Academic literature on the topic 'Innate-like T cells'
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Journal articles on the topic "Innate-like T cells"
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Dadi, Saïda, Sagar Chhangawala, Benjamin M. Whitlock, Ruth A. Franklin, Chong T. Luo, Soyoung A. Oh, Ahmed Toure, et al. "Cancer Immunosurveillance by Tissue-Resident Innate Lymphoid Cells and Innate-like T Cells." Cell 164, no. 3 (January 2016): 365–77. http://dx.doi.org/10.1016/j.cell.2016.01.002.
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Dadi, Saida, Sagar Chhangawala, Benjamin M. Whitlock, Ruth A. Franklin, Chong Luo, Soyoung A. Oh, Ahmed Toure, et al. "Cancer Immunosurveillance by Tissue-resident Innate Lymphoid Cells and Innate-like T Cells." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 74.9. http://dx.doi.org/10.4049/jimmunol.196.supp.74.9.
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Abstract Malignancy can be suppressed by the immune system in a process termed immunosurveillance. However, to what extent immunosurveillance occurs in spontaneous cancers and the composition of participating cell types remain obscure. Here we show that cell transformation triggers a tissue-resident lymphocyte response in oncogene-induced murine cancer models. Non-circulating cytotoxic lymphocytes, derived from innate, TCRαβ and TCRγδ lineages, expand in early tumors. Characterized by high expression of NK1.1, CD49a and CD103, these cells share a gene expression signature distinct from those of conventional NK cells, T cells and invariant NKT cells. Generation of these lymphocytes is dependent on the cytokine IL-15, but not the transcription factor Nfil3 that is required for the differentiation of tumor-infiltrating NK cells, and IL-15, but not Nfil3, deficiency results in accelerated tumor growth. These findings reveal a tumor-elicited immunosurveillance mechanism that engages unconventional type 1-like innate lymphoid cells and type 1 innate-like T cells.
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Wu, L., C. L. Gabriel, V. V. Parekh, and L. Van Kaer. "Invariant natural killer T cells: innate-like T cells with potent immunomodulatory activities." Tissue Antigens 73, no. 6 (June 2009): 535–45. http://dx.doi.org/10.1111/j.1399-0039.2009.01256.x.
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Hildreth, Andrew, and Timothy O’Sullivan. "Tissue-Resident Innate and Innate-Like Lymphocyte Responses to Viral Infection." Viruses 11, no. 3 (March 19, 2019): 272. http://dx.doi.org/10.3390/v11030272.
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Infection is restrained by the concerted activation of tissue-resident and circulating immune cells. Recent discoveries have demonstrated that tissue-resident lymphocyte subsets, comprised of innate lymphoid cells (ILCs) and unconventional T cells, have vital roles in the initiation of primary antiviral responses. Via direct and indirect mechanisms, ILCs and unconventional T cell subsets play a critical role in the ability of the immune system to mount an effective antiviral response through potent early cytokine production. In this review, we will summarize the current knowledge of tissue-resident lymphocytes during initial viral infection and evaluate their redundant or nonredundant contributions to host protection or virus-induced pathology.
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Herbelin, Andre, Florence Jacomet, Emilie Cayssals, Deborah Desmier, Alice Barbarin, Sara Basbous, Anaïs Levescot, et al. "EOMESODERMIN-EXPRESSING INNATE-LIKE CD8+ T CELLS IN HUMANS ARE IMPAIRED IN CHRONIC MYELOID LEUKEMIA PATIENTS AT DIAGNOSIS." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 142.12. http://dx.doi.org/10.4049/jimmunol.196.supp.142.12.
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Abstract Starting with our recent identification in healthy individuals of a new distinct CD8+ T cell subset harboring Eomes and exhibiting a marked “innate” (panKIR/NKG2A+) phenotype, we present here the first report on this unique T cell population in a physiopathological context, namely chronic myelogenous leukemia (CML), a clonal myeloproliferative disorder. The current first-line therapies for this hematopoietic malignancy are tyrosine kinase inhibitors such as Imatinib (IM). Knowing that the generation of innate Eomes-expressing CD8+ T cells in mice depends on PLZF-expressing NKT cells and that iNKT cells are functionally deficient in CML, we surmised that panKIR/NKG2A+Eomes+ CD8+ T cells could be altered during CML. Accordingly, in CML patients at diagnosis, the pool of blood KIR/NKG2A(+)Eomes(+) CD8(+) T cells was found to be severely reduced. Moreover, like for iNKT and NK cells, the functions of these innate-like CD8(+) T cells were impaired, as attested by their lost of potent antigen-independent cytotoxic activity and IFN-γ production in response to innate-like stimulation by IL-12+IL-18. Remarkably, both innate-like CD8(+) T cells and iNKT cells returned to normal after complete CML remission upon IM therapy, supporting evidence for an iNKT cell-dependent generation of circulating KIR/NKG2A+Eomes+ CD8+ T cells in CML patients, as in mice. Our study reveals a possible contribution of iNKT/innate-like CD8(+) T cells as a new innate immune axis to tumor control in CML.
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Raberger, Julia, Beatrice Grabner, Shinya Sakaguchi, Alexandra Schebesta, Nicole Boucheron, K. Emelie M. Blomberg, Anna Berglöf, et al. "Characterization of CD44-high memory phenotype T cells induced by enforced expression of the transcription factor PLZF (85.12)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 85.12. http://dx.doi.org/10.4049/jimmunol.182.supp.85.12.
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Abstract We and others have shown that transgenic expression of the transcription factor PLZF in the T cell lineage induces the appearance of CD44-high memory-phenotype (MP) T-cells (Savage et al. Immunity 2008; Raberger et al. PNAS, 2008). These MP T cells arise already in the thymus and produce IFNã upon PMA/ionomycin stimulation, thus sharing certain features with innate-like T cells. Furthermore, we observed that PLZF expression is up-regulated in Itk-deficient T cells, which are enriched with innate-like T cell subsets. To study the PLZF-induced MP T cell population in more detail, we are investigating whether these cells, like other innate-like T cells, are selected on classical or non-classical MHC molecules. Furthermore, PLZF transgenic mice are intercrossed with several knockout mice (e.g. Itk-/- or IL-15-/- mice) to determine signaling pathways/molecules required for their development and maintenance. Our studies will provide more insight into transcription pathways controlling the development of MP T cells with "innate-like" functions. Supported by the Austrian Science Fund FWF (SFB-F23, P19930).
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Nakajima, Shihoko, Asako Chiba, Ayako Makiyama, Eri Hayashi, Goh Murayama, Ken Yamaji, Shigeto Kobayashi, Naoto Tamura, Yoshinari Takasaki, and Sachiko Miyake. "Association of mucosal-associated invariant T cells with different disease phases of polymyalgia rheumatica." Rheumatology 59, no. 10 (March 3, 2020): 2939–46. http://dx.doi.org/10.1093/rheumatology/keaa054.
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Abstract Objectives Although T cells are thought to be involved in the pathogenesis of PMR, whether innate-like T cells are involved in the process remains unknown. Methods The serum levels of 27 cytokines/chemokines in patients with PMR were measured by a multiplex immunoassay (Bio-Plex Assay). The cytokine-producing capacity of T and innate-like T cells was assessed by intracellular cytokine staining and flow cytometry. The frequency and activated status of T and innate-like T cells were investigated by flow cytometry and their associations with clinical parameters were assessed. Results The levels of inflammatory cytokines were associated with disease activity in PMR. The cytokine-producing capacity by CD8+ T and innate-like T cells was associated with disease activity. The frequency of HLA-DR+ CD38+ cells among CD8+ T cells was increased in patients with active disease. The frequencies of HLA-DR+ CD38+ cells among CD4+ T, mucosal-associated invariant T (MAIT) and γδ T cells were higher in patients with inactive disease. The frequency of HLA-DR+ CD38+ MAIT cells was associated with the PMR activity score and CRP levels in patients in remission. Conclusion The inflammatory cytokine-producing capacity and expression of activation markers of CD8+ T and innate-like T cells were associated with the disease activity of PMR. MAIT cell activation in patients in remission may contribute to the subclinical activity of the disease.
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Allali, Slimane, Céline Dietrich, François Machavoine, Rachel Rignault-Bricard, Valentine Brousse, Mariane de Montalembert, Olivier Hermine, Thiago Trovati Maciel, and Maria Leite-de-Moraes. "Innate-like T cells in children with sickle cell disease." PLOS ONE 14, no. 6 (June 28, 2019): e0219047. http://dx.doi.org/10.1371/journal.pone.0219047.
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Kurioka, Ayako, Paul Klenerman, and Christian B. Willberg. "Innate-like CD8+ T-cells and NK cells: converging functions and phenotypes." Immunology 154, no. 4 (April 11, 2018): 547–56. http://dx.doi.org/10.1111/imm.12925.
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Wencker, Melanie, Gleb Turchinovich, Rafael Di Marco Barros, Livija Deban, Anett Jandke, Andrew Cope, and Adrian C. Hayday. "Innate-like T cells straddle innate and adaptive immunity by altering antigen-receptor responsiveness." Nature Immunology 15, no. 1 (November 17, 2013): 80–87. http://dx.doi.org/10.1038/ni.2773.
Full textDissertations / Theses on the topic "Innate-like T cells"
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Minoda, Yosuke. "Innate-like T cells in patients with cancer." Thesis, Federation University Australia, 2017. http://researchonline.federation.edu.au/vital/access/HandleResolver/1959.17/166481.
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Innate-like T cells, including invariant natural killer T (NKT), mucosal associated invariant T (MAIT) cells or g T cells are associated with regulation of anti-tumour responses in humans and mice, although their exact role remains controversial. We have studied innate-like T cells from tumour infiltrating lymphocytes (TILS), peripheral blood mononuclear cells (PBMCs) and bone marrow (BM) derived cells from patients undergoing treatment for cancer and compared their characteristics to cells from healthy donors. We identifed that the overall frequency of innate-like T cells was variably deficient in patients with blood or solid cancers. Interestingly, the deficiency of innate-like T cells appeared to be more severe than that of other T cells suggesting a specific impact. An increased proportion of activated g T cells and MAIT cells suggested they could have a functional role in responses to cancer cells. Despite the deficiency of these subsets in patient tissue samples, we showed that anti-tumour capacity of innate-like T cells was intact as innate-like T cells in most patient groups had a similar cytokine response to stimulation as cells from healthy donors. Finally, we also showed that innate-like T cells appeared not to broadly recognize cancer cells, as no direct impact was identified in their overall frequency or cytokine expression when exposed to autologous tumour cells, cancer lysates or lipids extracted from patient tumours, or colorectal cancer cell lines. This project was aimed at providing an overview of potential defects in innate-like T cells based on my analysis of a wide range of samples in the Fiona Elsey Cancer Research Institute (FECRI) Tissue Bank. As a result of my studies, we have established a clear understanding of innate cells in cancer, which provides a basis for future studies. Our novel findings include analysis of frequency distribution and functional capacity of MAIT cells in solid tumours other than colorectal cancer and in patients with blood cancers such as chronic lymphocytic leukaemia (CLL), non-Hodgkin's lymphoma (NHL), multiple myeloma (MM) or other haematological malignancies, something not previously reported. Taken together, we showed that a deficiency of innate-like T cells is common in patient groups with cancer and could be a risk factor for disease and possibly a target for immunotherapies, but the functional capacity was intact for cytokine responses.Doctor of Philosophy
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Yonkers, Nicole L. "Toll-like Receptor Tolerance in Dendritic Cells During Hepatitis C and HIV Infections: Collapsing the Bridge Between Innate and Adaptive Immunity." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1298412448.
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Taylor, Rebecca Chantelle. "Effects of toll-like receptor 2 ligands on T-cell responses to mite allergen in humans." University of Western Australia. School of Paediatrics and Child Health, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0107.
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[Truncated abstract] The last few decades have witnessed an increase in the prevalence, morbidity and economic burden associated with asthma and allergic disease. This rising incidence cannot be completely explained by changes in genetic factors or by improvements in diagnostic procedures. Environmental factors, particularly those associated with a westernised lifestyle, are considered to be involved in this increase. In the late 1980’s Strachan was the first to link environmental factors with allergic disease, this theory became to be known as the ‘hygiene hypothesis’. This hypothesis links the “cleaner” more “healthy ” environment we now live in, with an increased risk of developing allergic disease. This effect is highlighted by studies linking farm and animal exposure (rich in microbial compounds) during early life with a decrease in allergic disease. Since then numerous studies have been undertaken to ascertain the factors present in the microbe rich environment, which elicit this protective effect. Many studies have revolved around endotoxin, however microbial components (mainly from Gram-positive bacteria) which signal through Toll-like receptor 2 (TLR2), have also shown that they can alter the allergic immune response. In mice models TLR2 has been shown to both exacerbate and inhibit allergic disease. The above research highlights the need for further studies into the effect of TLR2 ligands, and to define the mechanisms by which they exert their effects in human allergic disease. These mechanisms will be relevant to understanding the pathogenesis of allergy, but also might provide novel ways to treat allergy. The aims of the study outlined in this thesis were to determine whether in vitro exposure to TLR2 ligands could modify the established immune response to house dust mite allergen (HDM), and to examine the mechanisms by which this occurs. ... The addition of glucocorticoids to LTA enhanced the ability of this TLR2 ligand to inhibit IL-5 and IL-13 production by HDM-activated blood mononuclear cells. In conclusion, this study shows that TLR2 ligands have the ability to inhibit the Th2 response to mite allergen in previously sensitized individuals by an as yet unknown mechanism. However the findings described herein do provide an impetus for future studies designed to uncover novel mechanisms by which allergic responses can be ameliorated, and may open new treatment modalities.
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Isaksson, Magnus. "Initiation of Autoimmunity in Experimental Autoimmune Encephalomyelitis." Doctoral thesis, Uppsala universitet, Molekylär medicin, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-173427.
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The events that trigger an autoimmune disease remain largely unknown. To study these events animal models are necessary because symptoms of autoimmune diseases are preceded by a long asymptomatic period in humans. Experimental autoimmune encephalomyelitis (EAE) is the best characterized model for cell mediated autoimmunity and an animal model for the human disease multiple sclerosis. EAE is induced in rodents by immunization with myelin antigens (Ags) together with adjuvants. After immunization, T cells are primed in the periphery by Ag presenting cells and subsequently invade the central nervous system where they mediate parenchymal inflammation, resulting in demyelination and clinical symptoms of an ascending paralysis. It is now generally recognised that the main cell type mediating EAE is the T helper type 17 (Th17) cell. Tolerance to EAE can be attained by DNA vaccination, but how the immune response against the myelin Ags is abrogated after DNA vaccination is not known. By employing short interfering RNA technology, induction of the innate immune signalling molecule interferon (IFN) -β was found to be necessary for the protective effect of DNA vaccination in EAE. In addition, DNA vaccination inhibited subsequent autoimmune Th17 cell responses. The Toll-like receptors (TLRs) of the innate immune system have evolved to recognise conserved molecular structures on microbes and signalling through them almost exclusively converge on the molecule MyD88. Signalling via MyD88 was found to be required for induction of EAE since mice deficient in this molecule did not develop disease. Upstream signalling via TLR4 and TLR9 had tolerogenic properties. In studies of Ag presentation in EAE, two major subtypes of dendritic cells (DCs) were examined. Plasmacytoid DCs were found to have a promoting role in the induction of EAE, partly via type 1 IFNs. Myeloid DCs had a redundant role in the induction phase of EAE, neither disease severity nor encephalitogenic Th17 responses were affected by their absence during priming. These studies further demonstrate that the cells and molecules of the innate immune system exhibit a crucial role in controlling the adaptive immune system which mediates tissue damage in autoimmune diseases.
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Gutzeit, Cindy. "Interference of Varicella-Zoster Virus (VZV) with the CD1 antigen presenting system on immature dendritic cells." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2009. http://dx.doi.org/10.18452/16059.
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Das human pathogene Varicella-Zoster Virus (VZV) gehört zur Familie der Herpesviren und ist weltweit verbreitet. Die Primärinfektion verursacht Varicellen, welche durch einen bläschenartigen Hautausschlag charakterisiert ist. Im Anschluss daran etabliert VZV eine lebenslange Latenz und verursacht nach Reaktivierung Herpes Zoster. Seit 2004 ist der Lebendimpfstoff aus attenuierten Virionen des VZV-Stammes V-Oka in Deutschland empfohlen. Im Gegensatz zur Infektion mit zirkulierenden virulenten VZV Stämmen tritt nach Verimpfung des Vakzin-Stammes V-Oka kein Exanthem auf. Die Haut ist der Hauptreplikationsort von VZV und immunologische Unterschiede zwischen virulentem VZV und dem Vakzin-Stamm treten hier am deutlichsten auf. In der vorliegenden Arbeit konnte eine neue Immunevasionsstrategie virulenter VZV Stämme aufgedeckt werden, welche erklären könnte, wie virulente VZV Stämme frühe antivirale Immunantworten umgehen. In Hautläsionen von Herpes Zoster Patienten konnte eine massive Infiltration von myeloiden inflammatorischen Dendritischen Zellen beobachtet werden. In vitro Studien mit Monozyten abgeleiteten Dendritischen Zellen (DC), welche inflammatorische DC repräsentieren, zeigten, eine signifikant erhöhte Expression von CD1c Molekülen nach Infektion mit dem Vakzin-Stamm, sowie virulentem VZV. Funktionelle Untersuchungen mit intraepithelialen CD1c-restringierten gamma delta T Zellen zeigten, dass DC nach Infektion mit dem Vakzin-Stamm phänotypisch und funktionell reiften und somit die T Zellen zur IFN-gamma Sekretion stimulierten. Im Gegensatz dazu wurde die funktionelle Reifung von DC, die mit virulentem VZV infiziert waren, geblockt. Folglich wurde kein bioaktives IL-12 sezerniert, welches als entscheidendes Cytokin zum Aufbau einer antiviralen T-Helfer 1 Immunantwort beiträgt. Darüber hinaus konnte gezeigt werden, dass virulentes VZV die Signalkaskade des Toll-like Rezeptors 2 (TLR2) in DC inhibiert und somit die IL-12 Produktion verhindert.Varicella-zoster virus (VZV) which belongs to the family of herpesviruses is restricted to humans and distributed worldwide. Primary infection of VZV causes chickenpox characterized by a disseminated rash. Thereafter, VZV establishes a lifelong latency and can be reactivated to cause herpes zoster. Since 2004 the attenuated strain V-Oka of VZV was licensed for Germany to immunize children against VZV infection. In contrast to infection by circulating virulent VZV strains, vaccination with V-Oka remains asymptomatic. The skin is the major replication site of VZV and immunological differences between virulent VZV and the vaccine should become most apparent within this immune organ. In summary, this study discovered a new immune evasion strategy of virulent VZV strains which might explain how virulent VZV strains overcome innate antiviral responses. A strong infiltration of myeloid-derived inflammatory DCs has been detected in skin lesions of herpes zoster patients. In vitro studies with monocyte-derived dendritic cells (DCs), reflecting inflammatory DCs, showed that they were efficiently infected by both, the vaccine and a virulent VZV strain. Intriguingly, a significant upregulation of CD1c molecules on VZV-infected DCs was observed. Functional investigations using intraepithelial CD1c-restricted gamma delta T cells revealed that DCs infected with the vaccine virus were fully instructed to mature, thereby promoting IFN-gamma secretion of gamma-delta T cells. In striking contrast, DCs infected with virulent VZV strains were efficiently blocked to mature functionally. In detail, they did not secrete bioactive IL-12 which is an instrumental cytokine for generation of antiviral T helper 1 responses. Moreover, virulent VZV blocked Toll-like receptor 2 (TLR2) signaling in DCs thereby preventing production of bioactive IL-12 which in turn inhibited IFN-gamma secretion by gamma-delta T cells.
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Morrison, Vicky L. "Innate and cognate roles of B cells in T cell differentiation and memory." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/4873.
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B cells recognise antigens on micro-organisms through their B cell receptor (BCR) and via Toll-like receptors (TLRs), and thus respond in both innate and adaptive manners during the subsequent immune response. Innate recognition through TLRs has the potential to alter the behaviour of whole B cell populations. I show, here, that MyD88-dependent activation of B cells via TLR2 or TLR9 causes the rapid loss of expression of CD62L, by metalloproteinasedependent shedding, resulting in the exclusion of these cells from lymph nodes and Peyer’s patches, but not the spleen. Moreover, systemic infection with Salmonella typhimurium causes shedding of CD62L and the subsequent focussing of B cell migration to the spleen. I reveal that splenic B cells undergo further changes during S. typhimurium infection, including TLR-dependent differentiation of marginal zone B cells into IgM-secreting plasma cells. Together, these TLR-mediated alterations to B cells are likely to influence the development of immunity to pathogens carrying the appropriate ligands. In addition to these innate responses of B cells, endocytosis of cognate antigen through their BCR allows antigen presentation. This, together with their ability to secrete cytokines, means they have the potential to drive T helper cell responses. I investigate the role of B cells in such CD4+ T cell responses by following antigen-specific T cells in vivo, using both a peptide immunisation strategy and the S. typhimurium infection model. I use anti-CD20 B cell depletion antibodies to deplete B cells at various stages of the immune response, and analyse the effects on T follicular helper and memory cell populations. I show that both the generation and maintenance of T follicular helper cells is dependent on the presence of B cells. Furthermore, I demonstrate that B cells are necessary very early in immune responses, during the first 10 days, for efficient generation of memory T cells.
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Yamamoto, Ryusuke. "Thymic Development of a Unique Bone Marrow-Resident Innate-like T Cell Subset with a Potent Innate Immune Function." Kyoto University, 2019. http://hdl.handle.net/2433/244522.
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Villanueva, Alexander Ian. "The influence of Toll-like receptors on murine invariant natural killer T cell activation." Thesis, 2013. http://hdl.handle.net/10214/7252.
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Invariant natural killer T (iNKT) cells are a versatile subclass of T lymphocytes which recognize glycolipid antigens. iNKT cells are capable of rapidly producing a broad array of cytokines in response to stimulation; thus, they play an important role in the early regulation of a variety of immune responses. It was hypothesized that iNKT cells express functional Toll-like receptors (TLRs) and that stimulation of TLRs by their ligands modulates iNKT cells responses. In the first objective, it was revealed that upon stimulation with anti-CD3 monoclonal antibody and interferon (IFN)-α, expression of TLRs was enhanced in iNKT cells. Furthermore, stimulation of iNKT cells with TLR ligands led to a significant increase in the expression of several cytokines. In the second objective, the mechanisms behind the modulatory effects of the TLR9 ligand (CpG-ODN) on iNKT cells were determined. Altogether, these findings suggest a direct role for TLRs in iNKT cell activation.Ontario Graduate Scholarship
Books on the topic "Innate-like T cells"
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Voll, Reinhard E., and Barbara M. Bröker. Innate vs acquired immunity. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0048.
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The innate and the adaptive immune system efficiently cooperate to protect us from infections. The ancient innate immune system, dating back to the first multicellular organisms, utilizes phagocytic cells, soluble antimicrobial peptides, and the complement system for an immediate line of defence against pathogens. Using a limited number of germline-encoded pattern recognition receptors including the Toll-like, RIG-1-like, and NOD-like receptors, the innate immune system recognizes so-called pathogen-associated molecular patterns (PAMPs). PAMPs are specific for groups of related microorganisms and represent highly conserved, mostly non-protein molecules essential for the pathogens' life cycles. Hence, escape mutants strongly reduce the pathogen's fitness. An important task of the innate immune system is to distinguish between harmless antigens and potentially dangerous pathogens. Ideally, innate immune cells should activate the adaptive immune cells only in the case of invading pathogens. The evolutionarily rather new adaptive immune system, which can be found in jawed fish and higher vertebrates, needs several days to mount an efficient response upon its first encounter with a certain pathogen. As soon as antigen-specific lymphocyte clones have been expanded, they powerfully fight the pathogen. Importantly, memory lymphocytes can often protect us from reinfections. During the development of T and B lymphocytes, many millions of different receptors are generated by somatic recombination and hypermutation of gene segments making up the antigen receptors. This process carries the inherent risk of autoimmunity, causing most inflammatory rheumatic diseases. In contrast, inadequate activation of the innate immune system, especially activation of the inflammasomes, may cause autoinflammatory syndromes.
Book chapters on the topic "Innate-like T cells"
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Neagu, Monica, and Carolina Constantin. "Signal Transduction in Immune Cells and Protein Kinases." In Advances in Experimental Medicine and Biology, 133–49. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-49844-3_5.
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AbstractImmune response relies upon several intracellular signaling events. Among the protein kinases involved in these pathways, members of the protein kinase C (PKC) family are prominent molecules because they have the capacity to acutely and reversibly modulate effector protein functions, controlling both spatial distribution and dynamic properties of the signals. Different PKC isoforms are involved in distinct signaling pathways, with selective functions in a cell-specific manner.In innate system, Toll-like receptor signaling is the main molecular event triggering effector functions. Various isoforms of PKC can be common to different TLRs, while some of them are specific for a certain type of TLR. Protein kinases involvement in innate immune cells are presented within the chapter emphasizing their coordination in many aspects of immune cell function and, as important players in immune regulation.In adaptive immunity T-cell receptor and B-cell receptor signaling are the main intracellular pathways involved in seminal immune specific cellular events. Activation through TCR and BCR can have common intracellular pathways while others can be specific for the type of receptor involved or for the specific function triggered. Various PKC isoforms involvement in TCR and BCR Intracellular signaling will be presented as positive and negative regulators of the immune response events triggered in adaptive immunity.
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Voll, Reinhard E., and Barbara M. Bröker. "Innate vs acquired immunity." In Oxford Textbook of Rheumatology, 356–64. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0048_update_001.
Full textAbstract:
The innate and the adaptive immune system efficiently cooperate to protect us from infections. The ancient innate immune system, dating back to the first multicellular organisms, utilizes phagocytic cells, soluble antimicrobial peptides, and the complement system for an immediate line of defence against pathogens. Using a limited number of germline-encoded pattern recognition receptors including the Toll-like, RIG-1-like, and NOD-like receptors, the innate immune system recognizes so-called pathogen-associated molecular patterns (PAMPs). PAMPs are specific for groups of related microorganisms and represent highly conserved, mostly non-protein molecules essential for the pathogens’ life cycles. Hence, escape mutants strongly reduce the pathogen’s fitness. An important task of the innate immune system is to distinguish between harmless antigens and potentially dangerous pathogens. Ideally, innate immune cells should activate the adaptive immune cells only in the case of invading pathogens. The evolutionarily rather new adaptive immune system, which can be found in jawed fish and higher vertebrates, needs several days to mount an efficient response upon its first encounter with a certain pathogen. As soon as antigen-specific lymphocyte clones have been expanded, they powerfully fight the pathogen. Importantly, memory lymphocytes can often protect us from reinfections. During the development of T and B lymphocytes, many millions of different receptors are generated by somatic recombination and hypermutation of gene segments making up the antigen receptors. This process carries the inherent risk of autoimmunity, causing most inflammatory rheumatic diseases. In contrast, inadequate activation of the innate immune system, especially activation of the inflammasomes, may cause autoinflammatory syndromes.
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Monteiro, Andreia, Ana Mafalda Fonseca, and Artur Paiva. "Peripheral Biomarkers in Multiple Sclerosis Patients Treated with Interferon-Beta." In Recent Advances in Neurochemistry [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99006.
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Multiple sclerosis is a relapsing and eventually progressive disorder of the central nervous system that continues to challenge researchers who try to understand the pathogenesis of the disease and prevent its progression. Interferon-beta is the most widely prescribed treatment for MS. Peripheral blood seems to mirror the immunological disturbances that underlie MS, which could represent the migration patterns between periphery and other tissues according to the clinical phase of the disease. Based on this assumption, several studies point to significant alterations in peripheral blood homeostasis of different subpopulations of T cells, like γδ T cells or Th1, Th2 and Th17 functional subsets; of B cells subpopulations; and of innate cells like monocytes and dendritic cells. The main goal of this chapter is to make an in-depth review of the major findings described in the literature that correlate specific alterations on different leukocytes subpopulations with disease status, and which therefore have the potential to constitute a peripheral biomarker of disease progression.
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Lambourne, Jonathan, and Ruaridh Buchanan. "Basic Immunology." In Tutorial Topics in Infection for the Combined Infection Training Programme. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198801740.003.0012.
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There are four major components of the immune system. These include: 1. mechanical barriers to pathogen entry. 2. the innate immune system. 3. the adaptive immune system. 4. the lymphoid organs. Mechanical barriers include skin and mucous membranes and tight junctions between epithelial cells prevent pathogen entry. Breaches can be iatrogenic, for example, IV lines, surgical wounds, and mucositis, and are a large source of healthcare- associated infections. The innate immune system provides the first internal line of defence, as well as initiating and shaping the adaptive immune response. The innate system comprises a range of responses: phagocytosis by neutrophils and macrophages (guided in part by the adaptive immune system), the complement cascade, and the release of antimicrobial peptides by epithelial cells (e.g. defensins, cathelicidin). The adaptive immune system includes both humoral (antibody- mediated) and cell-mediated responses. It is capable of greater diversity and specificity than the innate immune system, and can develop memory to pathogens and provide increased protection on re-exposure. Immune cells are divided into myeloid cells (neutrophils, eosinophils, basophils, mast cells, and monocytes/macrophages) and lymphoid cells (B, T, and NK cells). These all originate in the bone marrow from pluripotent haematopoietic stem cells. The lymphoid organs include the spleen, the lymph nodes, and mucosal-associated lymphoid tissues—which respond to antigens in the blood, tissues, and epithelial surfaces respectively. The three main ‘professional’ phagocytes are macrophages, dendritic cells, and neutrophils. They are similar with respect to how they recognize pathogens, but differ in their principal location and effector functions. Phagocytes express an array of Pattern Recognition Receptors (PRRs) e.g. Toll-like receptors and lectins (proteins that bind carbohydrates). PRRs recognize Pathogen- Associated Molecular Patterns (PAMPs)— elements which are conserved across species, such as cell-surface glycoproteins and nucleic acid sequences. Though limited in number, PRRs have evolved to recognize a huge array of pathogens. Binding of PRRs to PAMPs enhances phagocytosis. Macrophages are tissue-resident phagocytes, initiating and co-ordinating the local immune response. The cytokines and chemokines they produce cause vasodilation and alter the expression of endothelial cell adhesion factors, recruiting circulating immune cells.
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Carvalho, Fabiana Rabe, Débora Familiar-Macedo, and Andrea Alice Silva. "Mitochondrial DNA Role in Zika Virus Infection." In Mitochondrial DNA and the Immuno-inflammatory Response: New Frontiers to Control Specific Microbial Diseases, 86–100. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815051698122030009.
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Zika virus (ZIKV) is a member of the Flavivirus family. ZIKV infection ranges from asymptomatic to a mild disease in adults. However, in 2015, ZIKV infection became a public health emergency in the Americas associated with neurological alterations such as Guillain-Barré syndrome (GBS) in adults and congenital zika syndrome (CZS). By blocking type I IFN interferon signaling pathways, ZIKV evades the immune system and infects cells expressing the T cell immunoglobulin mucin domain-1 (TIM-1) and TAM (Tyro3, AXL, and Mer) receptors, such as neural progenitor cells. Moreover, ZIKV seems to orchestrate a process of astrocytic hypoxia that leads to the production of reactive oxygen species (ROS), mitochondrial DNA (mtDNA) fragmentation, and apoptosis. In recent decades, the active participation of mitochondria in the immuno-inflammatory response has been reported in several pathologies. In this context, mtDNA seems to have an essential role in triggering the innate immune response by activating inflammasomes, activating the cyclic GMP–AMP synthase (cGAS)–stimulator of interferon genes (STING) pathway, and also activating toll-like receptors that lead to IFN production and viral clearance. Here, we present an overview of some mechanisms of inflammatory response present in ZIKV infection, which contributes to mitochondrial dysfunction, mtDNA release, and tissue damage.
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E. Olguín, Jonadab, and Luis Ignacio Terrazas. "Regulation of the Immune Response in Cysticercosis: Lessons from an Old Acquainted Infection." In Current State of the Art in Cysticercosis and Neurocysticercosis. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.100137.
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In the last decades, we have learned some critical lessons about the relationship between the human body and its interaction with many infectious diseases, where regularly, the immune system has a major role in protection. We learned to differentiate between the immune response occurring in either an intracellular or extracellular parasitic infection, between innate and adaptive immune response, between either inflammatory or anti-inflammatory responses, and finally, we learned to recognize very particular mechanisms, such as the inability of the immune system to respond during very particular scenarios, such as the inability of T cells to both proliferate and produce cytokines even after their exposure to mitogens or specific-antigens. Along with our increase in the knowledge in immunology, we figured out that immunoregulation and immunosuppression are processes used by many parasites to reduce the capacity of the immune system to eliminate them, and to persist in the host favoring their transmission and also to complete their life cycles. Immunoregulation involves several mechanisms such as anergy, apoptosis, induction of both suppressive cytokines and membrane-bound molecules, as well as specialized cell populations of the immune system like regulatory T cells, Alternative Activated Macrophages, or Myeloid-derived Suppressor Cells, that together modify the outcome of the immune response. In this chapter we will review the general differences between the different types of immunoregulation, the kind of cellular populations of the immune system used by the helminths Taenia solium and Taenia crassiceps to induce immunoregulation and immunosuppression and also, the mechanisms used by these parasites such as mimicking molecules of the immune system to replace directly these mechanisms. Understanding and deciphering all these regulatory mechanisms could be useful to develop new tools to control this infection.
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Saadi, Fareeha, Debanjana Chakravarty, Grishma Kasle, and Jayasri Das Sarma. "Neurotropic Virus-Induced Meningoencephalomyelitis." In Recent Advances in Encephalitis Research [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.102674.
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Meningoencephalomyelitis emanates under the umbrella relating inflammatory changes of the Central Nervous System (CNS). Meningitis denotes inflammation in the meningeal layers, encephalitis is an acute diffuse inflammation of the brain, and inflammation in the spinal cord is denoted as myelitis. These can be interrelated or independent of each other depending on the etiology. The entire mechanism of meningoencephalomyelitis is governed by an acute innate inflammatory branch followed by a chronic progressive, adaptive branch of immunity with clinical signs like hyperthermia, weight loss, hypoxia, leukocytosis. This book chapter will focus on viral-induced meningitis, encephalitis, and myelitis. Thirty years of experience working with a murine-β-coronavirus (m-CoV); Mouse hepatitis virus (MHV)-A59 induced experimental model system provided us a thorough understanding of neuroglial cell-mediated acute neuroinflammation, denoted by the accumulation of leukocyte-common-antigen (LCA) positive or CD45+ leukocytes in perivascular infiltrates referred to as perivascular cuff formation and microglial nodules in the brain parenchyma, which mimics specific pathology of human neurological disease multiple sclerosis (MS). Additionally, in this chapter, we summarized the role of CNS resident microglial activation and its interaction with peripheral migratory T cells in mounting neuropathogenesis and host immunity in different families of neurotrophic encephalomyelitis viruses that cause CNS inflammation.
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Peakman, Mark. "Immunology of type 1 diabetes mellitus." In Oxford Textbook of Endocrinology and Diabetes, 1723–33. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.1319.
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The concept that the pathological hallmark of type 1 diabetes—namely, irreparable damage to β cells—is the result of an autoimmune process has gained sustained credence since it was first intimated in the 1970s. Forty years on, a robust set of criteria can be applied to settle this important question. As a result of numerous, reproducible research findings (Table 13.2.3.1), there is now an overwhelming case to support the assertion that type 1 diabetes is an autoimmune disease. Perhaps the most persuasive evidence is provided by the case reports of diabetes arising in recipients of bone marrow from patients with type 1 diabetes (1, 2). In these cases, the recipients underwent bone marrow ablation as part of the treatment for their underlying condition (e.g. relapsed haematological cancers) that effectively removed all autologous innate and adaptive immune cells. To reconstitute their immune system, they then received bone marrow from a sibling with type 1 diabetes. They developed the disease themselves some years later. It is hard to argue against the proposal that immune cells transferred in the bone marrow inoculum were responsible for β cell destruction. Indeed, current practice in these circumstances is to ensure immune depletion of any mature T lymphocytes that may be present in the transplanted bone marrow using specific monoclonal antibodies. This successfully circumvents the problem—and also provides clear evidence for the pivotal role for T lymphocytes in causing β cell damage. It should be noted that the overwhelming majority of patients with type 1 diabetes—especially those inhabiting the Western, developed world—have evidence of the underlying autoimmune processes, as discussed in this chapter. However, there is a recognition that type 1 diabetes may be heterogeneous, as, in some patients, evidence of autoimmunity is lacking (WHO diabetes classification type 1B). In Japan, a fulminant form of diabetes has been described as representing 15–20% of type 1 disease (15). Presentation is characterized by a high prevalence of preceding common cold-like and gastrointestinal symptoms, a near-normal level of HbA1c (despite very high plasma glucose levels and ketoacidosis), raised serum pancreatic enzyme levels, and absent C-peptide—but only rarely any evidence of autoantibodies against islet cell autoantigens (16). Some cases of type 1 diabetes arising in sub-Saharan Africa have also been described as lacking evidence of autoimmunity against islet cells (see Chapter 13.4.3.4); however, these data require clarification, since it is known that the autoantibodies decline and may disappear from the circulation soon after diagnosis, making retrospective classification of cohorts with established disease highly problematic (17). Future studies in these locations will need to establish evidence of autoimmunity at diagnosis in currently equivocal situations, using the most comprehensive, up-to-date range of serological markers (see Table 13.2.3.2, below), as well as to establish the clinical and immunogenetic features of the disease.
Conference papers on the topic "Innate-like T cells"
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Hussain, Khiyam, Pierre Vantourout, Maria Poole, Josephine Eum Eum, Thomas Hayday, Adam Laing, Seb Battaglia, et al. "1392 An atypical central memory like phenotype can be induced in human T cells by Innate TCRαβ engagement." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.1392.
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Chou, Chun, Saida Dadi, Briana G. Nixon, and Ming Li. "Abstract A181: Origin of tumor-elicited cytotoxic innate-like T-cell responses." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-a181.
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