Relevant bibliographies by topics / Th1 and Th17 cells

Academic literature on the topic 'Th1 and Th17 cells'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Th1 and Th17 cells"

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Chen, Junwei, Junxia Li, Huiying Gao, Caihong Wang, Jing Luo, Zhiqin Lv, and Xiaofeng Li. "Comprehensive Evaluation of Different T-Helper Cell Subsets Differentiation and Function in Rheumatoid Arthritis." Journal of Biomedicine and Biotechnology 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/535361.

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Rheumatoid arthritis (RA) is the most common autoimmune disorder. Loss of Th1/Th2 and Th17/Treg balance has been reported in several inflammatory autoimmune diseases. This study was to investigate Th1, Th2, Th17, and Treg differentiation and related cytokines in RA patients. The frequencies of Th1, Th2, Th17, and Treg cells in peripheral blood of RA patients (n=76) and healthy controls (n=18) were determined by flow cytometry. Eight serum cytokines were analyzed using cytometric bead array. The results demonstrated that RA patients exhibited increased peripheral Th1/Th17 cells and Th1/Th17-related cytokines. However, Th1 cells only reached significant difference at advanced stage, but Th17 at all stages, suggesting more important roles in Th17 cells. For Th2 and Treg cells, there was a different function pattern in RA progression. Although with the increase of DAS28 score, Th2 cell experienced some degree of decrease in RA patients, no significant difference was observed. IL-4 and IL-10 showed a significant increase in RA patients. These indicated that Th2 cells might exert immunosuppression effects mainly by secreting cytokines. Treg cells were found significantly decreased in RA patients, but no difference was observed in TGF-βexpression, indicating a cell-cell interaction pattern in Treg cell.
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Damsker, Jesse M., Anna M. Hansen, and Rachel R. Caspi. "Th1 and Th17 cells." Annals of the New York Academy of Sciences 1183, no. 1 (January 2010): 211–21. http://dx.doi.org/10.1111/j.1749-6632.2009.05133.x.

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FANG, Yujiang, Shiguang YU, and Helen MULLEN. "Differential sensitivity of Th1, Th2 and Th17 cells to Fas-mediated apoptosis (47.15)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 47.15. http://dx.doi.org/10.4049/jimmunol.182.supp.47.15.

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Abstract In response to T cell receptor crosslinking, naïve CD4+ T cells can differentiate into three major subsets, Th1, Th2 and Th17 cells. Th17 cells play an important role in the pathogenesis of autoimmune diseases, but little is known about the regulation of apoptosis in Th17 cells. This study was undertaken to directly determine and compare the sensitivity of in vitro polarized Th1, Th2 and Th17 cells to Fas-mediated apoptosis and to determine if the anti-apoptotic molecule FLIP could inhibit apoptosis of each of the three subsets. Using several different methods, the order of sensitivity of T cell subsets to Fas-mediated apoptosis is: Th1>Th17>Th2. The greater sensitivity of Th17 cells compared to Th2 cells correlated with their higher expression of FasL. The decreased sensitivity of Th17 compared to Th1 cells correlated with higher expression of FLIP by Th17 cells. Transgenic overexpression of FLIP in T cells protected all three subsets from Fas-mediated apoptosis. Using splenocytes from IFNγ-/- mice, Fas-mediated apoptosis of T cells activated under Th1 polarization-inducing conditions were shown to be dependent on IFN-γ, while Fas-mediated apoptosis of Th17 and Th2 cells was IFN-γ independent. These findings provide new knowledge for understanding how survival of different subsets of T cells is regulated. This information might be useful for the design of new strategies to treat autoimmune diseases (NIH DK35527).
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Banuelos, Jesus, and Nick Lu. "Distinct apoptotic machinery and selective gene regulation by glucocorticoids in Th17 cells (P1294)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 119.6. http://dx.doi.org/10.4049/jimmunol.190.supp.119.6.

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Abstract Glucocorticoids (GCs) are extensively used in the treatment of inflammatory disorders and surprisingly, are ineffective in suppressing Th17 responses. We sought to determine the mechanisms underlying the insensitivity of Th17 cells to GCs. We found that in vitro polarized murine Th1 and Th2 cells, but not Th17 cells, were sensitive to GC-induced apoptosis as determined by various apoptotic markers such as annexin-V staining. At the mRNA level, GCs suppressed IL-4 and IFN-γ, and unexpectedly IL-22 but not IL-17 (A and F). Despite the distinct GC responses, Th1, Th2, and Th17 cells showed similar levels of GC receptor (GR) isoforms. Using PCR array to survey 84 genes involved in apoptosis, we found significant differences in the apoptotic machinery between Th1 and Th17 cells. Th17 cells showed increased expression of anti-apoptotic survivin and Bfl-1 whereas Th1 cells showed increased expression of pro-apoptotic Bim, Fas ligand, caspase 1, and death receptor 5. GCs induced Bim in both Th1 and Th17 cells while the same treatment decreased the expression of Nod1 and Bcl-xL in Th1 but not Th17 cells. Altered apoptotic machinery and differences in genes regulated after GC treatment may underlie the inability of GCs to induce apoptosis in Th17 cells. These studies on the mechanisms underlying the selective insensitivity of Th17 cells to GCs may provide a basis for improved treatment regimens for severe asthma and other Th17-mediated disorders.
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Nelson, Michelle, Stefanie Bailey, Logan Huff, Sreenath Kundimi, and Chrystal Paulos. "Multifunctional CD26hi Th17 cells eradicate large human tumors (TUM2P.902)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 71.26. http://dx.doi.org/10.4049/jimmunol.192.supp.71.26.

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Abstract Human CD4+ T cells differentiate into multiple effector subsets, but their distinct roles in anti-tumor immunity remain elusive. CD4+ T cell subsets enriched from bulk human CD4+ T cells [Th1 (CXCR3+), Th2 (CCR4+), and Th17 (CCR6+ or CD26hi)] were stimulated with anti-CD3 beads bearing agonists to either CD28 or ICOS and were then engineered with a chimeric antigen receptor that recognizes human mesothelioma. In vitro, ICOS costimulation proved superior to CD28 for augmenting the function of human Th1, Th2, CCR6+ Th17 and CD26hi Th17 cells, as indicated by elevated production of IFN-γ, IL-4 and IL-17A, respectively. Moreover, CD26hi Th17 cells possessed strikingly enhanced polyfunctionality compared to Th1, Th2 or CCR6+ Th17 cells, as demonstrated by their heightened capacity to co-secrete IL-17A, IFN-γ, IL-22, IL-2, and TNF-α simultaneously. Compared to other enriched T cell subsets, a greater percentage of CD26hi Th17 cells exhibit an effector memory phenotype. In vivo, CD26hi Th17 cells more efficiently reconstituted immunodeficient hosts and persisted long-term. Furthermore, CD26hi Th17 cells possessed a superior ability to kill large human tumors (>150mm2) when infused into mice compared to Th1, Th2 or CCR6+ Th17 cells. These results suggest that the generation of multifunctional, long-lived human Th17 populations could be instrumental to the design of novel, effective T cell-based cancer therapies.
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Liu, Houpu, Ting Feng, Qingjie Li, Wenbo Zhang, Suxia Yao, Charles Elson, and Yingzi Cong. "TGFβ converts Th1 cell into Th17 cells through stimulation of Runx1 expression under inflammatory conditions in intestines (MUC2P.819)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 68.3. http://dx.doi.org/10.4049/jimmunol.192.supp.68.3.

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Abstract Although accumulating evidence demonstrates that differentiated CD4 cells preserve plasticity to alter phenotypes under various conditions, it is still unclear how stable Th1 cells are and whether Th1 cells can convert into Th17 cells. The high stability of Th1 is supported by some epigenetic studies and numerous reports of Treg and Th17 cells conversion into Th1 cells but not vice versa. However, recent reports of Th1 cell conversion to Treg, Th2 and Tfh cells argue the absolute stability of Th1 lineage. By using IFNγThy1.1 CBir1 TCR transgenic reporter mice, whose TCR is specific for an immunodominant microbiota antigen, we investigate the stability of Th1 cells under intestinal inflammatory conditions. Transfer of purified CBir1 specific IFNγ+Th1 cells induces colitis in RAG-/- mice and IFNγ+Th1 cells convert into IL-17+ Th17 but not Foxp3+ Treg cells in the inflamed intestines. TGFβ, IL-6 and IL-2, but not hypoxia factors, differentially regulate Th1 to Th17 conversion. TGFβ induction of transcriptional factors, Runx1 and RORγt, is crucial for the conversion, in that silencing Runx1 by siRNA inhibits Th1 conversion into Th17 cells. Furthermore, using ChIP assay, we show that TGFβ enhances histone acetylation but inhibits trimethylation of Runx1 and RORγt binding sites on il-17 or rorc gene in Th1 cells. In conclusion, our data demonstrate that Th1 cells convert into Th17 cells under inflammatory conditions in intestines, which is mediated by TGFβ-induction of Runx1.
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Annunziato, Francesco, and Sergio Romagnani. "Do studies in humans better depict Th17 cells?" Blood 114, no. 11 (September 10, 2009): 2213–19. http://dx.doi.org/10.1182/blood-2009-03-209189.

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Abstract CD4+ T helper (Th) lymphocytes represent a heterogeneous population of cells. In addition to type 1 (Th1) and type 2 (Th2) cells, another subset of CD4+ effector Th cells has been discovered and named as Th17, because of its unique ability to produce interleukin (IL)–17. Studies in mice initially suggested that Th17 cells are the pathogenic cells in autoimmune disorders, whereas Th1 cells may behave rather as protective. Subsequent studies in humans demonstrated the plasticity of Th17 cells and their possibility to shift to Th1. The plasticity of Th17 to Th1 cells has recently been confirmed in mice, where it was found that Th17 cells seem to be pathogenic only when they shift to Th1 cells. Studies in humans also showed that Th17 cells are different than in mice because all of them express CD161 and exclusively originate from CD161+ precursors present in umbilical cord blood and newborn thymus. While murine Th17 cells develop in response to IL-6, IL-1, and transforming growth factor (TGF)–β, human Th17 cells originate from these CD161+ precursors in response to IL-1β and IL-23, the need for TGF-β being controversial. Thus, we believe that studies in humans have better depicted human Th17 cells than studies in mice.
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Paulos, Chrystal, Michelle Nelson, Logan Huff, Sreenath Kundimi, and Morgan Goodyear. "Human CD26hi Th17 cells eradicate large established mesothelioma (P2139)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 170.26. http://dx.doi.org/10.4049/jimmunol.190.supp.170.26.

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Abstract Human CD4+ T cells can differentiate into multiple effector subsets, but their role in anti-tumor immunity remains incompletely elucidated. Further, the costimulatory molecules that effectively bolster their antitumor activity are unknown. To uncover the role of CD28 versus ICOS costimulation, we sorted Th1 (CXCR3+), Th2 (CCR4+), or Th17 (CCR6+ or CD26hi) subsets from bulk human CD4+ T cells and stimulated them with CD3/CD28 or CD3/ICOS beads. We found that ICOS costimulation not only augmented human Th17 cells’ function, but also enhanced the function of human Th1 and Th2 cells superior to CD28 costimulation. Moreover, CD26hi Th17 cells were more polyfunctional than the other T cells subsets, as indicated by increased secretion of IL-17, IFN-γ, IL-22 and TNF-α. To determine the therapeutic potential of these subsets, we sorted Th1, Th2 and Th17 cells from human peripheral blood, expanded them with CD3/ICOS beads, and engineered them to recognize mesothelioma. We found that CD26hi Th17 cells mediated superior regression of large human mesothelioma in mice compared to CXCR3+Th1, CCR4+Th2 or CCR6+Th17 cells. The therapeutic effectiveness of CD26hi Th17 cells was associated with enhanced functionality and persistence in vivo. Taken together, these data indicate that the appropriate selection of effector CD4+ T cells is critical for successful tumor eradication. These findings will help guide next generation clinical trials for patients with advanced malignancies.
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Carvalheiro, Tiago, Carlos Rafael-Vidal, Beatriz Malvar-Fernandez, Ana P. Lopes, Jose M. Pego-Reigosa, Timothy R. D. J. Radstake, and Samuel Garcia. "Semaphorin4A-Plexin D1 Axis Induces Th2 and Th17 While Represses Th1 Skewing in an Autocrine Manner." International Journal of Molecular Sciences 21, no. 18 (September 22, 2020): 6965. http://dx.doi.org/10.3390/ijms21186965.

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Semaphorin (Sema)4A is a transmembrane glycoprotein that is elevated in several autoimmune diseases such as systemic sclerosis, rheumatoid arthritis and multiple sclerosis. Sema4A has a key role in the regulation of Thelper Th1 and Th2 differentiation and we recently demonstrated that CD4+ T cell activation induces the expression of Sema4A. However, the autocrine role of Sema4A on Th cell differentiation remains unknown. Naïve Th cells from healthy controls were cell sorted and differentiated into Th1, Th2 and Th17 in the presence or absence of a neutralizing antibody against the Sema4A receptor PlexinD1. Gene expression was determined by quantitative PCR and protein expression by ELISA and flow cytometry. We found that the expression of Sema4A is induced during Th1, Th2 and Th17 differentiation. PlexinD1 neutralization induced the differentiation of Th1 cells, while reduced the Th2 and Th17 skewing. These effects were associated with an upregulation of the transcription factor T-bet by Th1 cells, and to downregulation of GATA3 and RORγt in Th2 cells and Th17 cells, respectively. Finally, PlexinD1 neutralization regulates the systemic sclerosis patients serum-induced cytokine production by CD4+ T cells. Therefore, the autocrine Sema4A-PlexinD1 signaling acts as a negative regulator of Th1 skewing but is a key mediator on Th2 and Th17 differentiation, suggesting that dysregulation of this axis might be implicated in the pathogenesis of CD4+ T cell-mediated diseases.
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Clay, Slater L., Alberto Bravo-Blas, Daniel M. Wall, Megan K. L. MacLeod, and Simon W. F. Milling. "Regulatory T cells control the dynamic and site-specific polarization of total CD4 T cells following Salmonella infection." Mucosal Immunology 13, no. 6 (May 26, 2020): 946–57. http://dx.doi.org/10.1038/s41385-020-0299-1.

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Abstract FoxP3+ regulatory T cells (Tregs) control inflammation and maintain mucosal homeostasis, but their functions during infection are poorly understood. Th1, Th2, and Th17 cells can be identified by master transcription factors (TFs) T-bet, GATA3, and RORγT; Tregs also express these TFs. While T-bet+ Tregs can selectively suppress Th1 cells, it is unclear whether distinct Treg populations can alter Th bias. To address this, we used Salmonella enterica serotype Typhimurium to induce nonlethal colitis. Following infection, we observed an early colonic Th17 response within total CD4 T cells, followed by a Th1 bias. The early Th17 response, which contains both Salmonella-specific and non-Salmonella-specific cells, parallels an increase in T-bet+ Tregs. Later, Th1 cells and RORγT+ Tregs dominate. This reciprocal dynamic may indicate that Tregs selectively suppress Th cells, shaping the immune response. Treg depletion 1–2 days post-infection shifted the early Th17 response to a Th1 bias; however, Treg depletion 6–7 days post-infection abrogated the Th1 bias. Thus, Tregs are necessary for the early Th17 response, and for a maximal Th1 response later. These data show that Tregs shape the overall tissue CD4 T cell response and highlight the potential for subpopulations of Tregs to be used in targeted therapeutic approaches.
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Dissertations / Theses on the topic "Th1 and Th17 cells"

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Prendergast, Catriona Taguma. "Exploring the pathogenic potential of myelin-reactive Th1 and Th17 cells in central nervous system autoimmune disease." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5285.

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The activation of naïve T cells results in their proliferation and differentiation into a particular T-helper (Th) phenotype, namely Th1, Th2 or Th17 cells. This thesis focuses on the role of pro-inflammatory Th1 and Th17 cells in the induction of autoimmune disease of the central nervous system (CNS), using murine experimental autoimmune encephalomyelitis (EAE) as the model. Classically, EAE has been considered to be a Th1-mediated disease. However, since the emergence of the Th17 cells, there has been a paradigm shift towards Th17 cells being the key pathogenic subset in autoimmune disease. This thesis established robust protocols for the differentiation of naïve T cells into myelin-reactive Th1 or Th17 cells, producing ‘clean’ populations devoid of any contaminating cells. Passive T cell-transfer experiments revealed that myelin-reactive Th1 cells could induce EAE, whereas Th17 cells could not. This lack of disease correlated with the inability of the Th17 cells to accumulate in the non-inflamed CNS. Myelin-reactive Th1 cells did have this capability and only once inflammation was established, could Th17 cells be identified in the CNS, potentially exacerbating the disease. After these differences were observed, the project investigated two main aims: 1) to identify differences in homing molecule expression on Th1 and Th17 cells which could explain the difference in their ability to home to the CNS, and to investigate the functional significance of such differences, by molecular blockade; 2) to investigate the requirements for three key cytokines in EAE pathogenesis in passive T cell transfer models, investigating IFN-γ,IL-17 and TNF-α. P-selectin glycoprotein ligand-1 appeared to be important for the initial entry of inflammatory T cells into the CNS. Th1 cells deficient in IFN-γ were capable of IFNinducing EAE. A proportion of the mice developed “atypical” clinical signs, which correlated with T cell infiltration predominantly of the brain, rather than the spinal cord. This atypical EAE may be IL-17 dependent. In conclusion, this thesis indicates the importance of not focusing all resources and therapeutic approaches on Th17- induced inflammation as Th17 cells may not play such a major role as previously thought.
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Costa, Fernando Augusto Miranda da. "Resposta imune in vitro aos antígenos de Papilomavírus Humano (HPV) em homens na cidade de São Paulo, Brasil." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5133/tde-04022014-155625/.

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Introdução: O Papilomavírus Humano está muito bem associado com diversos tipos de cânceres humanos, como câncer anogenital e oral. Alguns estudos demonstram que o aparecimento de lesões e a progressão para o câncer estão relacionados ao tipo de resposta imune do hospedeiro. Deste modo, evidências indicam que a resposta imune do hospedeiro tem um papel muito importante para o curso da infecção pelo HPV. Objetivo: Avaliar a resposta imune específica in vitro ao Papilomavírus Humano (HPV) em homens com lesões causadas por HPV e sem lesão por HPV. Material e Métodos: Foram recrutados 31 pacientes e 11 voluntários, que formaram 4 grupos de estudo; sendo 12 pacientes no Grupo A (HIV +/ HPV +); 09 pacientes no Grupo B (HIV-/HPV+); 10 pacientes no Grupo C (HIV+/ HPV-); e 11 indivíduos saudáveis no Grupo D (HIV-/HPV-). Foram realizados ensaios de cultura celular para mensurar a resposta celular específica \"in vitro\" do tipo Th1/Th2/Th17 (INF-y, IL-2, TNFalfa, IL-4, IL-10 e IL-17) sob o estímulo da vacina quadrivalente do HPV (HPV 6, 11, 16 e 18) e à proteína E7 de HPV-16. Resultados: O grupo coinfectado (HIV +/ HPV+) apresentou níveis mais elevados de citocinas, principalmente do perfil Th2, comparando-se com os dados dos demais grupos de estudo. O grupo coinfectado apresentou níveis elevados de IL-6 e IL-10 (Perfil Th2) em relação ao grupo controle (HIV-/HPV-), com significância estatística (p < 0.0001 e p < 0.0001, respectivamente). Conclusão: Foi demonstrada uma elevada produção de citocinas no grupo HPV+/HIV+, sugerindo uma forte imunomodulação pela coinfecção HIV/HPV. Entretanto, novos estudos devem ser realizados para comprovar estes dados. Além de apresentar um perfil essencialmente Th2 do grupo coinfectado, principalmente pelos níveis elevados de IL-6 e IL-10 apresentados, sugerindo que estas duas citocinas possam servir como biomarcadores para persistência viral, uma vez que, os pacientes soropositivos para HIV apresentam maior persistência de HPV, e monitorar a progressão para lesões mais graves
Introduction: Human Papillomavirus is associated with different types of human cancers, such as anogenital and oral cancer. Some studies show that the appearance of lesions and progression to cancer are related to the type of host immune response. Thus, evidence indicates that the host immune response has a role key in the course of HPV infection. Objective: To evaluate the specific immune response in vitro to HPV in men with lesions caused by HPV and without injury caused by HPV. Methods: We recruited 31 patients and 11 volunteers, who formed four groups, with 12 patients in Group A (HIV+/HPV+); 09 patients in Group B (HIV-/HPV+); 10 patients in Group C (HIV+/HPV-) and 11 healthy subjects in Group D (HIV-/HPV-). Cells culture assay was performed to measure the specific immune response \"in vitro\" Th1/Th2/Th17 (IFN-y, IL-2, TNF-alfa, IL-4, IL-10 and IL-17) under the stimulation of quadrivalent HPV vaccine (HPV 6, 11, 16 and 18) and the E7 protein of HPV-16. Results: The coinfected group (HIV+/HPV+) had higher levels of cytokines, especially Th2 profile, compared with data from the other study groups. The coinfected group showed high levels of IL-6 and IL-10 (Th2 profile) compared to the control Group (HIV- /HPV-), with statistical significance (p < 0.0001 and p < 0.0001, respectively). Conclusion: This study demonstrated a high production of cytokines in the coinfected group, suggesting a strong immunomodulation by coinfection HIV/HPV. However, further studies should be conducted to confirm these data. In addition to presenting essentially a Th2 profile, especially by high levels of IL-6 and IL-10 presented, suggesting that these two cytokines may serve as biomarkers for viral persistence, since HIV seropositive patients have a higher persistence of HPV, and monitor the progression to more serious injuries
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Zhang, W., X. Tian, F. Mumtahana, J. Jiao, T. Zhang, K. D. Croce, D. Ma, B. Kong, and B. Cui. "The existence of Th22, pure Th17 and Th1 cells in CIN and Cervical Cancer along with their frequency variation in different stages of cervical cancer." BioMed Central Ltd, 2015. http://hdl.handle.net/10150/610273.

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BACKGROUND: Recently, it is found that T-helper (Th) 22 cells are involved in different types of autoimmune and tumor diseases. But, till now, no study has been carried out to understand the involvement of these cells in cervical cancer (CC). METHODS: Flow cytometry was used to determine the expression of interferon gamma (IFN-gamma), Interleukin-22 (IL-22), IL-17 in the peripheral blood of healthy controls (HC), CIN and cervical cancer patients. From peripheral blood mononuclear cells (PBMCs), mRNA expression levels of Aryl hydrocarbon receptor (AHR), RAR-related orphan receptor C (RORC), TNF-alpha and IL-6 were respectively determined. Using the method of ELISA, plasma concentrations of IL-22, IL-17 and TNF-alpha were examined. RESULTS: Th22 and Th17 cells were elevated in CC and CIN patients. Th1 cells and the plasma concentrations of IL-22 in CC patients were significantly increased compared with HC. In CC patients, an increased prevalence of Th22 cells was associated with lymph node metastases. There was a positive correlation between Th22 and Th17 cells, but an approximately negative correlation between Th22 and Th1 cells in CC patients. The mRNA expression of RORC, TNF-alpha and IL-6 was significantly high in CC patients. CONCLUSIONS: Our results indicate that there is a higher circulatory frequency of Th22, Th17 and Th1 cells in CC which may conjointly participate in the pathogenesis and growth of CC.
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Pereira, Leonardo Biscaro. "Avaliação do perfil de citocinas no tecido subcutâneo de camundongos na presença de cimento endodôntico." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/58/58135/tde-03102013-151254/.

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Avaliou-se a capacidade dos cimentos endodônticos: Sealapex®, Activ-GP® e AH-Plus® de alterarem o perfil das citocinas nas respostas Th1, Th2 e Th17, após a implantação destes em subcutâneo de camundongos. A quantificação das citocinas IL-2, IL-6, TNF-α, IFN-γ, IL-4, IL-10 e IL-17 foi realizada in vivo, no tecido reacional circundante aos implantes, os quais foram confeccionados a partir de sondas nasogástricas estéreis e apirogênicas de cloreto de polivinila preenchidas com os cimentos, tendo um grupo controle com sondas vazias. Utilizou-se camundongos isogênicos da linhagem C57BL/6 machos de 6/8 semanas de vida sendo que cada um recebeu 2 implantes na região dorsal (lado direito e esquerdo). Após os períodos experimentais de 7, 21 e 63 dias, com os camundongos anestesiados, os implantes foram removidos juntamente com o tecido circundante, e os animais sacrificados em seguida por deslocamento cervical. As amostras de cada grupo foram divididas sendo: duas, contendo implante/tecido, processadas histotecnicamente e as demais com apenas tecido (sem implante) foram homogeneizadas e centrifugadas com solução formada por tampão RIPA e inibidor de protease. O sobrenadante, fruto deste processo, foi coletado e a dosagem das citocinas realizada através do kit CBA mouse-Th1/Th2/Th17 Cytokine Kit (BD Cytometric Bead Array, San Jose, CA, USA) em análise por citometria de fluxo. Os parâmetros avaliados foram a concentração da citocina em função do cimento testado em cada período experimental. Submeteu-se os resultados à análise estatística por meio do teste t com a correção de Welch\'s. Para todos os testes o nível de significância foi de 5%. Com relação à IL-2 houve diferenças estatísticas significantes entre os grupos Activ-GP® e AH-Plus® (p=0,0391). No período de 21 dias foram detectadas diferenças entre o grupo controle e AH-Plus® (p=0,0402) e entre o grupo Sealapex® e AH-Plus® (p=0,0244). O AH-Plus® induziou um maior aumento na IL-6, aos 7 dias em relação ao Activ-GP® (p=0,0286) e aos 21 dias entre o grupo controle (p=0.0402) e Activ-GP® (p=0.0244). Os níveis de TNF-α foram estatisticamente superiores após 7 dias quando comparou-se o grupo AH-Plus® com os demais. Observou-se que no grupo controle aos 7 e 21 dias ocorreram diferenças estatísticas em relação ao Sealapex® e AH-Plus® respectivamente quando avaliadas as concentrações de IFN-γ. Houve também diferenças estatísticas entre o grupo controle e Sealapex® (p=0,0158) no período de 7 dias para a citocina IL-4. Os valores de IL-10 foram estatisticamente superiores para o grupo controle em relação ao Activ-GP® no período de 21 dias (p=0,0471). Com relação a IL-17 no período de 21 dias, observou-se os maiores valores para o grupo controle, seguido pelo Sealapex®, Activ-GP® e AH-Plus®. Foram detectadas diferenças entre os grupos controle e AH-Plus® (p=0,0121), controle e Activ-GP® (p=0,0262) e entre Sealapex® e Activ GP® (p=0,0314). Baseado nesses resultados podê-se concluir que: os cimentos endodônticos são capazes de modular as respostas Th1, Th2 e Th17 através da inibição ou estimulação da liberação das citocinas testadas. O cimento AH-Plus® promoveu as maiores diferenças no perfil de resposta Th1.
It was evaluated the capacity of the following endodontic sealers: Sealapex, Activ-GP and AH-Plus to modify the cytokine profile in Th1, Th2 and Th17 responses, after their implantation in the subcutaneous tissue of mice. Quantification of IL-2, IL-6, TNF-α, IFN-γ, IL-4, IL-10 and IL-17 was performed in vivo, in the reactional tissue surrounding the implants, which were made from sterile nasogastric probes and apyrogenic of polyvinyl chloride filled with sealer, and a control group of empty probes. It was used isogenic mice of C57BL/6 lineage, 6/8 weeks old males, each of which received two implants in the dorsal region (left and right). After the experimental time of 7, 21 and 63 days, the mice were anesthetized and the implants were removed along with the surrounding tissue, the animals were then sacrificed by cervical dislocation. Samples from each group were divided as follows: two containing implant / tissue processed histologically and with only the remaining tissue (without implant) were mixed and centrifuged with a solution formed by RIPA buffer and protease inhibitors. The supernatant result of this process was collected and cytokine dosage accomplished by mouse-Th1/Th2/Th17 Cytokine CBA Kit Kit (BD cytometric Bead Array, San Jose, CA, USA) for flow cytometry analysis. The evaluated parameters were the cytokine concentration in function of sealer tested in each trial. The results were submitted to statistical analysis using the t test with Welch\'s correction. For all tests the significance level was 5%. With respect to IL-2 there were significant statistical differences between groups-Activ GP and AH-Plus (p=0.0391). In the period of 21 days differences were found between the control group and AH-Plus (p=0.0402) and between the group Sealapex and AH-Plus (p=0.0244). The AH-Plus induced a greater increase in IL-6, at 7 days compared to Activ-GP (p=0.0286) and at 21 days between the control group (p=0.0402) and Activ-GP (p=0.0244). The levels of TNF-α were significantly higher after 7 days when the AH-Plus group was compared with others. It was observed that in the control group at 7 and 21 days there were statistical differences in relation to Sealapex and AH-Plus respectively when evaluated concentrations of IFN-γ. There were also significant differences between the control group and Sealapex (p=0.0158) within 7 days for the cytokine IL-4. The amounts of IL-10 were statistically higher in the control group compared to the Activ GP in a period of 21 days (p=0.0471). With respect to IL-17 in a period of 21 days, it was observed the highest values for the control group, followed by Sealapex, Activ-GP and AH-Plus. Differences were found between the control groups and AH-Plus (p=0.0121), control and Activ-GP (p=0.0262) and between Sealapex and Activ-GP (p=0.0314). Based on the presented results theendodontic sealers are able to promote changes in the response cytokine profile Th1, Th2 and Th17; Sealer AH-Plus produced the greatest changes, in the Th1 response profile.
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Medina, Tiago da Silva. "Participação do eixo Th17/IL-27 no controle da infecção experimental com Trypanosoma cruzi." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/17/17147/tde-02052014-160055/.

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Produzida por macrófagos e células dendríticas, a IL-27 é uma citocina heterodimérica capaz de induzir células Tr1 produtoras de IL-10 e consequentemente regular linfócitos Th1, Th2 e Th17, dependendo da doença envolvida. Partindo-se do pressuposto de que a infecção causada por Trypanosoma cruzi normalmente induz miocardite refletida pela migração intensa de linfócitos Th1 para o tecido cardíaco, nós analisamos o papel regulador da IL-27 nesta condição inflamatória. Nós inicialmente verificamos que a IL-27 foi prontamente induzida in vitro em células infectadas com T. cruzi. Para gerar miocardite intensa coordenada por linfócitos Th1, nós polarizamos linfócitos T naïves para o padrão Th1 na ausência de moléculas relacionadas ao perfil Th17 (camundongos IL-17R-/-, IL-23-/- e IL-6-/-). Como esperado, a inflamação cardíaca intensa e o dano tecidual foram observados na ausência das moléculas do padrão Th17, o que contribuiu para a morte prematura dos animais IL-17R-/-, IL-23-/- e IL-6-/-, precisa e notoriamente pela indução da migração excessiva de linfócitos Th1 para o tecido cardíaco via CXCL-9 e CXCL-10. Para explorar os mecanismos pelos quais a IL-27 controla a miocardite induzida pelo T. cruzi, nós encontramos um recrutamento substancial de macrófagos produtores de IL-27 para o tecido cardíaco, o qual foi mediado pelas quimiocinas CCL3 e CCL4 na ausência de moléculas do padrão Th17. Para determinar quais os receptores necessários para a produção de IL-27, nós observamos que macrófagos derivados da medula óssea de camundongos deficientes de TLR4-/-, TLR9-/- e NLRP3-/- aboliram completamente a produção desta citocina após a infecção in vitro com T. cruzi, enquanto o receptor TLR2 foi dispensável. Nós também verificamos que macrófagos produtores de IL-27 suprimiram linfócitos Th1 através da indução de células Tr1 produtoras de IL-10 após a infecção com T. cruzi. Em seguida, nós avaliamos se a IL-27 foi correlacionada com a proteção cardíaca durante a doença de Chagas. Nós observamos níveis séricos elevados de IL-27 tanto em pacientes com a forma clínica indeterminada ou cardíaca leve, enquanto pacientes com cardiomiopatia moderada ou grave produziram níveis reduzidos de IL-27. Neste estudo, nós descrevemos um novo mecanismo regulador desempenhado por macrófagos produtores de IL-27 no controle da miocardite induzida por T. cruzi. Macrófagos produtores de IL-27 podem suprimir processos inflamatórios desencadeados por linfócitos Th1, os principais vilões na doença de Chagas.
IL-27 is a heterodimeric cytokine produced by macrophages and dendritic cells known to induce IL-10-producing Tr1 cells and to regulate Th1, Th2, and Th17 lymphocytes, depending on the underlying disease. Because the infection caused by Trypanosoma cruzi normally induces myocarditis mirrored by an outstanding migration of Th1 cells to the heart tissue, we analyzed the regulatory role of IL-27 in this inflammatory condition. We firstly verified that IL-27 was promptly induced by in vitro T. cruzi-infected spleen cells. To generate a robust myocarditis coordinated by Th1 lymphocytes, we polarized lymphocytes to a Th1 pattern by infecting mice in the absence of Th17-related molecules (IL-17R-/-, IL-23-/-, and IL-6-/- mice). As expected, an impressive cardiac inflammation and damage was observed in the absence of Th17-related molecules, leading IL-17R-/-, IL-23-/-, and IL-6-/- mice to the premature death, precisely and notably by inducing an exuberant Th1 migration to the heart tissue via CXCL9 and CXCL10 chemokines. To explore the mechanisms by which IL-27 controls T. cruzi-induced myocarditis, we found a striking recruitment of IL-27-producing macrophages to the heart tissue mediated by increased levels of CCL3 and CCL4 chemokines in the absence of Th17-associated molecules. To gain further insights into the receptors required to IL-27 production, we observed that bone marrow-derived macrophages from TLR4-/-, TLR9-/-, and NLRP3-/- mice completely abolished IL-27 production after in vitro T. cruzi infection, while TLR2 was dispensable. We also verified that IL-27-producing macrophages supressed Th1 lymphocytes by inducing IL-10-producing Tr1 cells after T. cruzi infection. We next assessed whether IL-27 was correlated to cardiac protection during Chagas Disease. We observed augmented serum levels of IL-27 in either patients with indeterminate (asymptomatic) form or mild cardiac form, whereas patients with moderate or severe cardiomyopathy were poor producers of IL-27. Here, we described a novel regulatory mechanism developed by IL-27-producing macrophages in the control of T. cruzi-induced myocarditis. IL-27-producing macrophages can suppress inflammatory processes caused by Th1 lymphocytes, the bona fide culprits of Chagas Disease.
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Tigno-Aranjuez, Justine Daphne Tiglao. "Adjuvant Guided T cell Responses." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1244035297.

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Yao, Chengcan. "Prostaglandin E2-EP4 signaling promotes immune inflammation through TH1 cell differentiation and TH17 cell expansion." Kyoto University, 2011. http://hdl.handle.net/2433/151930.

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Agorogiannis, Eleftherios. "TH17 cells in transplantation biology." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.540084.

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Hull, Dobrina Nikolaeva. "The dynamics of Th17 and Th1 cells during anti-TNF therapy in patients with inflammatory arthritis and relationship with treatment response." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/29116.

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Anti-TNF agents have revolutionised the treatment of rheumatoid arthritis (RA), ankylosing spondylitis (AS) and psoriatic arthritis (PsA), however a significant proportion of patients respond inadequately. Studies in murine and human arthritis have paradoxically shown that anti-TNF treatment can increase circulating Th17 and Th1 cells but the relationship of these changes to treatment response remains unclear. The aim of the work in this thesis was to conduct a prospective, longitudinal investigation of patients with inflammatory arthritis during anti-TNF treatment and using clinical, ultrasound and immunological assessments to gain an understanding of the immune correlates of treatment response. Patients with RA (n=25), AS (n=15) and PsA (n=8) were recruited and followed over the first 12 weeks of treatment. Improvement in validated disease activity scores defined treatment responders and non-responders. Power Doppler ultrasound (PDUS) provided a quantitative assessment of changes in synovial thickening and vascularity during treatment, with synovial vascularity showing faster and greater reduction with treatment than synovial thickening. PBMCs testing using IL17 and IFNy ELISpot assays and flow cytometry consistently showed increased frequencies of circulating Th1 and Th17 cells in all three disease groups during anti-TNF therapy. Multiplex cytokine testing demonstrated a decrease in serum levels of proinflammatory cytokines and chemokines. Analyses of relationships between clinical, ultrasonographic and T-cell immunological changes revealed significant negative correlations between the increased frequency of Th1 and Th17 cells and reduction in synovial thickening and vascularity from baseline to 12 weeks on treatment in the RA group. Higher numbers of circulating Th17 cells at baseline in the RA group were associated with poorer anti-TNFa treatment response as defined by DAS28 score and ultrasonographic measures. This is the first study to link changes in T-cell immunopathology evaluated by cellular assays with morphological changes in arthritis assessed by PDUS during anti-TNFa treatment.
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Zager, Adriano. "A ativação imune materna e os efeitos sobre a imunidade, neuroinflamação e desenvolvimento da encefalomielite autoimune experimental na prole de camundongos." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/10/10133/tde-21112013-113642/.

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Experiências vivenciadas durante o período pré-natal são determinantes para a saúde do feto. A ocorrência de infecções maternas e a consequente ativação do sistema imune da mãe ocasionam uma série de alterações estruturais e funcionais no cérebro da prole, podendo predispor o indivíduo a transtornos psiquiátricos na vida pós-natal, como esquizofrenia e autismo. No entanto, estudos que investigam as alterações imunes na prole ainda são escassos na literatura. Dessa forma, o objetivo do presente estudo foi avaliar, na prole, o impacto da ativação imune materna sobre a atividade imune periférica, a resposta imune-inflamatória no sistema nervoso central (SNC), e sobre o desenvolvimento da encefalomielite autoimune experimental (EAE), o modelo murino de Esclerose Múltipla. Camundongos fêmeas prenhes receberam uma administração de salina ou lipopolissacarídeo (LPS) ao final da gestação (dia gestacional 17) e, quando adulta, a prole foi submetida a 3 experimentos principais, analisando: (1) produção de citocinas, atividade de células da periferia e desenvolvimento da hipersensibilidade do tipo tardia; (2) produção de mediadores inflamatórios por células residentes do SNC e; (3) desenvolvimento dos sintomas clínicos e da resposta imune no decorrer da EAE. Nossos resultados mostraram que a ativação imune materna provocou na prole alterações imunes periféricas, como aumento da produção de Interleucina(IL)- 12 e exacerbação da resposta de hipersensibilidade do tipo tardia; potencialização da produção das citocinas IL-1β e IL-6 em cultura primária de células residentes do SNC e; piora na severidade dos sintomas clínicos causados pela EAE, que coincide com aumento do infiltrado de linfócitos e macrófagos no SNC e ativação imuneinflamatória das células da glia. Tomados em seu conjunto, os dados do presente trabalho sugerem que condições inflamatórias durante a gestação, particularmente durante o final da gestação, podem predispor o feto a distúrbios autoimunes e neurodegenerativos na vida adulta.
Prenatal period experiences are crucial for the fetal health. The occurrence of maternal infections and subsequent maternal immune system activation cause a number of structural and functional changes in the brain of the offspring that may predispose individuals to psychiatric disorders in post-natal life, such as schizophrenia and autism. However, studies investigating offspring´s immune alterations are still scarce in the literature. The aim of this study was to evaluate, in mice offspring taken from LPS-treated dams, the impact of maternal immune activation on peripheral immune cell activity, central nervous system (CNS) inflammatory response, and development of experimental autoimmune encephalomyelitis (EAE), the murine model of multiple sclerosis. Pregnant female mice received a dose of either saline or lipopolysaccharide (LPS) during late gestation (gestational day 17), and offspring were used in three experiments to analyze: (1) cytokine production and activity by peripheral immune cells and development of delayed type hypersensitivity, (2) production of inflammatory mediators by resident CNS cells and, (3) development of clinical symptoms and immune response during the course of EAE. Our results showed that maternal immune activation resulted in immune alterations in the offspring, such as increased peripheral production of interleukin (IL) -12 and exacerbated response of delayedtype hypersensitivity; enhancement of IL-1β and IL-6 productions in primary CNS resident cells culture and; increased severity of EAE clinical symptoms, which is positively correlated with the increased lymphocytes and macrophages infiltration within the CNS and also with the immune-inflammatory activation of glial cells. Taken together, the data from this study suggest that inflammatory conditions during pregnancy, especially during the late pregnancy, may predispose the fetus to autoimmune and neurodegenerative disorders in adulthood.
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Books on the topic "Th1 and Th17 cells"

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TH17 cells in health and disease. New York: Springer, 2011.

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Jiang, Shuiping, ed. TH17 Cells in Health and Disease. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-9371-7.

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The Th1-Th2 paradigm in disease. Austin, Tex: R.G. Landes Company, 1997.

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Romagnani, S. The Th1/Th2 paradigm in disease. New York: Springer, 1997.

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L, Adorini, ed. Immunointervention in autoimmunity by Th1/Th2 regulation. New York: Springer, 1997.

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Waisman, Ari, and Burkhard Becher. T-helper cells: Methods and protocols. New York: Humana Press, 2014.

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Espéli, Marion, and Michelle Linterman. T follicular helper cells: Methods and protocols. New York, NY: Humana Press, 2015.

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Velikova, Tsvetelina. Th17 Cells in Health and Disease. Nova Science Publishers, Incorporated, 2020.

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Velikova, Tsvetelina. Th17 Cells in Health and Disease. Nova Science Publishers, Incorporated, 2020.

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Jiang, Shuiping. TH17 Cells in Health and Disease. Springer, 2014.

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Book chapters on the topic "Th1 and Th17 cells"

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McGary, Colleen S., and Mirko Paiardini. "Th17 Cells." In Encyclopedia of AIDS, 1–9. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-9610-6_209-1.

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Noack, Mélissa, and Pierre Miossec. "Th17 Cells." In Inflammation - From Molecular and Cellular Mechanisms to the Clinic, 395–418. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2017. http://dx.doi.org/10.1002/9783527692156.ch16.

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Peiser, Matthias. "TH17 Cells." In Encyclopedia of Immunotoxicology, 875–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_1574.

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Peiser, Matthias. "TH17 Cells." In Encyclopedia of Immunotoxicology, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27786-3_1574-1.

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McGary, Colleen S., and Mirko Paiardini. "Th17 Cells." In Encyclopedia of AIDS, 1991–98. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7101-5_209.

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Annunziato, Francesco, Lorenzo Cosmi, Francesco Liotta, Enrico Maggi, and Sergio Romagnani. "Human TH17 Cells." In TH17 Cells in Health and Disease, 231–42. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-9371-7_12.

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Awasthi, Amit, and Vijay K. Kuchroo. "From TH1/TH2 Paradigm to TH17 Cells: Le Roi Est Mort, Vive Le Roi." In TH17 Cells in Health and Disease, 3–25. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-9371-7_1.

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Schmidt-Weber, C. B. "Th17 and Treg Cells Innovate the Th1/Th2 Concept and Allergy Research." In Chemical Immunology and Allergy, 1–7. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000154844.

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Liu, Xuebin, Stewart Leung, Lei Fang, Xi Chen, Taylor Guo, and Jingwu Zhang. "Interplay of Pathogenic TH1/TH17 Cells and Regulatory T Cells in Auto-immune Disease: A Tale of Yin and Yang." In TH17 Cells in Health and Disease, 367–89. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-9371-7_19.

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Paulos, Chrystal M., Michelle H. Nelson, and Xue-Zhong Yu. "Th17 Cells in Cancer." In Tumor-Induced Immune Suppression, 37–75. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4899-8056-4_2.

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Conference papers on the topic "Th1 and Th17 cells"

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Psarras, A., A. Antanaviciute, I. Carr, M. Wittmann, P. Emery, G. Tsokos, and E. M. Vital. "SAT0019 Tnf-Α regulates plasmacytoid dendritic cells by suppressing ifn-Α production and enhancing th1 and th17 cell differentiation." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.4688.

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Plank, Maximilian, Gerard Kaiko, Steven Maltby, Jessica Weaver, Hock Tay, Shen Wei, Mark Wilson, Scott Durum, and Paul Foster. "Th22 cells develop independently of the Th17 lineage with unique transcriptional properties and plasticity toward Th1-type cells during Influenza infection." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa1146.

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Furukawa, Toshiki, Takuro Sakagami, Asako Takiguchi, Kenji Shima, Hirotaka Sakamoto, Yosuke Kimura, Yoshifumi Hoshino, et al. "Th17 Cells In Peripheral Blood Play Pivotal Roles In Development Of Non-Eosinophilic Asthma Independent Of Th1/Th2 Paradigm." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3944.

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Segal, Leopoldo, Rohan Kulkarni, Anna Nolan, Michael D. Weiden, Doris B. Tse, and William N. Rom. "Regulatory T Cells And Th17 Cells In Bronchoalveolar Lavage." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1391.

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Lane, N., LC Fairclough, AM Jackson, JM Corne, and RA Robins. "T Regs and Th17 Cells in COPD." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4303.

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McAllister, Florencia, Jennifer M. Bailey, Jeffrey Roeser, Danielle T. Blake, Elizabeth C. Wick, Cynthia L. Sears, Elizabeth M. Jaffee, et al. "Abstract 2968: TH17 cells in early pancreatic tumorigenesis." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2968.

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McAllister, Florencia, Jennifer M. Bailey, Janivette Alsina, Chris Nirschl, Rachana Lankapalli, Jeffrey Roeser, Elizabeth Jaffee, et al. "Abstract 2867: TH17 cells promote early pancreatic tumorigenesis." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-2867.

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Kuchroo, V. "SP0150 Th17 cells drive and regulate tissue inflammation." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.7254.

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Chang, Ying, Laila Al-Alwan, Paul-André Risse, James Martin, David H. Eidelman, and Qutayba Hamid. "Th17 Cytokines Induce Human Airway Smooth Muscle Cells Migration." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2128.

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Ye, Jian, Xinming Su, Eddy C. Hsueh, Yanping Zhang, Joyce M. Koenig, Daniel F. Hoft, and Guangyong Peng. "Abstract 781: Plasticity of human tumor-infiltrating Th17 cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-781.

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Reports on the topic "Th1 and Th17 cells"

1

Lai, Vy P. CD4+ Th1 HER2-Specific T Cells as a Novel Treatment for HER2-Overexpresssing Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2008. http://dx.doi.org/10.21236/ada499837.

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Lai, Vy P. CD4+ Th1 HER2-Specific T Cells as a Novel Treatment for HER2-Overexpressing Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2007. http://dx.doi.org/10.21236/ada477515.

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3

Banai, Menachem, and Gary Splitter. Molecular Characterization and Function of Brucella Immunodominant Proteins. United States Department of Agriculture, July 1993. http://dx.doi.org/10.32747/1993.7568100.bard.

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The BARD project was a continuation of a previous BARD funded research project. It was aimed at characterization of the 12kDa immunodominant protein and subsequently the cloning and expression of the gene in E. coli. Additional immunodominant proteins were sought among genomic B. abortus expression library clones using T-lymphocyte proliferation assay as a screening method. The 12kDa protein was identified as the L7/L12 ribosomal protein demonstrating in the first time the role a structural protein may play in the development of the host's immunity against the organism. The gene was cloned from B. abortus (USA) and B. melitensis (Israel) showing identity of the oligonucleotide sequence between the two species. Further subcloning allowed expression of the protein in E. coli. While the native protein was shown to have DTH antigenicity its recombinant analog lacked this activity. In contrast the two proteins elicited lymphocyte proliferation in experimental murine brucellosis. CD4+ cells of the Th1 subset predominantly responded to this protein demonstrating the development of protective immunity (g-IFN, and IL-2) in the host. Similar results were obtained with bovine Brucella primed lymphocytes. UvrA, GroE1 and GroEs were additional Brucella immunodominant proteins that demonstrated MHC class II antigenicity. The role cytotoxic cells are playing in the clearance of brucella cells was shown using knock out mice defective either in their CD4+ or CD8+ cells. CD4+ defective mice were able to clear brucella as fast as did normal mice. In contrast mice which were defective in their CD8+ cells could not clear the organisms effectively proving the importance of this subtype cell line in development of protective immunity. The understanding of the host's immune response and the expansion of the panel of Brucella immunodominant proteins opened new avenues in vaccine design. It is now feasible to selectively use immunodominant proteins either as subunit vaccine to fortify immunity of older animals or as diagnostic reagents for the serological survaillance.
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4

Bercovier, Herve, Raul Barletta, and Shlomo Sela. Characterization and Immunogenicity of Mycobacterium paratuberculosis Secreted and Cellular Proteins. United States Department of Agriculture, January 1996. http://dx.doi.org/10.32747/1996.7573078.bard.

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Our long-term goal is to develop an efficient acellular vaccine against paratuberculosis based on protein antigen(s). A prerequisite to achieve this goal is to analyze and characterize Mycobacterium paratuberculosis (Mpt) secreted and cellular proteins eliciting a protective immune response. In the context of this general objective, we proposed to identify, clone, produce, and characterize: the Mpt 85B antigen and other Mpt immunoreactive secreted proteins, the Mpt L7/L12 ribosomal protein and other immunoreactive cellular proteins, Mpt protein determinants involved in invasion of epithelial cells, and Mpt protein antigens specifically expressed in macrophages. Paratuberculosis is still a very serious problem in Israel and in the USA. In the USA, a recent survey evaluated that 21.6% of the dairy herd were infected with Mpt resulting in 200-250 million dollars in annual losses. Very little is known on the virulence factors and on protective antigens of Mpt. At present, the only means of controlling this disease are culling or vaccination. The current vaccines do not allow a clear differentiation between infected and vaccinated animals. Our long-term goal is to develop an efficient acellular paratuberculosis vaccine based on Mpt protein antigen(s) compatible with diagnostic tests. To achieve this goal it is necessary to analyze and characterize secreted and cellular proteins candidate for such a vaccine. Representative Mpt libraries (shuttle plasmid and phage) were constructed and used to study Mpt genes and gene products described below and will be made available to other research groups. In addition, two approaches were performed which did not yield the expected results. Mav or Mpt DNA genes that confer upon Msg or E. coli the ability to invade and/or survive within HEp-2 cells were not identified. Likewise, we were unable to characterize the 34-39 kDa induced secreted proteins induced by stress factors due to technical difficulties inherent to the complexity of the media needed to support substantial M. pt growth. We identified, isolated, sequenced five Mpt proteins and expressed four of them as recombinant proteins that allowed the study of their immunological properties in sensitized mice. The AphC protein, found to be up regulated by low iron environment, and the SOD protein are both involved in protecting mycobacteria against damage and killing by reactive oxygen (Sod) and nitrogen (AhpC) intermediates, the main bactericidal mechanisms of phagocytic cells. SOD and L7/L12 ribosomal proteins are structural proteins constitutively expressed. 85B and CFP20 are both secreted proteins. SOD, L7/L12, 85B and CFP20 were shown to induce a Th1 response in immunized mice whereas AphC was shown by others to have a similar activity. These proteins did not interfere with the DTH reaction of naturally infected cows. Cellular immunity provides protection in mycobacterial infections, therefore molecules inducing cellular immunity and preferentially a Th1 pathway will be the best candidate for the development of an acellular vaccine. The proteins characterized in this grant that induce a cell-mediated immunity and seem compatible with diagnostic tests, are good candidates for the construction of a future acellular vaccine.
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D'Andrea, Annalisa. Inhibition of Th17 Cell Differentiation as a Treatment for Multiple Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada577274.

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6

D Andrea, Annalisa. Inhibition of Th17 Cell Differentiation as a Treatment for Multiple Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada589923.

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