Дисертації з теми "Immune cell activation"
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Delcassian, Derfogail. "Biomimetic substrates for immune cell activation." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/30729.
Tilney-Bassett, Amanda L. "Phospholipid metabolism in T-cell activation." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239331.
Cliff, Jacqueline Margaret. "The role of autocrine factors in B cell activation." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327054.
Mohib, Kanishka. "Embryonic Stem Cell Extracts Possess Immune Modulatory Properties That Prevent Dendritic Cell Maturation and T Cell Activation." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/22794.
Nugent, Alexandria Lynne. "Morphine activation of stress pathways alters peripheral immune cell signaling." Connect to Electronic Thesis (ProQuest), 2008. http://0-gateway.proquest.com.library.lausys.georgetown.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3315451.
Nyambuya, Tawanda Maurice. "Markers of chronic immune activation and T-cell function in hyperglycaemia." Thesis, Cape Peninsula University of Technology, 2017. http://hdl.handle.net/20.500.11838/2597.
Type 2 diabetes mellitus (T2DM) is a chronic inflammatory condition characterised by hyperglycaemia; continuous activation of T-lymphocytes and immune dysregulation. Although the exact mechanisms of these phenomena are not fully understood, there is strong evidence suggesting the involvement of T-cells in the chronic inflammatory environment which could predispose diabetics to infections and thrombotic events. The effect of hyperglycaemia on cells of the innate immune system in T2DM has been well described and implicated in the progression of the disorder and the development of its complications. However, studies investigating the adaptive immune response still remain scarce and controversial. Thus, investigating T-cells in hyperglycaemic conditions could provide further insight into the immune dysfunction observed in T2DM and assist in identifying pathways which could be targeted in the disease management and treatment. Therefore, this study aimed to investigate chronic immune activation by measuring the expression of T-cell activation markers in hyperglycaemia and compare the results to those in the normoglycaemic group.
Clary, Sara Reed. "The effects of nitrosoureas on Thymocyte differentiation and T cell activation." Thesis, Virginia Tech, 1990. http://hdl.handle.net/10919/41939.
Cantrell, Jessica. "Adjuvant Effect of Chaperone-Rich Cell Lysate: The Effects of CRCL on the Activation of Immune Cells." Diss., The University of Arizona, 2009. http://hdl.handle.net/10150/195380.
Taner, Sabrina Beliz. "The role of lipid rafts in natural killer cell activation and immune surveillance." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.423546.
Carlin, Lindsey Elizabeth. "Natural killer cell activation, trafficking, and contribution to immune responses to viral pathogens." Diss., University of Iowa, 2013. https://ir.uiowa.edu/etd/1302.
Freitas, Claudia Mercedes. "Regulation of Immune Cell Activation and Functionby the nBMPp2 Protein andthe CD5 Co-Receptor." BYU ScholarsArchive, 2019. https://scholarsarchive.byu.edu/etd/8257.
Smyth, Lucy J. C. "Activation of cells of the mast cell/basophil lineage in response to potential allergens in the absence of IgE sensitisation." Thesis, University of Sheffield, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324450.
De, Milito Angelo. "Immune activation during HIV-1 infection : implication for B cell dysfunctions and therapy monitoring /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-170-5.
Alberghini, F. "THE ROLE OF PRC1 IN B CELL DEVELOPMENT AND ADAPTIVE IMMUNE RESPONSES." Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/285499.
Li, Hongbo. "SELECTIVE CB2 RECEPTOR ACTIVATION AMELIORATES INFLAMMATION IN CENTRAL NERVOUS SYSTEM BY REDUCING TH17 CELL DIFFERENTIATION AND IMMUNE CELL ACCUMULATION." Diss., Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/288653.
Ph.D.
Modulation of the endocannabinoid system by the administration of exogenous agonists and selective antagonists has been shown to have potential to attenuate the contribution of inflammation to secondary injury in the CNS. The two most well-defined receptors are the CB1 and CB2 receptors. CB2, the cannabinoid receptor expressed primarily on hematopoietic cells and activated microglia, mediates the immunoregulatory functions of cannabinoids. The involvement of CB2 in central nervous inflammation has been demonstrated by using both endogenous and exogenous ligands. We showed previously that CB2 selective agonists inhibited leukocyte rolling and adhesion to CNS microvasculature and ameliorate clinical symptom in both chronic and remitting-relapsing EAE models; and our previous studies also demonstrated therapeutic potential of CB2 agonist improving recovery following spinal cord injury in the mouse. The goal of the current investigation was to evaluate the mechanisms through which administration of a selective cannabinoid-2 (CB2) agonist modifies inflammatory responses and helps to improve function following the injury in central nervous system. In the EAE project, we showed that Gp1a, a highly selective CB2 agonist with a four log higher affinity for CB2 than CB1, reduced clinical scores and facilitated recovery in EAE in conjunction with long term reduction in demyelination and axonal loss. We also established that Gp1a affected EAE through at least two different mechanisms, i.e. an early effect on Th1/Th17 differentiation in peripheral immune organs, and a later effect on the accumulation of pathogenic immune cells in the CNS, associated with reductions in the expression of CNS and T cell chemokine receptors, chemokines and adhesion molecules. This is the first report on the in vivo CB2-mediated Gp1a inhibition of Th17/Th1 differentiation. We also confirmed the Gp1a-induced inhibition of Th17/Th1 differentiation in vitro, both in non-polarizing and polarizing conditions. The CB2-induced inhibition of Th17 differentiation is highly relevant in view of recent studies emphasizing the importance of pathogenic self-reactive Th17 cells in EAE/MS. In spinal cord injury project, we showed that spinal cord injury mice CB2 agonist O-1966 (with affinities to the CB1 and CB2 receptors of 5055±984 and 23±2.1 nM, respectively) had improved motor function, autonomic function. They also had significant reductions in CXCL-9, CXCL-11, dramatic reductions in IL-23p19 expression and its receptor IL-23r, and reduction in the number of immunoreactive microglia. The results reported in this thesis, demonstrated that the combined effect on Th17 differentiation and immune cell accumulation into the CNS, may contribute to the usefulness of CB2 selective ligands as potential therapeutic agents in neuroinflammation.
Temple University--Theses
Ehrenberg, Stefanie [Verfasser], and Josef [Akademischer Betreuer] Mautner. "Notch2 signalling in B cell activation, immune response and lymphomagenesis / Stefanie Ehrenberg. Betreuer: Josef Mautner." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2015. http://d-nb.info/1096162849/34.
Patterson, Andrew R. "Gimap5: A Critical Regulator of CD4+ T Cell Homeostasis, Activation, and Pathogenicity." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1544098387129747.
Sousa, Daniela Alexandra Costeira de. "Stimulation of a pDC cell line with self-DNA immune complexes." Master's thesis, Universidade de Aveiro, 2017. http://hdl.handle.net/10773/22095.
Plasmacytoid dendritic cells (pDCs) are a subset of Dendritic Cells that when stimulated can produce pro-inflammatory mediators and type I IFNs. These cells play an important role in autoimmune disease such as systemic lupus erythematosus, as they can become activated by immune complexes formed with self-DNA, which trigger a type I IFN response through the TLR-9 signaling pathway. Here, we optimized activation of CAL-1 cells, a human pDC cell line, with immunocomplexes of self-nuclear or mitochondrial DNA with the antimicrobial peptide LL37. It was found that high concentrations of LL37 led to a reduced CAL-1 cell viability. Self-DNA-LL37 triggered expression of IFN-α and IFN-β in CAL-1 cells, without inducing expression of TNF-α, as in primary pDCs. The concentrations of DNA and LL37 in the complexes leading to a stronger CAL-1 activation were 0.2μg/ml and 10μg/ml, respectively. We also found that CAL-1 cells stimulated with immune complexes with self-nuclear DNA, but not self-mitochondrial DNA, were capable of secreting the proinflammatory cytokine IL-1β. Immunocytochemistry analysis revealed that early endosomes and TLR-9 were recruited 30-60 minutes upon activation with immune complexes. Thus, this work established CAL-1 cells as a cell model for pDC activation with immune complexes.
As células dendríticas plasmacitóides (pDCs) são um subtipo de Células Dendríticas que quando estimuladas podem produzir mediadores proinflamatórios e IFNs do tipo I. Estas células desempenham um papel importante em doenças autoimunes como o lúpus sistémico eritematoso, uma vez que podem ser ativadas por imunocomplexos formados por DNA do próprio, que desencadeia uma resposta de IFNs do tipo I através da via de sinalização do TLR-9. Aqui, otimizamos a ativação das células CAL-1, uma linha celular de pDCs, com imunocomplexos de DNA nuclear ou mitocondrial do próprio com o péptido antimicrobiano LL37, em paralelo com a estimulação com CpG-A. Descobrimos que elevadas concentrações de LL37 reduzem a viabilidade celular das CAL-1. O próprio DNA-LL37 despoletam a expressão de IFN-α e IFN-β nas células CAL-1, sem induzir a expressão de TNF-α, tal como em pDCs primárias. As concentrações ideais de DNA e LL37 nos complexos que levam a uma forte ativação das CAL-1 são 0.2μg/ml e 10μg/ml, respetivamente. Também descobrimos que as células CAL-1 estimuladas com imunocomplexos de DNA nuclear do próprio, mas não de DNA mitocondrial do próprio, foram capazes de secretar a citocina pro-inflamatória IL-1β. A análise imunocitoquímica revelou que os endossomas iniciais e o TLR-9 são recrutados após ativação por 30-60minutos com imunocomplexos. Assim, este trabalho estabele as células CAL-1 como um modelo celular para a ativação de com imunocomplexos.
Seamons, Audrey. "Implications of myelin basic protein processing and presentation on T cell activation and tolerance /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/10851.
Getahun, Andrew. "Antibody Feedback Regulation : From Epitope Masking to T Helper Cell Activation." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4580.
Schoggins, John Wesley. "Adenovirus host-cell interactions : the role of capsid proteins in transduction, immune activation, and gene targeting /." Access full-text from WCMC:, 2007. http://proquest.umi.com/pqdweb?did=1432771281&sid=1&Fmt=2&clientId=8424&RQT=309&VName=PQD.
Bhattarai, Nirjal. "GB virus C interactions with HIV: effects on immunoactivation and mechanisms of immunomodulation." Diss., University of Iowa, 2013. https://ir.uiowa.edu/etd/2437.
Hotchkiss, Kelly M. "Engineering Surface Properties to Modulate Inflammation and Stem Cell Recruitment through Macrophage Activation." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5492.
Ali, Qasim. "Contribution to the mathematical modeling of immune response." Phd thesis, Ecole Nationale Supérieure des Mines de Saint-Etienne, 2013. http://tel.archives-ouvertes.fr/tel-00905603.
Reid, Timothy Dawson. "B lymphocyte activation and exhaustion in chronic HIV : novel surrogate markers of generalised immune activation and selective modulation of aberrant B cell responses using vasoactive intestinal peptide (VIP)." Thesis, Stellenbosch : Stellenbosch University, 2015. http://hdl.handle.net/10019.1/96898.
ENGLISH ABSTRACT: Introduction: Chronic HIV-1 infection is characterized by immune activation and dysregulation of immune homeostasis, which impacts on multiple immune cell types. The B-cell compartment, which plays an important role in the producing neutralizing antibodies, is also dysregulated in HIV- 1 infection. In this study we investigated peripheral blood B-cell subset distribution, and changes in expression of cellular activation, inhibition, and apoptosis signaling markers in both untreated chronic HIV-1 infected individuals and healthy uninfected controls. The neuropeptide immune modulator, vasoactive intestinal peptide (VIP) is known to selectively down-regulate activation of CD4+ T-cells in various disease settings including HIV-1, however to our knowledge, no studies have investigated the effect of VIP inhibition on B-cell activation. Materials & Methods: A total of 21 HIV+ve (CD4 count >250 cells/µl), and 19 HIV-ve individuals were recruited from the Emavundleni voluntary testing and counseling clinic in Crossroads, Western Province, South Africa. Whole blood was stained to distinguish B-cell subsets (activated memory (AM: CD21-CD27+), resting memory (RM: CD21+CD27+), mature naïve (MN: CD21+CD27-), or tissue-like memory (TLM: CD21loCD27lo). In addition expression of markers of B-cell activation (CD126, CD86, CD38, CD284, CD287), inhibition (CD72, CD85j, CD300a, CD305, CD307d), and apoptosis signaling (CD95), was assessed ex vivo by flow cytometry (BD FACSCanto II). For determination of functional responsiveness isolated B-cells (RosetteSep, Stemcell Technologies) were cultured for 18h (37°C, 5%CO2) without stimulation or stimulated with TLR ligands (LPS or R848). Stimulation experiments were also performed in the presence or absence of VIP. Results: Chronic HIV-1 infection affected B-cell subset distribution. The percentage (%) of TLM was increased by 59.24%, and %RM was decreased by 22.73% (both p<0.01). Total expression of the VIP receptor VPAC2 was decreased by 47.35% (p=0.0296). Subsets had a mixed phenotype ex vivo; HIV infection upregulated CD38 (by 59.56%, p=0.0004), CD72 (by 60.70%, p=0.0396), CD307d (by 68.63%, p=0.0015) on AM, while RM B-cells had increased expression of TLR4 (by 107.04%, p=0.0057) and TLR7 (by 208.14%, p=0.0199). TLM B cells (i.e. exhausted phenotype) displayed upregulated TLR7 (by 550%, p=0.0128) and CD307d (by 72.40% p=0.045) expression. MN B-cells had increased CD72 expression (by 70.98%, p=0.0026). R848 upregulated CD86 expression by 42.20% on AM (p<0.01), and by 56.06% on RM B-cells (p<0.01), which was significantly downregulated with VIP inhibition (both p<0.05). Similarly, CD95 expression on RM, TLM, and MN B-cells increased by 31.10% (p<0.001), 21.46% (p<0.01), and 39.92% (p<0.01) with R848 stimulation respectively, which was also significantly downregulated with VIP inhibition. Conclusion: These data indicate that B-cells in untreated HIV infection display increased levels of activation, and also the potential for increased susceptibility to apoptosis as evidenced by increased FAS (CD95) expression. VIP significantly down-regulated markers of activation, inhibition, and apoptosis signaling. Dysregulation of B-cells is thus apparent in asymptomatic stable chronic HIV-1 infection, which may impact on both inefficient neutralizing antibody production and hypergammaglobulinemia. The ability of VIP to prevent stimulationassociated marker upregulation may indicate that VIP is a potential therapeutic agent. Its immuno-modulatory properties were demonstrated to limit B-cell hyperactivation, and selectively down-regulate apoptosis and mark it out for further investigation.
AFRIKAANSE OPSOMMING: Inleiding: Immunaktivering en ongekoppelde immuun-homeostase is kenmerke van chroniese MIVinfeksie. Ons het perifere bloed B-sel subgroep-verspreiding, en veranderinge in die uitdrukking van merkers van aktivering, inhibisie, en apoptose in 'n onbehandelde MIV-1 besmettende groep ondersoek (in vergelyk met 'n gesonde onbesmettende kontrole). Die immuun-moduleerder, vasoaktiewe intestinale peptied (VIP) is bekend om aktivasie van geaktiveerde CD4+ T-selle te verminder, maar tot ons kennis, is daar geen studies wat die effek van VIP-inhibisie op B-sel aktivering ondersoek het, in die konteks van MIV-1 infeksie. Materiaal & Metodes: MIV+we individue (CD4-telling >250 selle/µl) , en MIVwe kontroles is gewerf uit die vrywillige toetsing en berading Emavundleni kliniek, Crossroads, Westelike Provinsie, Suid-Afrika. Bsel subgroepe is gedefinieer as geaktiveerde geheue (AM: CD21- CD27+ ), rusende geheue (RM: CD21+ CD27+ ), volwasse naïef (MN: CD21+ CD27- ), of weefsel-agtige geheue (TLM: CD21loCD27lo). Merkers van aktivering (CD126, CD86, CD38, CD284, CD287), inhibisie (CD72, CD85j, CD300a, CD305, CD307d), en apoptose signalering (CD95) is via vloeisitometrie (BD FACSCanto II) op B-selle ex vivo en ook op geïsoleerde B-selle (RosetteSep, Cell Technologies) ondersoek. Vir die bepaling van funksionele responsiwiteit, geïsoleerde B-selle (RosetteSep, StemCell Technologies) was vir 18h (37°C, 5%CO2) gekweek, sonder stimulasie of gestimuleer met TLR ligande (LPS of R848). Stimulasie eksperimente het ook in die teenwoordigheid of afwesigheid van VIP plaasgevind. Resultate: Chroniese MIV-1 infeksie het B-sel subset verspreiding geraak. Die persentasie (%) van TLM is verhoog deur 59,24%, en% RM het met 22.73% afgeneem (beide p <0,01). Totale uitdrukking van die VIP reseptor VPAC2 het met 47,35% afgeneem (p = 0,0296). Subgroepe het 'n gemengde ex vivo fenotipe; MIV-infeksie het CD38 (deur 59,56%, p=0,0004), CD72 (deur 60,70%, p=0,0396), CD307d (deur 68,63%, p=0,0015) op AM verhoog, terwyl RM Bselle het verhoogde uitdrukking van TLR4 (deur 107,04%, p=0,0057) en TLR7 (deur 208,14%, p=0,0199). TLM B-selle (die uitgeputtende fenotiep) het verhoogde TLR7 (deur 550%, p=0,0128) en CD307d (deur 72,40% p=0.045) uitdrukking gewys. MN B-selle het verhoogde uitdrukking van CD72 (deur 70,98%, p = 0,0026). R848 het CD86 uitdrukking op AM deur 42,20%, en op RM deur 56,06% toegeneem (beide p <0,01). Dit het met VIP inhibisie beduidend afgeneem (beide p <0.05). CD95 uitdrukking was soortgelyk verhoog op RM, TLM, en MN B-selle met 31.10% (p <0.001), 21,46% (p <0,01), en 39,92% (p <0,01) met R848 stimulasie. Al drie het beduidend afgeneem met VIP inhibisie. Gevolgtrekking: Hierdie data dui daarop dat B-selle in onbehandelde MIV-infeksie vertoon verhoogde aktiveringsvlakke, en ook die potensiaal vir verhoogde vatbaarheid vir apoptose soos bewys deur verhoogde uitdrukking van FAS (CD95). VIP het beduidend merkers van aktivering, inhibisie, en apoptose af-gereguleer. Wanfunksie van B-selle is dus in asimptomatiese stabiele chroniese MIV-1 infeksie duidelik, wat impak kan hê op beide oneffektiewe neutraliserende teenliggaampie produksie, en hiepergammaglobulinimie. Die vermoë van VIP stimulasie-verwante merker opregulasie te voorkom kan aandui dat VIP 'n potensiële terapeutiese agent is. VIP se immuno-moduleerende eiendomme is gedemonstreer om Bsel hieperaktiveering te beperk, en selektief apoptose afreguleer, en merk dit vir verdere ondersoek.
Eickmeier, Ira. "Relevance of the activation and migration patterns of CD8 T cells for the development of immune-mediated liver injury." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2014. http://dx.doi.org/10.18452/17032.
Initial immunological processes leading to autoimmune liver diseases are largely unknown. Therefore this thesis analyzed the antigen presentation, the migration as well as the phenotype of in vivo activated CD8 T cells in the liver by employing a mouse model for autoimmune hepatitis. It was shown that hepatic dendritic cells are effective antigen-presenting cells, which contribute to the induction of functional effector CD8 T cells in the liver and hepatitis. In contrast, Kupffer cells have a tolerogenic role during autoimmune processes in the liver. CD8 T cells that were in vivo activated in the liver display specific surface markers and unusual migration patterns. On the one hand an unusual surface molecule Neuropilin-1 was identified, on the other hand expression of well-known markers defining the activation-status of CD8 T cells suggests a hybrid phenotype. They reflect aspects of naive and effector T cells, characteristics also found on central memory T cells. Liver-primed CD8 T cells do not only produce pro-inflammatory cytokines leading to hepatitis, but they also retain their ability to circulate through lymph nodes. However, they have no access to the gut, which suggests that a direct regulatory function in the gut can be excluded. Although specific adhesion molecules on CD8 T cells activated in the liver were identified, no exclusive tissue-specific migration into the liver exists, as was shown for CD8 T cells primed in the gut. CD8 T cells activated in the gut-associated lymphoid tissue accumulate in the liver, in principle enabling them to induce liver pathology in the context of inflammatory bowel disease. Thus, the here described findings contribute to the understanding of initial immunological processes in autoimmune liver diseases.
RAELI, LORENZO. "Effect of anti-TNF therapy on T cell activation and effector functions in patients with chronic inflammatory diseases." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2009. http://hdl.handle.net/10281/10634.
Paranjape, Anuya. "MAST CELL ACTIVATION BY DIVERSE STIMULI CAN BE SUPPRESSED BY STEROID THERAPY AND TARGETING THE FYN-STAT5B CASCADE." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/5069.
Wagner, Stephen Douglas. "Characterization of early activation of multi-isotypic antibody-producing B lymphocytes in the small intestine." CSUSB ScholarWorks, 1999. https://scholarworks.lib.csusb.edu/etd-project/3018.
Jellison, Evan Robert. "CD4 T Cell-Mediated Lysis and Polyclonal Activation of B Cells During Lymphocytic Choriomeningitis Virus Infection: A Dissertation." eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/349.
Schmidt, Madelyn R. "Virus-Lymphocyte Interactions: Virus Expression Is Differentially Modulated by B Cell Activation Signals: A Dissertation." eScholarship@UMMS, 1991. https://escholarship.umassmed.edu/gsbs_diss/51.
Nguyen, Lam. "Immune Activation Induces Telomeric DNA Damage, Reduces Memory Precursors, and Promotes Short-lived Effector T Cell Differentiation in Chronic HCV Infection." Digital Commons @ East Tennessee State University, 2020. https://dc.etsu.edu/etd/3828.
Horne, Phillip Howard. "Activation and effector function of unconventional acute rejection pathways studied in a hepatocellular allograft model." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1188397900.
Chivero, Ernest Tafara. "Tropism of human pegivirus (formerly known as GB virus C) and host immunomodulation : insights into viral persistence." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/1565.
Ringqvist, Emma. "Host-Pathogen Responses during Giardia infections." Doctoral thesis, Uppsala universitet, Mikrobiologi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-108980.
Massanella, Luna Marta 1983. "CD4 and CD8 T-cell activation reflect different pathogenic asprects in chronic HIV-treated subjects." Doctoral thesis, Universitat Pompeu Fabra, 2012. http://hdl.handle.net/10803/85720.
Human immunodeficiency virus (HIV-‐1) infection causes a progressive impairment of the immune system, characterized by a massive CD4 T-‐cell depletion and sustained immune activation and inflammation. Highly active antiretroviral therapy (HAART) induces a sustained effective suppression of viral replication in HIV-‐infected subjects and reduces immune activation, but does not normalize it. The causes of this persistent immunehyperactivation despite viral suppression remain unknown. Our results show a dichotomy between CD4 and CD8 T-‐cell driving forces of immune activation in HIV-‐infected HAART-‐suppressed individuals. The low (but detectable) levels of residual replication drive immune activation in CD8 T-‐cell compartment. Therefore, raltegravir intensification of HAART results in specific and reversible reduction of CD8 T-‐cell activation, which seems to be a sensor of replication events (in particular CD38 expression). Interestingly, CD38 expression is under the control of Type I IFN, suggesting that the virus also controls inflammatory responses and that these responses are intimately linked to CD8 T-‐cell activation markers. Conversely, in treated individuals, viral persitence has low effects on CD4 T-‐cell compartment, which still show the consequences of pre-‐HAART depletion and determine immune recovery. In fact, CD4 T-‐cell activation is not reduced after one year of raltegravir intensification. Instead, the homeostatic response to CD4 T-‐cell depletion might drive activation in this compartment, particularly in HAART-‐treated individuals with satisfactory virological response but poor immune recovery (immunodiscordant subjects). Our results suggest that, even though immunodiscordant individuals showed lower CD4 T-‐cell production and higher microbial translocation, activation and cell death, immunodiscordance seems to be related to increased cell-‐destruction of CD4 T-‐cells. The persistent immune activation and inflammation in these subjects provide a milieu of accelerated immunoexhaustion of CD4 T-‐cells and immunosenescence of the whole immune system, contributing to long-‐term co-‐morbidities and accelerated ageing observed in these subjects. Therefore, determining the causes of this increased hyperactivation and cell-‐death may be important for the development of therapeutic strategies aiming to improve immune recovery.
Loots, Stanley. "Erythrocyte apoptosis (erythroptosis) and anaemia in chronic HIV-1 infection : relationship with immune activation and viraemia." Thesis, Stellenbosch : Stellenbosch University, 2013. http://hdl.handle.net/10019.1/85803.
ENGLISH ABSTRACT: Chronic HIV-1 infection is characterized by extensive inflammation/immune activation and also by anaemia. Macrophages and neutrophils produce reactive oxygen species (ROS) which can cause damage to surrounding cells, including erythrocytes. Damaged erythrocytes may die by apoptosis (erythroptosis) or be tagged for clearance by monocytes/ macrophages. In this study we investigated HIV-1-associated anaemia and erythroptosis in asymptomatic, untreated HIV-1 infected individuals and how it relates to oxidative stress and immune activation.
AFRIKAANSE OPSOMMING: Chroniese MIV-1 infeksie word gekenmerk deur uitgebreide inflammasie/immuun aktivering en ook deur anemie. Makrofage en neutrofiele produseer reaktiewe suurstof spesies (ROS), wat kan skade aan omliggende selle, insluitend rooibloedselle veroorsaak. Beskadigde rooibloedselle kan sterf deur apoptose (erythroptosis) of gemerk vir klaring deur monosiete/makrofage. In hierdie studie het ons ondersoek MIV-1-verwante bloedarmoede en erythroptosis in asimptomatiese, onbehandelde MIV-1 besmette individue en hoe dit verband hou met oksidatiewe stres en immuun aktivering.
The Poliomyelitis Research Foundation (PRF
Rehr, Manuela. "The impact of HIV-1 replication on generalized immune activation and virus-specific T cell responses : implications for HIV-1 phatogenesis /." Zürich : ETH, 2007. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=17000.
Seifried, Janna [Verfasser]. "Mechanisms of down-regulation of immune activation and B-cell responses in the natural hosts of simian immunodeficiency virus / Janna Seifried." Berlin : Freie Universität Berlin, 2012. http://d-nb.info/1027276873/34.
Priyadharshini, Bhavana. "Regulation of Early T Cell Activation by TNF Superfamily Members TNF and FASL: A Dissertation." eScholarship@UMMS, 2010. https://escholarship.umassmed.edu/gsbs_diss/494.
Judge, Chelsey J. "IL-7-MEDIATED CD56BRIGHT NK CELL FUNCTION IS IMPAIRED IN HCV IN PRESENCE AND ABSENCE OF CONTROLLED HIV INFECTION, WHILE CD14BRIGHTCD16- MONOCYTES NEGATIVELY CORRELATE WITH CD4 MEMORY T CELLS AND HCV DECLINE DURING HCV-HIV CO-INFECTION." Case Western Reserve University School of Graduate Studies / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=case1481187921533387.
Rivière, Élodie. "Rôle des cellules épithéliales salivaires au cours du Syndrome de Sjögren primitif Salivary gland epithelial cells from patients with Sjögren’s syndrome induce B-lymphocyte survival and activation Interleukin-7/Interferon axis drives T-cell and salivary gland epithelial cell interactions in Sjögren’s syndrome." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASS124.
Primary Sjogren's syndrome (pSS) is an auto-immune disease characterized by a lymphocytic infiltration of lacrimal and salivary glands leading to an ocular and oral dryness. The objective of this work was to understand the role of salivary gland epithelial cells (SGECs) in the pathophysiology of pSS and especially via their interactions with B and T lymphocytes. We observed a differential effect of SGECs from pSS and controls subjects since, in coculture, SGECs from pSS were able to induce a better survival of B lymphocytes compared to SGECs from controls. The interaction between SGECs and B lymphocytes involved mainly soluble factors. Our hypothesis is that several factors are involved and act in synergy. Indeed, inhibition of one of each soluble factor individually did not block the support of SGECs to B lymphocytes. In contrast, the addition of leflunomide, or a BTK inhibitor or a PI3K inhibitor inhibited the induction of B lymphocytes viability by SGECs.Regarding the interactions between SGECs and T lymphocytes, we showed that SGECs secrete interleukin 7 (IL7) after type I or II interferon (IFN)stimulation. In turn, IL7 is able to induce the production of type II IFN by T lymphocytes, suggesting the existence of an amplification loop between IL7 and IFN. The addition of a monoclonal antibody inhibiting the IL7 receptor (anti-IL7R) downregulated the expression of IFN induced genes in cultured salivary glands explants.These mechanisms could induce and/or maintain locally, the chronic B lymphocytes hyperactivation during pSS, as well as, the IFN signature described in the salivary glands. Thus, these results confirmed the hypothesis that SGECs play an active role in the pathogenesis of pSS. A better understanding of their mechanisms of action could help to define new therapeutic strategies in pSS
Khairnar, Vishal S. [Verfasser], and Karl Sebastian [Akademischer Betreuer] Lang. "Role of Lymphotoxin Beta and Cell Adhesion Molecule (CEACAM1) in Innate and Adaptive Immune Activation / Vishal Shivajirao Khairnar ; Betreuer: Karl Sebastian Lang." Duisburg, 2017. http://d-nb.info/1137466618/34.
Khairnar, Vishal Shivajirao [Verfasser], and Karl Sebastian [Akademischer Betreuer] Lang. "Role of Lymphotoxin Beta and Cell Adhesion Molecule (CEACAM1) in Innate and Adaptive Immune Activation / Vishal Shivajirao Khairnar ; Betreuer: Karl Sebastian Lang." Duisburg, 2017. http://d-nb.info/1137466618/34.
Albergante, L. "A PETRI NET MODEL OF LIVER RESPONSE TO VISCERAL LEISHMANIASIS: SELF-REGULATION AND COMPLEX INTERPLAY IN THE VERTEBRATE IMMUNE SYSTEM." Doctoral thesis, Università degli Studi di Milano, 2010. http://hdl.handle.net/2434/150085.
Bogner, Simon Sebastian [Verfasser], та Markus [Akademischer Betreuer] Glatzel. "Immune activation in Aβ-related angiitis (ABRA) and a cell model of E280A presenilin-mutated Familial Alzheimer's Disease / Simon Sebastian Bogner. Betreuer: Markus Glatzel". Hamburg : Staats- und Universitätsbibliothek Hamburg, 2014. http://d-nb.info/1059859823/34.
Chung, Charlotte Yuk-Yan. "Tight Junctions - The Link Between HIV-Associated Intestinal Barrier Dysfunction and Loss of Immune Homeostasis." Case Western Reserve University School of Graduate Studies / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=case1417822947.
Samassa, Fatoumata. "New insights into the manipulation of the host adaptive immune response by Shigella : the immunological synapse as a target." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCC293.
Modulation of the host innate response during bacterial infections has been vastly documented in contrast to that of the adaptive immunity. This is the case for Shigella, the Gram negative entero-invasive bacterium responsible for bacillary dysentery, an acute rectocolitis. Shigella infection results in the invasion and inflammatory destruction of the human colonic mucosa, relying on the expression of a type three-secretion system (T3SS). Delivery of T3SS virulence effectors directly into the host cell cytoplasm results in hijacking of cellular functions that promotes bacterial survival. The humoral protective immunity elicited upon natural Shigella infection is poorly efficient and short-lasting. Recent studies have shown that Shigella promotes apoptosis of some B cell subsets and impairs T cell migration through the action of identified virulence effectors. Migratory capacities are essential for T lymphocytes to search for antigen presenting cells (APC) displaying cognate antigens. T cell-APC encountering results in the formation of a very dynamic signaling platform at the interface between the two cells, named the immunological synapse (IS), eventually leading to pathogen-specific T cell activation. IS formation is dependent on actin cytoskeleton and vesicular trafficking for spatiotemporal relocalization at the cell-cell interface of all the required molecules. Knowing that these cellular pathways are targets of Shigella T3SS effectors in intestinal epithelial cells, we hypothesized that such a targeting occurring into T lymphocytes would impact IS formation, thus preventing specific T cell activation. The aim of my thesis work was thus to quantitatively and qualitatively characterize the IS formed with Shigella-infected T lymphocytes. If impairment occurred as compared to non-infected T cells, the objectives were to decipher the underlying molecular and cellular mechanisms along with the T3SS effectors involved, as well as the impact on T cell activation. We report that Shigella, by limiting T cell migration, reduces the number of conjugates formed between T cells and APCs. When conjugates are formed, the building-up of a canonical IS is prevented by T3SS effectors-mediated targeting of actin cytoskeleton and vesicular trafficking, eventually leading to inhibition of T cell activation. In particular, besides IpgD impairing T cell scanning of APCs, two other T3SS effectors, VirA and IpaJ, are shown to induce Golgi fragmentation and disruption of Rab11 vesicular compartments, leading to mislocalization of Lck, a key protein downstream TCR signaling, and decrease of TCR recycling rate, while also participating to the down-regulation of TCR endocytosis. This study highlights the coordinated action of multiple T3SS effectors targeting diverse cellular pathways to dampen the priming of adaptive immunity. In parallel to this main study, I also contributed to demonstrate the occurrence of the translocation of Shigella effectors into B and T lymphocytes not resulting into subsequent invasion, thus leading to the establishment of a new paradigm for the pathogenicity of Shigella. Overall, this work gives rise to a more comprehensive understanding of the strategies evolved by pathogens to counteract host adaptive defenses
Glaría, Percaz Estibaliz. "Selective effects of Liver X Receptor activation in host-bacteria interaction." Doctoral thesis, Universitat de Barcelona, 2021. http://hdl.handle.net/10803/673708.
Auma, Ann Winniefred Nangobi. "THE IMPACT OF DIRECT-ACTING ANTI-VIRAL THERAPY ON NAIVE CD4+ T CELL LYMPHOPENIA AND CELLULAR IMMUNE ACTIVATION IN HCV INFECTION AND HCV/HIV CO-INFECTION." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1625764728651756.