ leads to the development of autoimmunity. In anti-GBM disease this appears to have a self-perpetuating, accelerating component, that may be to do with antibodies and altered antigen presentation. Lymphocyte depletion may also predispose to the disease. A number of second hits have been identified and they seem to share a theme of damage to the glomerulus. There may be a prolonged (months to years) and usually subclinical phase in anti-GBM disease in which usually relatively low level antibody titres are associated with variable haematuria, sometimes minor pulmonary haemorrhage, but often no symptoms. Damage to the lung seems to determine whether there is a pulmonary component to the disease. Without pulmonary damage caused typically by smoking, inhalation of other fumes, and potentially infection or oxygen toxicity, the disease remains an isolated kidney disease. Antibodies appear to be an important component of the disease, but cell-mediated immunity is also critical to the clinical picture. In animal models, cell-mediated immunity triggered by the GBM antigen can cause severe renal damage in the absence of pathogenic antibody. The development of specific antibody also requires T-cell sensitization and help, and suppressing the response is likely to require suppressing both antibody and cell-mediated immunity. Antibodies recognize one major and some other epitopes, which are now well described. T-cell epitopes are becoming better understood. Evidence from animal models also suggests that the damage in anti-GBM disease is dependent on complement, macrophages, and neutrophils.
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Book chapters on the topic "T-Lymphocyte Epitopes"

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Lundin, Knut E. A., Gustav Gaudernack, Gunnar Paulsen, Ludvig M. Sollid, and Erik Thorsby. "Epitopes on HLA-DQw3 Molecules Recognized by T-Lymphocyte Clones." In Immunobiology of HLA, 289–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-39946-0_104.

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Mitchison, N. A. "Epitope Selection and Autoimmunity." In T Lymphocytes, 75–87. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3054-1_8.

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Cerny, A., C. Ferrari, and F. V. Chisari. "The Class I-Restricted Cytotoxic T Lymphocyte Response to Predetermined Epitopes in the Hepatitis B and C Viruses." In Current Topics in Microbiology and Immunology, 169–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78530-6_10.

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Higashimoto, Yuichiro, Cara C. Wilson, Brent Palmer, Scott Southwood, John Sidney, Ettore Appella, Robert Chesnut, Alessandro Sette, and Brian D. Livingston. "Identification of Conserved HIV-1-Derived Helper T Lymphocyte Epitopes Using Synthetic Peptides and High Throughput Binding Assays." In Peptides: The Wave of the Future, 1039–40. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0464-0_486.

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Linnemann, Thomas, Carsten Brock, Katrin Sparbier, Marcus Muche, Arlett Mielke, Ansgar Lukowsky, Wolfram Sterry, Kelt Kaltoft, Karl-Heinz Wiesmüller, and Peter Walden. "Identification of Epitopes for CTCL-Specific Cytotoxic T Lymphocytes." In Advances in Experimental Medicine and Biology, 231–35. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5357-1_36.

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Hurtgen, Brady J., and Chiung-Yu Hung. "Rational Design of T Lymphocyte Epitope-Based Vaccines Against Coccidioides Infection." In Methods in Molecular Biology, 45–64. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7104-6_4.

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Adorini, L., C. Bove, M. Darsley, E. Appella, and G. Doria. "Mapping of Antigen Epitopes Interacting with Class II MHC Products and with the Antigen Receptor of T Lymphocytes." In Macromolecular Biorecognition, 279–87. Totowa, NJ: Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4600-8_24.

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Ozato, Keiko, David Koeller, Ronald Lieberman, Jun-ichi Miyazaki, Ettore Appella, Donald W. Mann, and James Forman. "Site Directed Mutagenesis Identifies Allo-Antigenic Epitopes of an H-2 Antigen Recognized by Antibodies and by Cytotoxic T-Lymphocytes." In H-2 Antigens, 177–84. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4757-0764-9_17.

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H. Ravindranath, Mepur, and Fatiha E.L. Hilali. "Monospecific and Polyreactive Monoclonal Antibodies against Human Leukocyte Antigen-E: Diagnostic and Therapeutic Relevance." In Monoclonal Antibodies. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95235.

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A monoclonal antibody (mAb) binds to an antigen recognizing an epitope (a sequence of amino acids). A protein antigen may carry amino acid sequence unique to that antigen as well as sequences found in other proteins. Human leukocyte antigens (HLA), a family of proteins expressed by the Major Histocompatibility Complex gene family represent a special case, in that it displays a high degree of polymorphism. Every HLA molecule possesses both specific (private) epitopes and epitopes shared (public) with other HLA class Ia and class Ib molecules. HLA-E is overexpressed in cancer cells more than any other HLA Class I molecules. Therefore specific localization of HLA-E with mAbs is pivotal for developing targeted therapy against cancer. However, the commercially available mAbs for immunodiagnosis are polyreactive. We have developed anti-HLA-E mAbs and distinguished monospecific from polyreactive mAbs using Luminex multiplex single antigen bead (SAB) assay. HLA-E-binding of monospecific-mAbs was also inhibited by E-restricted epitopes. The amino acid sequences in the region of the epitopes bind to CD94/NKG2A receptors on CD8+ T cells and NK cells and block their antitumor functions. Monospecific-HLA-E mAbs recognizing the epitopes sequences can interfere with the binding to restore the anti-tumor efficacy of NK cells. Also, monospecific-mAbs augment the proliferation of CD4-/CD+ cytotoxic T-lymphocytes. Therefore, anti-HLA-E monospecific-mAb can serve as a double-edged sword for eliminating tumor cells.
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"Distinct Epitopes for Kd-Restricted Cytolytic T Cells Specific for HLA-CW3 or HLA-A24 Map to the same Region of HLA." In Lymphocyte Activation and Differentiation, 819–22. De Gruyter, 1988. http://dx.doi.org/10.1515/9783110850253-136.

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Conference papers on the topic "T-Lymphocyte Epitopes"

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Wang, Fei-peng, and Xian-hui He. "Prediction of HLA-A*0201 Restricted Cytotoxic T Lymphocyte Epitopes in Influenza A H1N1 Virus and the Similarity Analysis of These Epitopes with Those Existing in Other Influenza Viruses." In 2010 4th International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2010. http://dx.doi.org/10.1109/icbbe.2010.5515558.

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Reports on the topic "T-Lymphocyte Epitopes"

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Hogan, Kevin T. Identification and Characterization of Ovarian Carcinoma Peptide Epitopes Recognized by Cytotoxic T Lymphocytes. Fort Belvoir, VA: Defense Technical Information Center, November 2006. http://dx.doi.org/10.21236/ada462674.

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Hogan, Kevin T. Identification and Characterization of Ovarian Carcinoma Peptide Epitopes Recognized by Cytotoxic T Lymphocytes. Fort Belvoir, VA: Defense Technical Information Center, November 2007. http://dx.doi.org/10.21236/ada482936.

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3

Hogan, Kevin T. Identification and Characterization of Ovarian Carcinoma Peptide Epitopes Recognized by Cylotoxic T Lymphocytes. Fort Belvoir, VA: Defense Technical Information Center, November 2008. http://dx.doi.org/10.21236/ada510798.

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