Relevant bibliographies by topics / Cd40lg-

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Academic literature on the topic 'Cd40lg-'

Author: Grafiati
Published: 9 March 2023
Last updated: 11 March 2023

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Journal articles on the topic "Cd40lg-"

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Hubbard, Nicholas, David Hagin, Karen Sommer, Yumei Song, Iram Khan, Courtnee Clough, Hans D. Ochs, David J. Rawlings, Andrew M. Scharenberg, and Troy R. Torgerson. "Targeted gene editing restores regulated CD40L function in X-linked hyper-IgM syndrome." Blood 127, no. 21 (May 26, 2016): 2513–22. http://dx.doi.org/10.1182/blood-2015-11-683235.

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Key PointsThe CD40LG locus can be specifically targeted and repaired in primary human T cells by insertion of a spliced CD40LG complementary DNA. Gene editing restores regulated CD40L expression in X-HIGM T cells, reconstituting B-cell immunoglobulin class switching.
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Hubbard, Nicholas Wesley, David Hagin, Karen Sommer, Yumei Song, Iram Khan, Courtnee Clough, Hans D. Ochs, David J. Rawlings, Andrew Scharenberg, and Troy R. Torgerson. "Targeted Gene Editing Restores Regulated CD40L Expression and Function in X-HIGM T cells." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 214.28. http://dx.doi.org/10.4049/jimmunol.196.supp.214.28.

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Abstract Loss of CD40L expression or function results in X-Linked Hyper-IgM Syndrome (X-HIGM), characterized by recurrent infections due to impaired immunoglobulin class-switching and somatic hypermutation. Previous attempts using retroviral gene transfer to correct murine CD40L expression restored immune function; however, treated mice developed lymphoproliferative disease, likely due to viral-promoter dependent constitutive CD40L expression. These observations highlight the importance of preserving endogenous gene regulation in order to safely correct this disorder. Here we report efficient, on-target, homology directed repair (HDR) editing of the CD40LG locus in primary human T cells using a combination of a TALEN-induced double-strand break and a donor template delivered by recombinant Adeno-Associated Virus (rAAV). HDR mediated insertion of a coding sequence (GFP or CD40L) upstream of the translation start site within Exon 1 allowed transgene expression to be regulated by endogenous CD40LG promoter/enhancer elements. Additionally, inclusion of the CD40LG 3′-untranslated region (3′-UTR) in the transgene preserved post-transcriptional regulation. Expression kinetics of the transgene paralleled that of endogenous CD40L in unedited T cells, both at rest and in response to T cell stimulation. The use of this method to edit X-HIGM patient T cells restored normal expression of CD40L and CD40-muIg binding, and rescued IgG class switching of naïve B-cells in vitro. These results demonstrate the feasibility of engineered nuclease-directed gene repair to restore endogenously regulated CD40L, and the potential for its use in T cell therapy for X-HIGM syndrome.
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Kutukculer, Necil, Neslihan Edeer Karaca, Guzide Aksu, Ayca Aykut, Erhan Pariltay, and Ozgur Cogulu. "An X-Linked Hyper-IgM Patient Followed Successfully for 23 Years without Hematopoietic Stem Cell Transplantation." Case Reports in Immunology 2018 (October 14, 2018): 1–4. http://dx.doi.org/10.1155/2018/6897935.

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When caring for patients with life-limiting diseases, improving survival and optimizing quality of life are the primary goals. For patients with X-linked hyper-IgM syndrome (XHIGM), the treatment modality has to be decided for a particular patient regarding hematopoietic stem cell transplantation or intravenous immunoglobulin replacement therapy with P. jiroveci prophylaxis. A seven-year-old male patient was admitted with recurrent upper and lower respiratory tract infections and recurrent otitis media. His initial immunologic evaluation revealed low IgG and normal IgA and IgM levels with normal lymphocyte phenotyping and inadequate specific antibody responses. He was diagnosed as common variable immunodeficiency and began to receive intravenous immunoglobulin (IVIG) (0.5 gm/kg) with four-week intervals. During follow-up for 23 years under IVIG therapy, he was extremely well and never had severe infections. In 2017, targeted next generation sequencing was performed in order to understand his molecular pathology. A previously described hemizygous c.31C>T(p.Arg11Ter) mutation was found in CD40LG gene. The mother was heterozygous carrier for this mutation and his sister did not have any mutation. Flow cytometric analysis for CD40LG expression on activated T cells showed highly decreased, but not absent, CD40LG expression. In conclusion, diagnostic delay is a clinical problem for patients with CD40LG deficiency, because of low or normal IgM levels, showing that all the hypogammaglobulinemic patients, not only with high serum IgM levels, but also with normal to low IgM levels, have to be examined for CD40LG expression on activated T lymphocytes. Secondly, type of CD40LG mutations leads to enormous interpatient variations regarding serum IgM levels, CD40LG levels on activated T cells, age at diagnosis, severity of clinical findings, and follow-up therapies with or without hematopoietic stem cell therapy.
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Kato, Kazunori, Yukari Masuta, Kei Tomihara, Katsunori Sasaki, and Hirofumi Hamada. "A Novel Non-Cleavable Cell Surface Mutant of CD40-Ligand Induces Anti-Leukemic Immune Response and Prevent Systemic Inflammatory Reaction." Blood 104, no. 11 (November 16, 2004): 3174. http://dx.doi.org/10.1182/blood.v104.11.3174.3174.

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Abstract CD40-ligand (CD40L), a member of the TNF family, is expressed transiently on activated CD4-positive T cells and mediates cognate interaction between T cell and antigen-presenting cell (APC) such as dendritic cells. We and other investigators have reported previously that transduction of human leukemia cells with adenovirus encoding full-length CD40-ligand resulted in upregulation of immune costimulatory molecules, enhance APC activity and generation of CTL to leukemia B cells. However, CD40L is cleaved to a soluble form (sCD40L) by metalloproteases and high levels of sCD40L may contribute to the systemic inflammatory diseases including systemic lupus erythematosus and rheumatoid arthritis, suggesting a potentially deleterious side effect of CD40L gene therapy. In this study we generated a non-cleavable mutant of CD40L to develop a potentially less toxic molecule for CD40L gene therapy. Four mutants of human CD40L (termed CD40Lm1, m2, m3 and m4) with point mutation of amino acids from E112 to P120 (suggested cleavage site) were created by RT-PCR and cloned into retrovirus and adenovirus vectors. These four mutants of CD40L were transduced into tumor cells and assessed sCD40L production by ELISA, demonstrating that all four mutants resulted in a fully non-cleavable mutant of CD40L. We also confirmed that CD40L mutants could stimulate CD40-positive B and dendritic cells and induce phenotypic alterations and IL-12 production. In order to examine systemic side effect of CD40L, we transplanted tumor cells expressing wild-type (CD40Lwt) or non-cleavable mutant of CD40L (CD40Lm3) in nude mice and have observed for one month period. Two weeks after transplantation, mice with tumors expressing CD40Lwt exhibited arthritis, systemic edema and slight diarrhea, but CD40Lm3 did not induce any systemic inflammatory effect. We also found increased plasma levels of sCD40L (>800 pg/ml) in mice transplanted with CD40Lwt transfectant but not in CD40Lm3 transplanted mice. Additionally, mice with CD40Lwt resulted in increased number of infiltrating mononuclear cells in the liver and kidney, whereas no inflammatory cells were observed in the liver of mice with CD40Lm3. Overall, non-cleavable mutant of CD40L is fully capable of inducing immune response with less toxic molecule and useful tool for CD40L gene therapy of leukemia and lymphoma.
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Yeh, Yu-Min, Peng-Chan Lin, Wu-Chou Su, and Meng-Ru Shen. "CD40 Pathway and IL-2 Expression Mediate the Differential Outcome of Colorectal Cancer Patients with Different CSF1R c.1085 Genotypes." International Journal of Molecular Sciences 22, no. 22 (November 22, 2021): 12565. http://dx.doi.org/10.3390/ijms222212565.

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Colony-stimulating factor 1 receptor (CSF-1R) acts as the receptor for colony stimulating factor 1, a cytokine that controls the production, differentiation, and function of macrophages. Prior studies showed cancer patients harboring germline CSF1R c.1085A>G genetic variant had better survival. Here, primary tumor samples from a stage III colorectal cancer (CRC) cohort were analyzed by a targeted gene expression assay containing 395 immune-related genes to study the immune mechanism underlying the different outcomes. CRC patients with CSF1R c.1085 genotype A_G had a better disease-free and overall survival than those with CSF1R genotype A_A. Compared to the group of patients without CSF1R variant, higher CD40LG expression, a surface marker of T cells, was found in the tumor tissues of patients with CSF1R c.1085 variant. In parallel with the higher CD40LG gene expression, immunofluorescent staining also showed more CD3+CD40L+ T cell infiltrates in tumors with CSF1R c.1085 genotype A_G. Moreover, higher IL-2 expression, known to be regulated by CD40 pathway, was also observed in tumors with CSF1R c.1085 genotype A_G than genotype A_A. Higher IL-2 expression generated by the interaction of CD40 ligand and CD40 between T cells and macrophages with CSF1R c.1085A>G variant is the potential mechanism explaining the different outcomes.
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Dong, Qiuting, Jinxia Zhao, Zhongqiang Yao, Xiangyuan Liu, and Huiying He. "A Case Report of X-Linked Hyperimmunoglobulin M Syndrome with Lipoma Arborescens of Knees." Case Reports in Medicine 2016 (2016): 1–4. http://dx.doi.org/10.1155/2016/5797232.

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The X-linked hyperimmunoglobulin M syndrome (HIGM), caused by mutations in the CD40LG gene, is a kind of primary immunodeficiency disease (PID). Patients with X-linked HIGM are susceptible to infection as well as autoimmune diseases. Lipoma arborescens (LA) is a rare benign tumor, of which the pathogenesis mechanism has not been clearly understood. We report a case of HIGM combined with LA in a 22-year-old male patient. A new deletion mutation of CD40LG gene was detected in this case. The possible relationship between HIGM and LA was also discussed.
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Rigaud, Stéphanie, Eduardo Lopez-Granados, Sophie Sibéril, Geoffrey Gloire, Nathalie Lambert, Christelle Lenoir, Cindy Synaeve, et al. "Human X-linked variable immunodeficiency caused by a hypomorphic mutation in XIAP in association with a rare polymorphism in CD40LG." Blood 118, no. 2 (July 14, 2011): 252–61. http://dx.doi.org/10.1182/blood-2011-01-328849.

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Abstract The present study focuses on a large family with an X-linked immunodeficiency in which there are variable clinical and laboratory phenotypes, including recurrent viral and bacterial infections, hypogammaglobulinemia, Epstein-Barr virus–driven lymphoproliferation, splenomegaly, colitis, and liver disease. Molecular and genetic analyses revealed that affected males were carriers of a hypomorphic hemizygous mutation in XIAP (XIAPG466X) that cosegregated with a rare polymorphism in CD40LG (CD40 ligandG219R). These genes are involved in the X-linked lymphoproliferative syndrome 2 and the X-linked hyper-IgM syndrome, respectively. Single expression of XIAPG466X or CD40LG219R had no or minimal effect in vivo, although in vitro, they lead to altered functional activities of their gene products, which suggests that the combination of XIAP and CD40LG mutations contributed to the expression of clinical manifestations observed in affected individuals. Our report of a primary X-linked immunodeficiency of oligogenic origin emphasizes that primary immunodeficiencies are not caused by a single defective gene, which leads to restricted manifestations, but are likely to be the result of an interplay between several genetic determinants, which leads to more variable clinical phenotypes.
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Horrillo, Angélica, Tomás Fontela, Elena G. Arias-Salgado, Dolores Llobat, Gracia Porras, Matilde S. Ayuso, and Consuelo González-Manchón. "Generation of mice with conditional ablation of the Cd40lg gene: new insights on the role of CD40L." Transgenic Research 23, no. 1 (September 13, 2013): 53–66. http://dx.doi.org/10.1007/s11248-013-9743-2.

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Brune, Zarina, Bharati Matta, and Betsy Barnes. "IRF5 regulation of CD4+ T cell metabolism controls CD40L expression." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 165.02. http://dx.doi.org/10.4049/jimmunol.208.supp.165.02.

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Abstract Systemic Lupus Erythematosus (SLE) is a devastating autoimmune disease that results from failure of the immune system to distinguish “self” from “non-self”. Studies in our lab and others demonstrated that human SLE CD4+ T cells have elevated levels of IRF5 and increased metabolism, while Irf5 knockout murine CD4+ T cells show diminished utilization of oxidative phosphorylation and glycolysis, respectively. However, how IRF5 contributes to CD4+ T cell support of B cell function and dysfunction has not been fully elucidated. Here, using IRF5 KO C57BL/6J mice, we show that loss of IRF5 in CD4+ T cells directly contributes to defects in plasmablast generation. Examination of the CD40-CD40L interaction shows significant decreases in CD40L expression in Irf5 KO CD4+ T cells. Examination of Cd40lg transcript expression shows no difference in mRNA expression in Irf5 KO murine CD4+ T cells when compared to WT. This finding indicated a novel post-transcriptional regulatory role for IRF5. Examination of the canonical mTOR pathway, a key translational regulator, shows decreased phosphorylation of the S6 ribosomal protein upon loss of Irf5, indicating diminished activity of the mTOR pathway. mTOR inhibition with rapamycin in turn results in decreased CD40L expression, supporting a role for mTOR in CD40L regulation. As mTOR signaling is known to be regulated by cellular metabolism, we examined if loss of IRF5 results in altered T cell metabolism. We found that Irf5 KO T cells have decreased glucose metabolism and increased glutamine metabolism. This data has increased our understanding of how metabolism influences CD4+ T cell function and provided insight into novel post-translational regulatory roles for IRF5 via T cell metabolic regulation.
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López-Herrera, Gabriela, José Luis Maravillas-Montero, Alexander Vargas-Hernández, Laura Berrón-Ruíz, Emmanuel Ramírez-Sánchez, Marco Antonio Yamazaki-Nakashimada, Francisco Javier Espinosa-Rosales, and Leopoldo Santos-Argumedo. "A novel CD40LG deletion causes the hyper-IgM syndrome with normal CD40L expression in a 6-month-old child." Immunologic Research 62, no. 1 (March 10, 2015): 89–94. http://dx.doi.org/10.1007/s12026-015-8638-0.

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Dissertations / Theses on the topic "Cd40lg-"

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MERCURI, ELISABETTA. "PRECLINICAL MODELING HIGHLIGHTS THE THERAPEUTIC POTENTIAL OF THE ADOPTIVE TRANSPLANT OF GENE CORRECTED T CELLS IN X-LINKED HYPER-IGM IMMUNODEFICIENCY." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2020. http://hdl.handle.net/10281/263922.

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La terapia genica di cellule staminali ematopoietiche (HSC) ha prodotto benefici clinici in diversi pazienti affetti da una varietà di malattie genetiche. Tuttavia, l’uso di vettori che si integrano nel genoma in modo semi-casuale pone il rischio di mutagenesi inserzionale e di una espressione del transgene ectopica/non regolata. Quest’ultimo problema è particolarmente rilevante quando si trattano geni strettamente regolati attivi sulla proliferazione cellulare, come il gene CD40LG, la cui espressione sulle cellule T attivate porta all’attivazione contatto-dipendente delle cellule B, alla loro proliferazione ed allo scambio di classe delle immunoglobuline. Poichè le sue mutazioni causano l’immunodeficienza legata all’X con iper-IgM (HIGM1), il trasferimento genico in HSC è stato proposto come potenziale trattamento per questa sindrome. Anche se piccole quantità di cellule trasdotte hanno ripristinato la funzione immunitaria umorale e cellulare in un modello murino di HIGM1, l’espressione costitutiva di CD40LG in timociti o in cellule T periferiche ha portato a linfoproliferazioni, molte delle quali sono progredite a linfom. Le strategie di riparazione genica che preservano il controllo fisiologico dell’espressione del gene corretto potrebbero quindi rappresentare un approccio più promettente per il trattamento di HIGM1. In questo studio sfruttiamo il meccanismo Homology Directed Repair (HDR) per la correzione in situ della maggior parte delle mutazioni responsabili della sindrome HIGM1 presenti nel gene CD40L, con l’obiettivo di ristabilirne la funzione e il controllo dell’espressione. In particolare sfruttiamo il sistema CRISPR/Cas9 per promuovere l’integrazione sito-specifica di una copia funzionale di parte del gene CD40L a valle del suo promotore endogeno, correggendo così la maggior parte delle mutazioni responsabili della malattia. Dato che il difetto genetico non è deleterio per le cellule T, questo tipo di malattia ci offre l’opportunità unica di sviluppare una terapia genica basata sulla correzione di cellule T autologhe. Al fine di stabilire quali sono le dosi terapeutiche e le condizioni di trapianto necessarie per ottenere la ricostituzione immunitaria e il ripristino delle funzioni immunologiche con cellule corrette, abbiamo infuso diverse dosi di cellule T WT in topi HIGM1 pre-condizionati o meno con diversi regimi linfodepletanti ed eseguito trapianti competitivi di cellule staminali ematopoietiche WT e Cd40lg - / - nel modello animale. Mentre l’ analisi del sangue periferico ha dimostrato la persistenza a lungo termine di cellule T in tutte le condizioni, sono stati ottenuti livelli di attecchimento più elevati nei topi trapiantati dopo il trattamento chemioterapico con ciclofosfamide (CPA). Tutti i topi trapiantati hanno mostrato un parziale ripristino della risposta IgG specifica dopo immunizzazione con TNP-KLH, ma è stato osservato un ripristino più elevato nei topi pre-condizionati con CPA. Questi topi hanno anche mostrato la presenza di centri germinativi nella milza. Topi HIGM1 ricostituiti con dosi crescenti di HSPC WT hanno mostrato un ripristino dose-dipendente della risposta immunitaria T dipendente. In particolare, abbiamo dimostrato che il 10% di HSPC funzionali è sufficiente a ripristinare parzialmente la capacità di produrre anticorpi specifici contro diversi antigeni oltre che ad attenuare l'infezione in topi HIGM1 inoculati con il patogeno Pneumocystis murina. Il nostro obiettivo futuro è quello di dimostrare il ripristino della risposta immunitaria contro l'infezione da pneumocystis murina in topi HIGM1 trapiantati con cellule T CD4 + WT. In caso di successo, i nostri risultati saranno strumentali per stabilire il potenziale terapeutico di un approccio di correzione genica basato sulle cellule T per il trattamento della sindrome HIGM1 che potrebbe fungere da terapia ponte per una terapia definitiva basata sul trapianto di HSPC corrette.
Background The X-linked hyper-IgM syndrome type I (HIGM1) is caused by inactivating mutations in the CD40 ligand gene (CD40LG) that disrupt the T cell helper function on B cells and macrophages. This disease represents an ideal candidate for a gene correction strategy because preclinical studies of Hematopoietic Stem Cell (HSC) gene therapy have already shown i) evidence of potential efficacy even with few amounts of transduced cells; ii) critical safety issues due to unregulated transgene expression. Since in HIGM1 the genetic defect is not lethal to T cells, we aim to apply our gene editing strategy on autologous T cells that could be used to provide immediate therapeutic benefit to the patients by resolving pre-existing infections prior to a definitive HSPC transplant. Methods To establish which are the therapeutic threshold levels and transplant conditions required to achieve immune reconstitution and functional immunologic restoration with corrected cells, we infused different doses of WT T cells into HIGM1 mice pre-conditioned or not with different lymphodepleting regimens and performed competitive transplants of WT and Cd40lg-/- HSPC in the mouse model. Results While longitudinal blood analyses showed a long-term, stable T cell engraftment in all the conditions, highest engraftment rates were obtained in mice transplanted after chemotherapy treatment with cyclophosphamide (CPA). All the transplanted mice showed a partial rescue of the antigen-specific IgG response after immunization with Keyhole Limpet Hemocyanin (TNP-KLH) but a higher rescue was observed in mice pre-conditioned with CPA. These mice also showed the presence of TNP-KLH specific IgG producing B cells and germinal centers within splenic lymphoid follicles. HIGM1 mice reconstituted with increasing proportions of WT HSPC displayed a dose-dependent rescue of the T cell mediated immune response. In particular we found that 10% of WT HSPC is sufficient to partially restore serologic immunity against different antigens as well as to attenuate infection in HIGM1 mice challenged with Pneumocystis murina. Conclusions Our current efforts are aimed to demonstrate functional restoration of the immune response against Pneumocystis murina infection in HIGM1 mice that received adoptive transfer of WT CD4+ T cells. If successful, our findings will be instrumental to establish the therapeutic potential of a T cell gene correction approach for the treatment of the HIGM1 disease that could act as a bridge therapy to the HSPC-based strategy.
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Yeboah, Sybil A. Parise Leslie V. "Do CD40L and CD40 contribute to sickle cell anemia?" Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,1640.

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Thesis (M.S.)--University of North Carolina at Chapel Hill, 2008.
Title from electronic title page (viewed Sep. 16, 2008). "... in partial fulfillment of the requirements for the degree of Master of Science in the Department of Biochemistry." Discipline: Biochemistry and Biophysics; Department/School: Medicine.
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Martins, Ryan Stephen. "Tumor-Bearing Host Macrophage Dysfunction: Role of CD40/CD40L Interactions." Thesis, Virginia Tech, 2001. http://hdl.handle.net/10919/32405.

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A functional immune system is a potential barrier to tumor growth and progression. Cancer is caused, in part, by the loss of immune surveillance leading to the inability of the immune system to destroy the cancer cells. Macrophages (Mfs) are essential cellular components of the immune system; they influence immune responses in diverse and fundamental ways. As a consequence, Mfs present targets for tumors to evade, thereby enhancing tumor survival and growth. An interaction between CD40 on Mfs and CD40L on T cells is required for cell-mediated inflammatory responses. The CD40/CD40L interaction is bi-directional; suppressed expression of either protein by the tumor will prevent activation of both Mfs and T cells. We showed that tumor growth suppresses T-cell CD40L expression. Decreased CD40L expression disrupted Mf activation pathways, leading to impaired production of immunostimulatory cytokines, interleukin (IL)-12 and IL-18 by tumor-bearing host (TBH) Mfs. Disruption of CD40L expression, via dysregulation of IL-12 and IL-18 production, impeded T-cell interferon (IFN)-g production, which in turn exacerbated Mf dysfunction. We showed that IFN-g induced interferon consensus sequence binding protein (ICSBP) expression is impaired in TBH Mfs due to tumor cell-derived TGF-b and, to a lesser extent, IL-10. ICSBP induces CD40L, IL-12, and IL-18 expression. Disruption of the CD40/CD40L interaction via lowered CD40L expression generates an immunosuppressive loop that may be a strategy for tumor survival and growth. This was demonstrated by impaired cytotoxicity; via impaired tumor necrosis factor (TNF)-a and nitric oxide (NO) production by TBH Mfs against Meth-KDE tumor cells. Collectively, these studies show that multiple antitumor mechanisms could be enhanced by restoration of CD40L expression.
Master of Science
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Oxer, Daniella Stefani. "Interação entre as vias de sinalização CD40/CD40L e os PPARs." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5159/tde-17062009-122735/.

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O receptor CD40 e seu ligante CD40L possuem um papel importante na interface entre a resposta imune inata e a adaptativa. Disfunções desta via de sinalização são descritas em doenças de origem inflamatória e autoimunes. Em Lúpus eritematoso sistêmico (LES) foi descrito um aumento nos níveis séricos de CD40L solúvel, que participa na produção de autoanticorpos. Receptores ativados por proliferadores de peroxisomos (PPARs) são fatores de transcrição que inicialmente foram descritos como envolvidos apenas no metabolismo lipídico, mas que atualmente são também descritos como atuantes no controle da resposta imune. Com isso, nosso objetivo é determinar se a ativação dos PPARs modula o processo inflamatório através da interação com CD40/CD40L in vitro ou in vivo. Células de linhagem monocítica humana THP-1 foram tratadas por 24 horas com forbol-éster (PMA, 40 nM) e posteriormente estimuladas com CD40L recombinante (rhCD40L, 1 g/ml) por diferentes períodos. Transcritos de mRNA foram analisados por real time PCR e os resultados expressos como razão da expressão do gene housekeeping GAPDH. As células THP-1 apresentam um aumento na expressão de PPAR e após 16 e 2 horas de estímulo com rhCD40L, respectivamente. Estas células também foram estimuladas com LPS (10 g/ml) e LPS+rhCD40L para sabermos se a resposta obtida anteriormente era específica ao estímulo com rhCD40L. O resultado mostra que há uma diminuição na expressão de PPAR e após o estimulo com LPS ou LPS+rhCD40L, indicando que nessas condições a modulação da expressão de PPARs é especifica para a via de sinalização CD40/CD40L. Foi medida também a expressão de CD36, que é descrito na literatura como um indicador da atividade de PPARs. O resultado mostra que o estímulo com CD40L promove um aumento de CD36, o que indica indiretamente que o PPAR estava ativo neste modelo experimental. Para mostrar a interação direta destas duas vias de sinalização, silenciamos o gene de PPAR por siRNA e posteriormente anlisamos a expressão de CD80, cuja expressão encontra-se aumentada logo após a ativação do CD40 de acordo com a literatura. O resultado mostra que, com o silenciamento de PPAR , há um aumento de CD80 logo após a ativação do CD40, evidenciando assim a interação entre essas duas vias de sinalização. A fim de verificar se os achados encontrados in vitro poderiam ser observados in vivo, foi isolada a fração mononuclear de sangue periférico de pacientes com LES com a doença em atividade (n=17), a doença inativa (n=21) ou doadores saudáveis (n=12) e foi medida a expressão de PPAR e por real time PCR. PPAR apresenta um aumento em pacientes com a doença ativa ou inativa em comparação aos doadores saudáveis. Já a expressão de PPAR apresenta aumento apenas em lúpicos em atividade quando comparados com lúpicos inativos ou doadores saudáveis. Quando considerado nesta análise o efeito do tratamento dos pacientes com corticosteróides nos níveis de PPAR, obsevou-se que a expressão de PPAR apresenta o mesmo padrão anterior. Estes resultados sugerem a hipótese de que PPAR seja um possível marcador de atividade de LES. Para confirmar esta especificidade, foram adicionadas à analise células mononucleares retiradas de pacientes com tuberculose e com infecções agudas. Os dados mostram que os níveis elevados de PPAR se mantém apenas em pacientes com lúpus ativo, o que confirma nossa hipótese. Nossos achados sugerem que PPAR e são regulados especificamente em reposta a ativação da via do CD40/CD40L, em monócitos em cultura e em células obtidas de pacientes com LES. Podemos também sugerir que PPAR possa ser um marcador para a atividade de LES. Estes resultados podem representar um novo mecanismo de controle da via de sinalização do CD40/CD40L, participando no controle da resposta inflamatória em cultura e em células de pacientes lúpicos
The membrane receptor CD40 and its ligand CD40L play an important role in the interface between innate and acquired immunity. Dysfunction of this signaling pathway was described in inflammatory and autoimmune diseases. In systemic lupus erythematosus (SLE), increased serum levels of soluble CD40L have been detected, where it plays a significant role in the generation of auto-antibodies. Peroxisome proliferator activator receptors (PPARs) are transcription factors originally described in lipid metabolism. More recently, they were also characterized as inflammatory modulators. Therefore, our objective was to determine whether the activation of PPARs may modulate the inflammatory process through interaction with the CD40/CD40L signaling pathway in vitro and in vivo. Macrophages derived from the human monocytic cell line THP-1 by 24h-treatment with PMA (40 nM) were stimulated with human recombinant CD40L (rhCD40L, 1 g/ml) for different periods. Messenger RNA (mRNA) transcripts for PPAR , and were determined by real time PCR and expressed as a ratio of the housekeeping gene GAPDH transcripts. THP-1 cells express a basal level of PPAR and gene transcription, which is increased 16 and 2 hours after exposure to rhCD40L, respectively. We also stimulated the THP-1 cells with LPS (10 g/ml) and LPS+rhCD40L to see if the increase of PPAR was a response specific to the rhCD40L stimuli. The data show that there is a decrease in PPAR and genes expression upon LPS or LPS+rhCD40L stimulation, indicating that in these times (2 and 16 hours) the response is specific for the CD40/CD40L signaling pathway. Increased expression of CD36 is known as an indicator of PPARs activity. We measured CD36 and saw an increase of this receptor after rhCD40L stimulus, indicating indirectly that PPARs were active in this experimental model. To prove the direct interaction between CD40/CD40L and PPAR , we silenced the PPAR gene by siRNA and analyzed the expression of CD80, which is known to increase after CD40 activation. The results show an increase in CD40L-stimulated CD80 expression upon silencing of PPAR , showing that there is an interaction between these signaling pathways. To confirm whether these findings also occur in vivo, mononuclear cells were isolated from whole blood samples from SLE patients with active (n=17) and inactive disease (n=21), and healthy donors (n=12). The mRNA transcripts for PPARs were detected by real time PCR. In both active and inactive SLE patients, monocytes show an increase in PPAR mRNA expression, as compared to healthy donors. PPAR mRNA is increased only in active patients when compared to healthy donors and inactive lupus patients. Further in this analysis, when we separated the patients with and without the administration of corticosteroids, PPAR displayed the same pattern as above. These results suggested that PPAR may be a marker for lupus activity. To validate this hypothesis, we compared the results obtained from patients with tuberculosis and acute infections. Results showed that only active-lupus patients have an increase in PPAR , confirming the specificity of this phenomenon and hence our hypothesis Our findings suggest that PPAR and are up-regulated specifically in response to CD40/CD40L activation, in both cultured macrophages and in monocytes obtained from SLE patients. We could also suggest that PPAR may be marker for lupus activity. Our results may represent a new control mechanism of the CD40/CD40L signaling pathway and seem to be implicated in the control of the inflammatory response in both human macrophages in vitro and SLE patients
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Macina, Denis. "Étude de l'implication du système CD40/CD40L dans le syndrome hyper-IGM." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq33704.pdf.

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Morgenroth, Iris. "Charakterisierung des CD40-CD40L-Systems als wichtiger Regulator der B-Zellfunktion des Haushuhns." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-77513.

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Bürger, Christina [Verfasser], and Sabine [Akademischer Betreuer] Steffens. "Cell type-specific CD40-CD40L interaction in atherosclerosis / Christina Bürger ; Betreuer: Sabine Steffens." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2017. http://d-nb.info/1142787141/34.

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Pluvinet, Ortega Raquel. "Paper del receptor CD40 en l'activació de les cèl·lules endotelials. Rellevància de la interacció CD40-CD40L en processos immunoinflamatoris." Doctoral thesis, Universitat de Barcelona, 2007. http://hdl.handle.net/10803/1884.

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CD40 (TNFRSF5) és una glicoproteïna de membrana que pertany a la família de receptors del factor de necrosi tumoral (TNF-R). La interacció amb el seu lligand fisiològic (CD40L o CD154) regula una àmplia varietat de funcions biològiques, des de l'activació del sistema immune, tant humoral com cel·lular, a diferents aspectes de la resposta inflamatòria.
Els principals objectius d'aquesta tesi han estat 1) l'estudi a nivell molecular del paper de CD40 en l'activació de les cèl·lules endotelials, i 2) les conseqüències del bloqueig d'aquesta via de senyalització en la resposta immunoinflamatòria.
S'ha obtingut un siRNA potent i específic capaç de reduir l'expressió del receptor CD40 humà en un 85%, tant a nivell de mRNA com a nivell de proteïna. Aquest siRNA expressat en forma de shRNA en un vector lentiviral permet assolir un silenciament gènic eficient i estable de CD40 al llarg del temps. S'ha validat l'activitat antiinflamatòria d'aquest siRNA analitzant les conseqüències funcionals del silenciament d'aquest receptor en cèl·lules endotelials. Aquest siRNA bloqueja l'activació endotelial via CD40L impedint la inducció de l'expressió de les molècules d'adhesió ICAM-1, VCAM-1 i E-selectina, i inhibint l'adhesió leucocitària en aquestes cèl·lules en un 87%.
S'ha utilitzat el potencial antiinflamatori del siRNA dirigit contra CD40 humà per estudiar el paper d'aquest receptor en cèl·lules endotelials en inflamació. Utilitzant microarrays, s'ha realitzat una anàlisi comparativa del perfil global d'expressió gènica en cèl·lules endotelials humanes en les quals s'inactiva específicament aquesta via de senyalització mitjançant RNAi, en el context de la interacció cèl·lula endotelial i limfòcit T activat (CD40L+), com a primer pas en l'inici de la resposta immunoinflamatòria. Aquest estudi d'expressió gènica ha permès identificar nous gens i noves vies de senyalització implicades en la inducció de la resposta inflamatòria desencadenada per l'activació de CD40 en endoteli.
Per altra banda, es volia avaluar l'eficàcia del silenciament gènic de CD40 per a la inducció de tolerància immunològica en un model experimental d'al·lotrasplantament renal. Amb aquesta finalitat s'ha obtingut un siRNA anti-CD40 de rata amb una potent eficiència silenciadora i s'ha optimitzat la transferència d'aquest siRNA en el ronyó a trasplantar mitjançant electroporació in vivo de l'òrgan. L'objectiu d'aquest estudi era silenciar temporalment l'expressió d'aquest receptor en les cèl·lules renals i bloquejar la interacció CD40-CD40L essencial per a la inducció de procés inflamatori que dóna lloc al rebuig del ronyó trasplantat. Resultats preliminars mostren que la teràpia gènica local amb siRNA redueix la resposta inflamatòria posttrasplantament. El siRNA anti-CD40 causa una reducció significativa de l'expressió del mRNA de CD40, disminuint l'aparició de rebuig agut humoral i allargant el temps mig de supervivència dels animals trasplantats amb els ronyons tractats amb siRNA en comparació amb els animals control.
CD40 (TNFRSF5) belongs to the tumor necrosis factor receptor family (TNF-R). Its interaction with its physiological ligand (CD40L or CD154) regulates a wide variety of biological functions, from the activation of the immune system, to different aspects of the inflammatory response.
The main goals of this work have been 1) the molecular study of the role of CD40 in the activation of the endothelial cells, and 2) the consequences of blocking this signaling in the immunoinflammatory response. We have obtained a powerful and specific siRNA able to reduce human CD40 expression by 85%. The anti-inflammatory activity of this siRNA has been validated by analyzing the functional consequences of CD40 silencing in endothelial cells activated via CD40L. This siRNA blocks the induction of ICAM-1, VCAM-1 and E-selectin expression, and inhibits leukocyte adhesion in these cells by 87%.
We have used the anti-inflammatory potential of this siRNA directed against human CD40 to carry out a global gene expression profiling analysis in order to study the role of CD40 in endothelial cells during inflammation. Using microarrays, we have performed a comparative transcriptome analysis in human endothelial cells, in the context of the endotelial cell interaction with activated T lymphocyte (CD40L+), as the first step of the immunoinflammatory response. This study has allowed us to identify new genes and signaling pathways involved in the induction of the inflammatory response by CD40 activation in endothelium.
On the other hand, we have obtained an siRNA against rat CD40 with a powerful silencing activity and we have optimized its transfer to the kidney through in vivo electroporation. The purpose of this study was to determine the CD40 gene silencing effectiveness in inducing immunological tolerance in an experimental model of renal allotransplantation. Preliminary results show that local gene therapy with siRNA reduces the inflammatory response post-transplantation. The anti-CD40 siRNA treatment causes a significant reduction of the incidence of acute humoral rejection and increases the survival half life of animals transplanted with kidneys treated with siRNA compared to control animals.
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Meunier, Sylvain. "Impact de l’interaction CD40/CD40L sur les différents intervenants de la réponse immunitaire T CD8." Paris 5, 2011. http://www.theses.fr/2011PA05T039.

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Mon sujet de thèse consiste à étudier le rôle des différentes voies possible à l’interaction CD40/CD40L au cours de la réponse primaire des lymphocytes T CD8 et à caractériser la réponse des lymphocytes T CD8 CD40-/-. Les résultats obtenus jusqu’à présent semblent montrer deux effets à une interaction CD40/CD40L en fonction de la localisation de la molécule CD40 selon le type cellulaire (sur les lymphocytes T CD8 ou sur les cellules présentatrices d’antigène). Le premier effet est la mis en place d’une réponse primaire optimale de la part des lymphocytes T CD8 et est dû à l’expression de CD40 par les cellules présentatrices d’antigène. Le deuxième effet est la génération de la mémoire immunitaire T CD8 au cours de la réponse primaire et est dû à l’expression de CD40 par les lymphocytes T CD8. Nos résultats montrent que l’interaction CD40/CD40L passant par les cellules présentatrices d’antigène envoie les signaux suffisants pour la prolifération et la cytotoxicité de la réponse primaire T CD8. En revanche, l’interaction CD40/CD40L passant par les lymphocytes T CD8 est indispensable à la génération de la mémoire T CD8. Si la déficience en CD40 par les lymphocytes T CD8 n’affecte pas la réponse primaire, ce n’est pas le cas de la réponse secondaire. En effet, dans ce cas, les lymphocytes T CD8 présentent une réponse secondaire altérée. Comparé à une réponse secondaire classique, les lymphocytes T CD8 CD40-/- présentent une amplitude de réponse diminuée et un pic de réponse décalé, une réponse plus proche d’une réponse primaire. Ces cellules présentent également une cytotoxicité et une survie altérées, ainsi qu’une sensibilité aux facteurs immunorégulateurs accrue
My thesis project is to study the role of different possible pathways possible for the CD40/CD40L interaction during the primary response of CD8 T cells and to characterize the response of CD8 T cell CD40-/-. The results suggest two CD40/CD40L interaction effects depending on the location of the CD40 molecule expressed on different cell types (on CD8 T cells or on antigen presenting cells). The first effect is to set up an optimal primary response from the CD8 T cells and is due to the expression of CD40 by antigen presenting cells. The second effect is the generation of memory CD8 T cells during the primary response and is due to the expression of CD40 by CD8 T cells. Our results show that the CD40/CD40L interaction via the antigen presenting cells sends signals sufficient for proliferation and cytotoxicity of CD8 primary response. However, the CD40/CD40L interaction via the CD8 T cells is essential for the generation of memory CD8 T cells. If the deficiency of CD40 by CD8 T cells does not affect the primary response, it is not the case of the secondary response. Indeed, in this case, CD8 T cells exhibit altered secondary response. Compared to a classical secondary response, the CD8 T cells CD40-/- exhibit a decreased response amplitude and delayed peak response, a response closer to a primary response. These cells also exhibit impaired cytotoxicity and survival. Finally these cells have a more sensitivity to immunoregulatory factors
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Sakai, Hidemasa. "The CD40-CD40L axis and IFN-γ play critical roles in Langhans giant cell formation." Kyoto University, 2012. http://hdl.handle.net/2433/158049.

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Books on the topic "Cd40lg-"

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Cooke, Peter William. CD40 expression in bladder cancer. Birmingham: University of Birmingham, 2001.

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Davies, Clare Charlotte. Mechanisms of CD40 signalling and apoptosis in carcinoma cells. Birmingham: University of Birmingham, 2003.

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Wheeler, Kay. The role of CD40 in human B cell activation. Birmingham: University of Birmingham, 1993.

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Armour, Carolyn Anne. The role of CD40 in the regulation of cell growth. Birmingham: University of Birmingham, 1998.

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Baker, Matthew Paul. Functional and molecular aspects of CD40 signalling in human B cells. Birmingham: University of Birmingham, 1997.

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Teale, Glyn Robert. Characterisation of the CD40 cell surface receptor in cervical invasive and preinvasive disease. Birmingham: University of Birmingham, 2001.

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Total integrated dose testing of solid-state scientific CD4011, CD4013, and CD4060 devices with CO-60 gamma rasys. [Washington, DC: National Aeronautics and Space Administration, 1985.

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Lucas, Carrie Lynn. Mechanisms of deletional tolerance of peripheral CD8⁺ T cells induced by anti-CD40L and allogeneic bone marrow transplantation. 2010.

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Goldstein, Marni Diane. Differential signal transduction by the B cell activation receptor CD40. 1998.

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Differential Induction of Nuclear Factor-κB and Activator Protein-1 Activity after CD40 Ligation Is Associated with Primary Human Hepatocyte Apoptosis or Intrahepatic Endothelial Cell Proliferation. Molecular Biology of the Cell, 2003.

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Book chapters on the topic "Cd40lg-"

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Kotlyar, David, and Anthony Leonardi. "Anti-CD40/Anti-CD40L." In Cancer Therapeutic Targets, 31–42. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4419-0717-2_92.

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Kotlyar, David, and Anthony Leonardi. "Anti-CD40/Anti-CD40L." In Cancer Therapeutic Targets, 1–12. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6613-0_92-1.

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Law, Che-Leung, and Iqbal S. Grewal. "Therapeutic Interventions Targeting CD40L (CD154) and CD40: The Opportunities and Challenges." In Advances in Experimental Medicine and Biology, 8–36. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-89520-8_2.

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Wenzel, Folker. "Soluble CD40L in Stem Cell Products." In Stem Cells and Cancer Stem Cells, Volume 12, 241–45. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-017-8032-2_21.

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Bishop, Gail A., and Bruce S. Hostager. "CD40." In Encyclopedia of Signaling Molecules, 886–93. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_148.

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Covey, Lori R. "CD40." In Encyclopedia of Medical Immunology, 254–63. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-0-387-84828-0_32.

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Bishop, Gail A., and Bruce S. Hostager. "CD40." In Encyclopedia of Signaling Molecules, 1–8. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_148-1.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "CD40." In Encyclopedia of Signaling Molecules, 313–20. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_148.

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Burkly, Linda C. "CD40L Pathway Blockade as an Approach to Immunotherapy." In Advances in Experimental Medicine and Biology, 135–52. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1277-6_12.

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Schultz, A., A. Greiner, R. Nenninger, D. Schömig, A. Wilisch, E. Oswald, R. A. Kroczek, B. Schalke, H. K. Müller-Hermelink, and A. Marx. "CD40-Expression in Thymoma." In Epithelial Tumors of the Thymus, 235–45. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-0033-3_31.

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Conference papers on the topic "Cd40lg-"

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França, Tábata Takahashi, Luiz Fernando Bacarini Leite, Tiago Arruda Maximo, Christiane Guedes Lambert, Nuria Bengala Zurro, Wilma Carvalho Neves Forte, and Antonio Condino Neto. "NOVA MUTAÇÃO NO GENE CD40LG EM PACIENTE COM FENÓTIPO BRANDO DE SÍNDROME DE HIPER- IGM LIGADA AO X." In 4º Congresso Internacional Sabará de Saúde Infantil. São Paulo: Editora Blucher, 2020. http://dx.doi.org/10.5151/cissi2020-54.

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Merz, Christian, Jaromir Sykora, Meinolf Thiemann, Viola Marschall, Karl H. Heinonen, Harald Fricke, Christian Gieffers, and Oliver Hill. "Abstract 1688: HERA-CD40L: A novel hexavalent CD40 agonist with superior biological activity." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1688.

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Sun, Zhijian, and Lusong Luo. "Abstract 1298: CD40L-CD40 signaling on B-cell lymphoma response to BTK inhibitors." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1298.

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Merz, Christian, Jaromir Sykora, Viola Marschall, David M. Richards, Meinolf Thiemann, Harald Fricke, Oliver Hill, and Christian Gieffers. "Abstract 1760: The hexavalent CD40 agonist HERA-CD40L augments multi-level crosstalk between T cells and antigen-presenting cells." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1760.

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Bauer, NN, JT Baker, J. Rai, and TM Moore. "Soluble CD40L Directly Regulates PMVEC Barrier Function." 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.a2327.

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Glick, Adam B., Jacob T. Bailey, Andrew Gunderson, Kyle Breech, and Michael Podolsky. "Abstract 2673: Divergent therapeutic responses to CD40L blockade or CD40 activation in Ras-driven skin cancers determined by origin of tumor initiating cell." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2673.

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Gieffers, Christian, David M. Richards, Jaromir Sykora, Christian Merz, Julian P. Sefrin, Katharina Billian-Frey, Karl Heinonen, et al. "Abstract 1076: Hexavalent HERA-CD40L induces a productive T cell-mediated anti-tumor immune response and shows superior activity in comparison to benchmark CD40 agonistic antibodies." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-1076.

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Trella, Emanuele. "Abstract A016: Multipotency of a CD40L-expressing recombinant vaccinia virus." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-a016.

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Gieffers, Christian, Jaromir Sykora, Christian Merz, Mauricio Redondo Müller, David M. Richards, Julian Sefrin, Katharina Billian-Frey, et al. "Abstract 5015: HERA-CD40L a hexavalent CD40 agonist induces T cell mediated anti-tumor immune response and shows superior activity in direct comparison to benchmark agonistic antibodies." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-5015.

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Gieffers, Christian, Jaromir Sykora, Christian Merz, Mauricio Redondo Müller, David M. Richards, Julian Sefrin, Katharina Billian-Frey, et al. "Abstract 5015: HERA-CD40L a hexavalent CD40 agonist induces T cell mediated anti-tumor immune response and shows superior activity in direct comparison to benchmark agonistic antibodies." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-5015.

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Reports on the topic "Cd40lg-"

1

Sorensen, Neil Robert. Failure analysis for the dual input quad NAND gate CD4011 under dormant storage conditions. Office of Scientific and Technical Information (OSTI), May 2007. http://dx.doi.org/10.2172/908064.

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Sorensen, Neil Robert. Failure analysis for the dual input quad NAND fate CD4011 under dormant storage conditions. Office of Scientific and Technical Information (OSTI), November 2004. http://dx.doi.org/10.2172/975246.

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