Academic literature on the topic 'Innate lymphocyte cells'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Innate lymphocyte cells.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "Innate lymphocyte cells"
1
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.
Full textAbstract:
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.
2
Turner, Jan-Eric, Martina Becker, Hans-Willi Mittrücker, and Ulf Panzer. "Tissue-Resident Lymphocytes in the Kidney." Journal of the American Society of Nephrology 29, no. 2 (November 1, 2017): 389–99. http://dx.doi.org/10.1681/asn.2017060599.
Full textAbstract:
It has become evident that nonlymphoid tissues are populated by distinct subsets of innate and adaptive lymphocytes that are characterized by minimal exchange with recirculating counterparts. Especially at barrier sites, such as the skin, gut, and lung, these tissue-resident lymphocyte populations are ideally positioned to quickly respond to pathogens and other environmental stimuli. The kidney harbors several classes of innate and innate-like lymphocytes that have been described to contribute to this tissue-resident population in other organs, including innate lymphoid cells, natural killer cells, natural killer T cells, mucosal-associated invariant T cells, and γδ T cells. Additionally, a substantial proportion of the adaptive lymphocytes that are found in the kidney displays a surface phenotype suggestive of tissue residency, such as CD69+CD4+ T cells. In this review, we summarize recent advances in the understanding of tissue-resident lymphocyte populations, review the available evidence for the existence of these populations in the kidney, and discuss the potential physiologic and pathophysiologic roles thereof in kidney.
3
Chen, Yi-Ling, Clare S. Hardman, Koshika Yadava, and Graham Ogg. "Innate Lymphocyte Mechanisms in Skin Diseases." Annual Review of Immunology 38, no. 1 (April 26, 2020): 171–202. http://dx.doi.org/10.1146/annurev-immunol-082919-093554.
Full textAbstract:
Innate lymphocyte populations are emerging as key effectors in tissue homeostasis, microbial defense, and inflammatory skin disease. The cells are evolutionarily ancient and carry conserved principles of function, which can be achieved through shared or unique specific mechanisms. Recent technological and treatment advances have provided insight into heterogeneity within and between individuals and species. Similar pathways can extend through to adaptive lymphocytes, which softens the margins with innate lymphocyte populations and allows investigation of nonredundant pathways of immunity and inflammation that might be amenable to therapeutic intervention. Here, we review advances in understanding of innate lymphocyte biology with a focus on skin disease and the roles of commensal and pathogen responses and tissue homeostasis.
4
Wiarda, Jayne E., Julian M. Trachsel, Sathesh K. Sivasankaran, Christopher K. Tuggle, and Crystal L. Loving. "Intestinal single-cell atlas reveals novel lymphocytes in pigs with similarities to human cells." Life Science Alliance 5, no. 10 (August 22, 2022): e202201442. http://dx.doi.org/10.26508/lsa.202201442.
Full textAbstract:
Lymphocytes can heavily influence intestinal health, but resolving intestinal lymphocyte function is challenging as the intestine contains a vastly heterogeneous mixture of cells. Pigs are an advantageous biomedical model, but deeper understanding of intestinal lymphocytes is warranted to improve model utility. Twenty-six cell types were identified in the porcine ileum by single-cell RNA sequencing and further compared with cells in human and murine ileum. Though general consensus of cell subsets across species was revealed, some porcine-specific lymphocyte subsets were identified. Differential tissue dissection and in situ analyses conferred spatial context, revealing similar locations of lymphocyte subsets in Peyer’s patches and epithelium in pig-to-human comparisons. Like humans, activated and effector lymphocytes were abundant in the ileum but not periphery of pigs, suggesting tissue-specific and/or activation-associated gene expression. Gene signatures for peripheral and ileal innate lymphoid cells newly discovered in pigs were defined and highlighted similarities to human innate lymphoid cells. Overall, we reveal novel lymphocyte subsets in pigs and highlight utility of pigs for intestinal research applications.
5
Meraviglia, Serena, Sary El Daker, Francesco Dieli, Federico Martini, and Angelo Martino. "γδT Cells Cross-Link Innate and Adaptive Immunity inMycobacterium tuberculosisInfection." Clinical and Developmental Immunology 2011 (2011): 1–11. http://dx.doi.org/10.1155/2011/587315.
Full textAbstract:
Protective immunity against mycobacterial infections such asMycobacterium tuberculosisis mediated by interactions between specific T cells and activated antigen presenting cells. To date, many aspects of mycobacterial immunity have shown that innate cells could be the key elements that substantially may influence the subsequent adaptive host response. During the early phases of infection, innate lymphocyte subsets play a pivotal role in this context. Here we summarize the findings of recent investigations onγδT lymphocytes and their role in tuberculosis immunity.
6
Gasteiger, Georg, Saskia Hemmers, Matthew A. Firth, Audrey Le Floc’h, Morgan Huse, Joseph C. Sun, and Alexander Y. Rudensky. "IL-2–dependent tuning of NK cell sensitivity for target cells is controlled by regulatory T cells." Journal of Experimental Medicine 210, no. 6 (May 6, 2013): 1167–78. http://dx.doi.org/10.1084/jem.20122462.
Full textAbstract:
The emergence of the adaptive immune system took a toll in the form of pathologies mediated by self-reactive cells. Regulatory T cells (T reg cells) exert a critical brake on responses of T and B lymphocytes to self- and foreign antigens. Here, we asked whether T reg cells are required to restrain NK cells, the third lymphocyte lineage, whose features combine innate and adaptive immune cell properties. Although depletion of T reg cells led to systemic fatal autoimmunity, NK cell tolerance and reactivity to strong activating self- and non-self–ligands remained largely intact. In contrast, missing-self responses were increased in the absence of T reg cells as the result of heightened IL-2 availability. We found that IL-2 rapidly boosted the capacity of NK cells to productively engage target cells and enabled NK cell responses to weak stimulation. Our results suggest that IL-2–dependent adaptive-innate lymphocyte cross talk tunes NK cell reactivity and that T reg cells restrain NK cell cytotoxicity by limiting the availability of IL-2.
7
Gasteiger, Georg, Saskia Hemmers, Paula D. Bos, Joseph C. Sun, and Alexander Y. Rudensky. "IL-2–dependent adaptive control of NK cell homeostasis." Journal of Experimental Medicine 210, no. 6 (May 6, 2013): 1179–87. http://dx.doi.org/10.1084/jem.20122571.
Full textAbstract:
Activation and expansion of T and B lymphocytes and myeloid cells are controlled by Foxp3+ regulatory T cells (T reg cells), and their deficiency results in a fatal lympho- and myeloproliferative syndrome. A role for T reg cells in the homeostasis of innate lymphocyte lineages remained unknown. Here, we report that T reg cells restrained the expansion of immature CD127+ NK cells, which had the unique ability to up-regulate the IL2Rα (CD25) in response to the proinflammatory cytokine IL-12. In addition, we observed the preferential accumulation of CD127+ NK cells in mice bearing progressing tumors or suffering from chronic viral infection. CD127+ NK cells expanded in an IL-2–dependent manner upon T reg cell depletion and were able to give rise to mature NK cells, indicating that the latter can develop through a CD25+ intermediate stage. Thus, T reg cells restrain the IL-2–dependent CD4+ T cell help for CD127+ immature NK cells. These findings highlight the adaptive control of innate lymphocyte homeostasis.
8
Matic, Sanja, Suzana Popovic, Predrag Djurdjevic, Danijela Todorovic, Natasa Djordjevic, Zeljko Mijailovic, Predrag Sazdanovic, et al. "SARS-CoV-2 infection induces mixed M1/M2 phenotype in circulating monocytes and alterations in both dendritic cell and monocyte subsets." PLOS ONE 15, no. 12 (December 31, 2020): e0241097. http://dx.doi.org/10.1371/journal.pone.0241097.
Full textAbstract:
Clinical manifestations of SARS-CoV-2 infection range from mild to critically severe. The aim of the study was to highlight the immunological events associated with the severity of SARS-CoV-2 infection, with an emphasis on cells of innate immunity. Thirty COVID-19 patients with mild/moderate symptoms and 27 patients with severe/critically severe symptoms were recruited from the Clinical Center of Kragujevac during April 2020. Flow cytometric analysis was performed to reveal phenotypic and functional alterations of peripheral blood cells and to correlate them with the severity of the disease. In severe cases, the number of T and B lymphocytes, dendritic cells, NK cells, and HLA-DR-expressing cells was drastically decreased. In the monocyte population proportion between certain subsets was disturbed and cells coexpressing markers of M1 and M2 monocytes were found in intermediate and non-classical subsets. In mild cases decline in lymphocyte number was less pronounced and innate immunity was preserved as indicated by an increased number of myeloid and activated dendritic cells, NK cells that expressed activation marker at the same level as in control and by low expression of M2 marker in monocyte population. In patients with severe disease, both innate and adoptive immunity are devastated, while in patients with mild symptoms decline in lymphocyte number is lesser, and the innate immunity is preserved.
9
Sharapova, T. N., E. A. Romanova, L. P. Sashchenko, N. V. Gnuchev, and D. V. Yashin. "Innate immune protein Tag7 stimulates the appearance of cytotoxic NK cells after incubation with lymphocytes." Доклады Академии наук 484, no. 6 (May 23, 2019): 777–80. http://dx.doi.org/10.31857/s0869-56524846777-780.
Full textAbstract:
Tag7 (PGRP-S) is an innate immune protein that is involved in the antibacterial and antitumor defense and stimulates the maturation of cytotoxic lymphocyte subpopulations. It was found that the incubation of lymphocytes with Tag7 for 3 days promotes the appearance of cytotoxic NK cells that are active against a number of tumor cell lines.
10
Kawabe, Takeshi, and Alan Sher. "Memory-phenotype CD4+ T cells: a naturally arising T lymphocyte population possessing innate immune function." International Immunology 34, no. 4 (December 13, 2021): 189–96. http://dx.doi.org/10.1093/intimm/dxab108.
Full textAbstract:
Abstract In conventional adaptive immune responses, upon recognition of foreign antigens, naive CD4+ T lymphocytes are activated to differentiate into effector/memory cells. In addition, emerging evidence suggests that in the steady state, naive CD4+ T cells spontaneously proliferate in response to self-antigens to acquire a memory phenotype (MP) through homeostatic proliferation. This expansion is particularly profound in lymphopenic environments but also occurs in lymphoreplete, normal conditions. The ‘MP T lymphocytes’ generated in this manner are maintained by rapid proliferation in the periphery and they tonically differentiate into T-bet-expressing ‘MP1’ cells. Such MP1 CD4+ T lymphocytes can exert innate effector function, producing IFN-γ in response to IL-12 in the absence of antigen recognition, thereby contributing to host defense. In this review, we will discuss our current understanding of how MP T lymphocytes are generated and persist in steady-state conditions, their populational heterogeneity as well as the evidence for their effector function. We will also compare these properties with those of a similar population of innate memory cells previously identified in the CD8+ T lymphocyte lineage.
Dissertations / Theses on the topic "Innate lymphocyte cells"
1
Esplin, Brandt L. "Replenishment of innate immune system in health and disease." Oklahoma City : [s.n.], 2009.
Find full text
2
Narayan, Kavitha. "The Function of Innate γδ T Cell Subsets is Molecularly Programmed in the Thymus in Three Stages: A Dissertation." eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/527.
Full textAbstract:
The immune system generates discrete lineages of cells that are designed to respond optimally to environmental cues and infectious agents. Two distinct lineages of T cells, distinguished by expression of either an αβ or γδ T cell receptor (TCR), arise from a common progenitor in the thymus. The type of pathogen and the cytokine milieu directs effector differentiation of αβ T cells in the periphery through the induction of specific transcriptional networks. γδ T cell development is distinct from that of αβ T cells in its ordered rearrangement of TCR genes and the pairing of Vγ and Vδ chains to generate γδ T cell subsets that home to specific tissues. Unlike conventional αβ T cells, γδ T cells express a preactivated or memory phenotype prior to pathogen encounter, and recent evidence indicates that effector functions may be programmed during thymic development. To better understand the development and function of γδ T cells, we analyzed the gene expression profiles of subsets of γδ T cells segregated by TCR repertoire and maturation state in the thymus. We also determined the impact of TCR signaling and trans-conditioning on γδ T cell subset-specific gene signatures by analysis of Itk-/- and Tcrb-/- γδ T cell subsets. Our analysis has defined three stages of γδ T cell subset-specific differentiation, and indicates that γδ T cells may consist of at least two separate lineages, distinguished by the expression of a Vγ2 or Vγ1.1 TCR, that arise from different precursors during thymic development. Key transcriptional networks are established in immature γδ T cells during the first phase of development, independent of TCR signaling and trans-conditioning, with Vγ2+ cells expressing modulators of WNT signaling, and Vγ1.1+ cells expressing high levels of inhibitor of DNA binding 3 (ID3), which regulates E2A/HEB proteins. The second stage involves the further specification of the Vγ2+ subset specific gene signature, which is dependent upon ITK-mediated signals. In the third stage, terminal maturation of γδ T cell subsets occurs, dependent on both TCR and trans-conditioning signals. The expression patterns of Vγ1.1+ subsets that differ in Vδ usage diverge, and all subsets further elaborate and reinforce their effector programming by the distinct expression of chemokine and cytokine receptors. Alteration of WNT signaling or E2A/HEB activity results in subset specific defects in effector programming, indicating that the transcriptional networks established at the immature stage are crucial for the functional maturation of γδ T cells. These data provide a new picture of γδ T cell development, regulated by multiple checkpoints that shape the acquisition of subset-specific molecular signatures and effector functions.
3
Thomas, Katja, Tony Sehr, Undine Proschmann, Francisco Alejandro Rodriguez-Leal, Rocco Haase, and Tjalf Ziemssen. "Fingolimod additionally acts as immunomodulator focused on the innate immune system beyond its prominent effects on lymphocyte recirculation." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-227035.
Full textAbstract:
Background
Growing evidence emphasizes the relevance of sphingolipids for metabolism and immunity of antigen-presenting cells (APC). APCs are key players in balancing tolerogenic and encephalitogenic responses in immunology. In contrast to the well-known prominent effects of sphingosine-1-phosphate (S1P) on lymphocyte trafficking, modulatory effects on APCs have not been fully characterized.
Methods
Frequencies and activation profiles of dendritic cell (DC) subtypes, monocytes, and T cell subsets in 35 multiple sclerosis (MS) patients were evaluated prior and after undergoing fingolimod treatment for up to 24 months. Impact of fingolimod and S1P on maturation and activation profile, pro-inflammatory cytokine release, and phagocytotic capacity was assessed in vitro and ex vivo. Modulation of DC-dependent programming of naïve CD4+ T cells, as well as CD4+ and CD8+ T cell proliferation, was also investigated in vitro and ex vivo.
Results
Fingolimod increased peripheral slanDC count—CD1+ DC, and monocyte frequencies remained stable. While CD4+ T cell count decreased, ratio of Treg/Th17 significantly increased in fingolimod-treated patients over time. CD83, CD150, and HLADR were all inhibited, but CD86 was upregulated in DCs after incubation in the presence of fingolimod. Fingolimod but not S1P was associated with reduced release of pro-inflammatory cytokines from DCs and monocytes in vitro and ex vivo. Fingolimod also inhibited phagocytic capacity of slanDCs and monocytes. After fingolimod, slanDCs demonstrated reduced potential to induce interferon–gamma-expressing Th1 or IL-17-expressing Th17 cells and DC-dependent T cell proliferation in vitro and in fingolimod-treated patients.
Conclusions
We present the first evidence that S1P-directed therapies can act additionally as immunomodulators that decrease the pro-inflammatory capabilities of APCs, which is a crucial element in DC-dependent T cell activation and programming.
4
Salem, Fatouma. "Identification de biomarqueurs prédictifs de la survenue d'une arthrite chez le patients atteints de maladie inflammatoire chronique de l'intestin (MICI)." Thesis, Université de Lorraine, 2021. http://www.theses.fr/2021LORR0341.
Full textAbstract:
De nombreuses données récentes suggèrent des liens entre les inflammations digestives et articulaires, dont le pourcentage élevé de patients avec une maladie inflammatoire chronique intestinale (MICI) développant une spondylarthropathie axiale (ax-SpA) et le succès clinique des biothérapies anti-cytokines dans ces 2 pathologies. On ignore cependant s'il s'agit d'un lien de causalité ou d'une co-existence entre les 2 maladies. D'un point de vue physiopathologique, la lamina propria (LP) de l'intestin contient une grande quantité de cellules de l'immunité de type 3 dont les lymphocytes TH17 et les cellules lymphoïdes innées de type 3 (ILC3s). Ces cellules jouent un rôle essentiel dans l'homéostasie intestinale en agissant comme un pare-feu contre les pathogènes extracellulaires mais peuvent générer une inflammation digestive voire de l'auto-immunité en cas d'activation excessive. Leur différenciation IL-23-dépendante est contrôlée par le facteur de transcription RORγt qui est lui-même réprimé par le récepteur nucléaire PPARγ. Ainsi, PPARγ est apparu comme un régulateur majeur de la voie IL-17/TH17-ILC3. Comme il est également capable de moduler la sécrétion de peptides antimicrobiens, il est un interacteur potentiel entre le microbiote fécal et la muqueuse digestive par sa capacité à réguler à la fois la réponse immune locale et la composition du microbiote. Pour étudier le rôle régulateur de PPARγ sur l'inflammation digestive, indépendamment de son impact métabolique général sur l'adipogénèse, nous avons généré des souris déficientes pour PPARγ dans les cellules immunitaires, i.e. une invalidation de PPARγ dans les cellules exprimant RORγt (RORγtcre+ PPARγfl/fl). En utilisant le modèle de colite induite par le DSS (sulfate de dextran sodique), nous n'avons pas montré d'aggravation de la maladie ni d'augmentation des cellules de l'immunité de type 3 dans la LP des souris déficientes en PPARγ. Cette absence d'effet n'a pas été modifiée par une déplétion cellulaire préalable par un anticorps anti-CD3 et a été reproduite dans le modèle de colite présumément plus ILC-3-dépendante induite par l'injection d'un anticorps anti-CD40. Ces résultats ne montrent pas un effet majeur de PPARγ sur les cellules de l'immunité innée de type 3 pendant l'inflammation digestive ou suggèrent que la réponse immune de type 3 n'est pas un mécanisme physiopathologique majeur dans les modèles animaux utilisés. Pour rechercher des biomarqueurs caractéristiques de l'apparition d'une ax-SpA chez les patients MICI, nous avons constitué la cohorte Floracrohn pour comparer des patients avec une maladie de Crohn (MC) sans inflammation articulaire, des patients avec une ax-SpA (SpA) sans inflammation digestive, des patients avec une MC ayant développé une ax-SpA (MC+SpA) et des patients non malades (contrôles). Les groupes de patients étaient majoritairement traités par des anti-TNFα et comparables en termes de consommation tabagique. Nous avons confirmé que les patients MC+SpA ont des maladies plus sévères et montré que le microbiote bactérien était plus fortement déséquilibré par la MC que par la ax-SpA avec l'émergence de quelques groupes bactériens. Au contraire, le fungome fécal était plus fortement déséquilibré par la ax-SpA que par la MC avec une diminution des certain genres comme une signature possible de l'apparition d'une ax-SpA chez les patients MC. Nous avons pas trouvé de différences parmi les 23 polymorphismes concernant les voies IL-17/IL-23 étudiées. La recherche d'une signature fungique spécifique pourrait être utile pour identifier les patients MC à risque de développer une ax-SpA, ce qui pourrait être complété par un profil cytokinique actuellement en cours d'évaluationSeveral pieces of evidence are in favor of a link between joint and gut inflammation including the high percentage of inflammatory bowel diseases (IBD) patients developing axial spondyloarthropathy (SpA) and the clinical success of cytokines-blocking therapies in both diseases. However, whether such co-occurrence is causative rather than correlative remains an open question. From a pathophysiological point of view, the lamina propria (lp) in the intestine is enriched in cells of type 3 immunity including TH17 cells and type 3 innate lymphoid cells (ILC3s). These cells play a homeostatic role in intestinal defense by acting as a firewall against extracellular pathogens but can lead to gut inflammation and possibly auto-immunity in case of excessive activation. Their IL-23-driven differentiation depends on the transcription factor RORγt which is repressed by the nuclear receptor PPARγ. As a consequence, PPARγ has emerged as a master regulator of the IL-17/TH17-ILC3 pathway and as it is also able to modulate the release of antimicrobial peptides, it is a possible key interactor between fecal microbiota and gut mucosa by regulating the local immune response and microbiota composition. To investigate the regulatory role of PPARγ in gut inflammation, independently from its overall metabolic impact on adipogenesis, we generated mice that are deficient for PPARγ in immune cells, namely PPARγ invalidation in RORγt expressing cells (RORγtcre+ PPARγfl/fl ). Using the DSS (dextran- sodium sulphate) colitis model, we failed to demonstrate any worsening of the disease nor increase in immune type 3 cell populations in the lp of PPARγ deficient mice. Such lack of effect was not modified by preliminary cell depletion with anti-CD3 antibody and was also observed in the expectedly more ILC3-dependent colitis model induced by anti-CD40 antibody injection. These data do not support a major role of PPARγ in type 3 immune cells during gut inflammation or alternatively that the underlying pathomechanisms poorly depend on type 3 immunity in these animal models. To search for biomarkers characteristic of axial SpA occurrence in IBD patients, we build the Floracrohn cohort to compare patients with Crohn's disease (CD) without joint inflammation, patients with axial SpA (SpA) without gut inflammation, patients with CD having developed axial SpA (CD+SpA) and non-diseased patients. Patients groups were mainly treated with anti-TNFα and were comparable in terms of smoking consumption. We confirmed that CD+SpA patients had more severe diseases and showed that bacterial microbiota was strongly influenced by CD over SpA with some emerging bacterial groups. In contrast, gut fungome was strongly influenced by SpA over CD with a decrease of certain fungi strain as a possible emerging signature of SpA in IBD patients. No distinct polymorphisms frequencies were found amongst the 23 studied in the IL-17/IL-23 pathways. The search for a specific fungome signature may be helpful to identify CD patients at risk of developing axial SpA and this could be completed by cytokines profiling currently under investigation
5
Shekhar, Sudhanshu. "A study on the role of lung dendritic cells and their interaction with innate lymphocytes in host defense against a bacterial lung infection." Karger, 2015. http://hdl.handle.net/1993/30622.
Full textAbstract:
Chlamydia is an obligate intracellular bacterial pathogen that causes a wide spectrum of diseases worldwide. At present, there are no vaccines to prevent chlamydial infections due to poor understanding of how anti-chlamydial immunity ensues. In this study, we employed a variety of in vitro and in vivo systems, including knockout (KO) mice and adoptive transfer, to investigate the role of lung dendritic cells (LDCs) and their relationship with innate lymphocytes, natural killer (NK) and invariant NKT (iNKT) cells, in host defense against chlamydial lung infections in mice. We found that iNKT cells altered the phenotype and cytokine production pattern of LDCs following C. pneumoniae infection. Adoptive transfer of LDCs from infected Jα18-KO mice, which lack iNKT cells, into naïve wild-type (WT) mice promoted Th2 (IL-4) immunity following infection challenge, whereas the transfer of LDCs from the infected WT mice induced protective Th1/Tc1 (IFN-γ) immunity. On the other hand, upon adoptive transfer, LDCs from C. muridarum-infected NK-cell-depleted mice (NK-LDCs) conferred reduced protection after chlamydial challenge than the recipients of LDCs from infected sham-treated mice (NK+LDCs). NK+LDC recipients exhibited an enhanced Th1/Th17, in contrast to Th2, response compared to the NK-LDC recipients. In coculture experiments, NK cells isolated from the infected mice promoted IL-12p70, IL-6, and IL-23 production by LDCs through NKG2D receptor signaling. These findings indicate that iNKT and NK cells condition LDCs to confer protective Th1/Tc1/Th17 immunity against chlamydial lung infection.
We also analyzed the contribution of major LDC subsets, CD103+ and CD11bhi LDCs, in host defense against C. muridarum infection. We found that CD103+ and CD11bhi LDC subsets expanded following chlamydial infection. CD103+ LDCs showed higher expression of costimulatory molecules and greater production of Th1- and Th17-inducing cytokines (IL-12, IL-6 and IL-23) than CD11bhi LDCs. Coculture of Chlamydia-specific CD4+ T cells with LDC subsets revealed that the T cells cultured with CD103+ LDCs produced larger amounts of IFN-γ and IL-17 compared to those with CD11bhi LDCs. To test their function in vivo, we isolated CD103+ and CD11bhi LDC subsets from infected mice and transferred them into naïve syngeneic mice that received chlamydial challenge. CD103+ LDC-recipients showed better protection, as evidenced by their reduced body weight loss, bacterial burden and lung pathology, than CD11bhi LDC recipients. Mice that received CD103+, compared to CD11bhi, LDCs produced enhanced Th1/Th17 cytokines (IFN-γ and IL-17) in the lung and the MLNs. In conclusion, these findings demonstrate that CD103+ LDCs are more efficient in inducing Th1/Th17 immunity to chlamydial infection than CD11bhi LDCs.
Taken together, our findings have provided direct in vivo evidence on the role of LDCs and their conditioning by iNKT and NK cells in generating mucosal T-cell immunity against a bacterial lung infection. The findings have added new knowledge to the field of lung immunology, which have implications for developing prophylactic and/or therapeutic strategies against respiratory diseases.October 2015
6
Prince, Amanda L. "The Role of Inducible T Cell Kinase (Itk) in the Development of Innate T Cells and in the Formation of Protective Memory Responses: A Dissertation." eScholarship@UMMS, 2013. https://escholarship.umassmed.edu/gsbs_diss/660.
Full textAbstract:
T cell development in the thymus produces multiple lineages of cells, including conventional naïve CD4+ and CD8+ T cells, regulatory T cells, and innate T cells. Innate T cells encompass γδ T cells, invariant natural killer (iNKT) cells, mucosal-associated invariant T (MAIT) cells, and H2-M3-restricted cells (Berg, 2007). Although they are a minor subset of all thymocytes, innate T cells develop in the thymus and share characteristics of the innate and adaptive immune systems (Berg, 2007). These lymphocytes undergo antigen receptor rearrangement and are able to exert their effector function immediately upon ex vivo stimulation (Berg, 2007). However, in several strains of mice harboring mutations in T cell signaling proteins or transcriptional regulators, conventional CD8+ T cells develop as innate cells that share characteristics with memory T cells (Atherly et al., 2006b; Broussard et al., 2006; Fukuyama et al., 2009; Gordon et al., 2011; Verykokakis et al., 2010b; Weinreich et al., 2010). One of these signaling proteins, inducible T cell kinase (Itk) is a nonreceptor protein tyrosine kinase that signals downstream of the T cell receptor (TCR) (Berg et al., 2005). Upon TCR activation, Itk is activated and recruited to the TCR signaling complex, where Itk interacts with Src homology 2 (SH2) domain-containing leukocyte phosphoprotein of 76 kDa (SLP-76), linker for activation of T cells (LAT), and phospholipase C γ1 (PLCγ1) (Berg et al., 2005). Thus, in Itk-deficient mice, TCR signaling is disrupted, which results in mature CD4- CD8+ (CD8SP) thymocytes that are CD44high, CD62Lhigh, CD122+, and CXCR3+ and that express high levels of the transcription factor, Eomesodermin (Eomes) (Atherly et al., 2006b; Broussard et al., 2006; Weinreich et al., 2010). Recently, it was determined that the development of these innate CD8SP thymocytes in itk-/- mice is dependent on IL-4 produced in the thymic environment by a poorly characterized subset of CD3+ thymocytes expressing the transcriptional regulator, promyelocytic leukemia zinc finger (PLZF) (Gordon et al., 2011; Verykokakis et al., 2010b; Weinreich et al., 2010). Here we show that a sizeable proportion of mature CD4+ CD8- (CD4SP) thymocytes in itk-/- mice also develop as Eomesodermin+ innate T cells. These Eomes+ innate CD4+ T cells are CD44high, CD62Lhigh, CD122+, and CXCR3+ (Atherly et al., 2006b; Broussard et al., 2006; Dubois et al., 2006; Weinreich et al., 2010). Surprisingly, neither CD4SP nor CD8SP innate thymocytes in itk-/- mice are dependent on γδ T cells for their development as was previously hypothesized (Alonzo and Sant'Angelo, 2011). Instead, both subsets of innate itk-/- T cells require the presence of a novel PLZF-expressing, SAP-dependent thymocyte population that is essential for the conversion of conventional CD4+ and CD8+ T cells into Eomesodermin-expressing innate T cells with a memory phenotype. This novel subset of PLZF-expressing SAP-dependent innate T cells preferentially home to the spleen and mesenteric lymph nodes and have a restricted TCR repertoire. Thus, we have christened this subset as CD4+ PLZF + MAIT-like cells. We have characterized multiple subsets of innate T cells that expand in the absence of Itk. Therefore, we were interested in how innate T cells respond to infection. Although Itk KO mice have defects in cytolytic function and cytokine production during an acute infection, these mice are able to clear viral infections (Atherly et al., 2006a; Bachmann et al., 1997). Hence, we hypothesized that Itk-deficient memory CD8+ T cells would be able to provide protection upon a challenge infection. Conversely, we found this not to be true although Itk-deficient memory CD8+ T cells were present in similar frequencies and cell numbers as WT memory CD8+ T cells at 42 days post-infection. Furthermore, Itk-deficient memory CD8+ T cells were able to produce IFNγ and exert cytolytic function upon stimulation. Although the function of Itk-deficient memory CD8+ T cells appeared to be intact, we found that these cells were unable to expand in response to a challenge infection. Remarkably, conventional memory CD8+ T cells lacking Itk were able to expand and form protective memory responses upon challenge. Thus, the inability of Eomes+ innate CD8+ T cells to form protective memory responses does not appear to be intrinsic to cells deficient in Itk. This thesis is divided into six major chapters. The first chapter will provide an introduction to T cell development and the role of Itk in T cell development. Additionally, it will introduce a variety of innate T cell subsets that will be discussed throughout this thesis and will provide an overview of CD4+ and CD8 + T cell differentiation during infection. This section will explain the role of Itk in CD4+ helper T cell differentiation and describe how Itk-deficient CD8+ T cells respond to acute infection. The introduction will also discuss the generation of conventional memory CD8+ T cells. The second chapter will provide the details of the experimental procedures used in this thesis. The third chapter will describe the characterization and development of Eomes+ innate CD4+ T cells that develop in the absence of Itk. Additionally, this chapter will address the subset of PLZF+ innate T cells that induce the expression of Eomes in innate T cells. The fourth chapter will further characterize and explore the development of itk-/- CD4+ PLZF+ MAIT-like T cells. The fifth chapter will examine the role of Eomes + innate CD8+ T cells in protective memory responses. Chapters three through five will display work that is in preparation to be submitted to a peer-reviewed journal. The sixth chapter will discuss the results of this thesis and their implications.
7
Prince, Amanda L. "The Role of Inducible T Cell Kinase (Itk) in the Development of Innate T Cells and in the Formation of Protective Memory Responses: A Dissertation." eScholarship@UMMS, 2002. http://escholarship.umassmed.edu/gsbs_diss/660.
Full textAbstract:
T cell development in the thymus produces multiple lineages of cells, including conventional naïve CD4+ and CD8+ T cells, regulatory T cells, and innate T cells. Innate T cells encompass γδ T cells, invariant natural killer (iNKT) cells, mucosal-associated invariant T (MAIT) cells, and H2-M3-restricted cells (Berg, 2007). Although they are a minor subset of all thymocytes, innate T cells develop in the thymus and share characteristics of the innate and adaptive immune systems (Berg, 2007). These lymphocytes undergo antigen receptor rearrangement and are able to exert their effector function immediately upon ex vivo stimulation (Berg, 2007). However, in several strains of mice harboring mutations in T cell signaling proteins or transcriptional regulators, conventional CD8+ T cells develop as innate cells that share characteristics with memory T cells (Atherly et al., 2006b; Broussard et al., 2006; Fukuyama et al., 2009; Gordon et al., 2011; Verykokakis et al., 2010b; Weinreich et al., 2010). One of these signaling proteins, inducible T cell kinase (Itk) is a nonreceptor protein tyrosine kinase that signals downstream of the T cell receptor (TCR) (Berg et al., 2005). Upon TCR activation, Itk is activated and recruited to the TCR signaling complex, where Itk interacts with Src homology 2 (SH2) domain-containing leukocyte phosphoprotein of 76 kDa (SLP-76), linker for activation of T cells (LAT), and phospholipase C γ1 (PLCγ1) (Berg et al., 2005). Thus, in Itk-deficient mice, TCR signaling is disrupted, which results in mature CD4- CD8+ (CD8SP) thymocytes that are CD44high, CD62Lhigh, CD122+, and CXCR3+ and that express high levels of the transcription factor, Eomesodermin (Eomes) (Atherly et al., 2006b; Broussard et al., 2006; Weinreich et al., 2010). Recently, it was determined that the development of these innate CD8SP thymocytes in itk-/- mice is dependent on IL-4 produced in the thymic environment by a poorly characterized subset of CD3+ thymocytes expressing the transcriptional regulator, promyelocytic leukemia zinc finger (PLZF) (Gordon et al., 2011; Verykokakis et al., 2010b; Weinreich et al., 2010). Here we show that a sizeable proportion of mature CD4+ CD8- (CD4SP) thymocytes in itk-/- mice also develop as Eomesodermin+ innate T cells. These Eomes+ innate CD4+ T cells are CD44high, CD62Lhigh, CD122+, and CXCR3+ (Atherly et al., 2006b; Broussard et al., 2006; Dubois et al., 2006; Weinreich et al., 2010). Surprisingly, neither CD4SP nor CD8SP innate thymocytes in itk-/- mice are dependent on γδ T cells for their development as was previously hypothesized (Alonzo and Sant'Angelo, 2011). Instead, both subsets of innate itk-/- T cells require the presence of a novel PLZF-expressing, SAP-dependent thymocyte population that is essential for the conversion of conventional CD4+ and CD8+ T cells into Eomesodermin-expressing innate T cells with a memory phenotype. This novel subset of PLZF-expressing SAP-dependent innate T cells preferentially home to the spleen and mesenteric lymph nodes and have a restricted TCR repertoire. Thus, we have christened this subset as CD4+ PLZF + MAIT-like cells. We have characterized multiple subsets of innate T cells that expand in the absence of Itk. Therefore, we were interested in how innate T cells respond to infection. Although Itk KO mice have defects in cytolytic function and cytokine production during an acute infection, these mice are able to clear viral infections (Atherly et al., 2006a; Bachmann et al., 1997). Hence, we hypothesized that Itk-deficient memory CD8+ T cells would be able to provide protection upon a challenge infection. Conversely, we found this not to be true although Itk-deficient memory CD8+ T cells were present in similar frequencies and cell numbers as WT memory CD8+ T cells at 42 days post-infection. Furthermore, Itk-deficient memory CD8+ T cells were able to produce IFNγ and exert cytolytic function upon stimulation. Although the function of Itk-deficient memory CD8+ T cells appeared to be intact, we found that these cells were unable to expand in response to a challenge infection. Remarkably, conventional memory CD8+ T cells lacking Itk were able to expand and form protective memory responses upon challenge. Thus, the inability of Eomes+ innate CD8+ T cells to form protective memory responses does not appear to be intrinsic to cells deficient in Itk. This thesis is divided into six major chapters. The first chapter will provide an introduction to T cell development and the role of Itk in T cell development. Additionally, it will introduce a variety of innate T cell subsets that will be discussed throughout this thesis and will provide an overview of CD4+ and CD8 + T cell differentiation during infection. This section will explain the role of Itk in CD4+ helper T cell differentiation and describe how Itk-deficient CD8+ T cells respond to acute infection. The introduction will also discuss the generation of conventional memory CD8+ T cells. The second chapter will provide the details of the experimental procedures used in this thesis. The third chapter will describe the characterization and development of Eomes+ innate CD4+ T cells that develop in the absence of Itk. Additionally, this chapter will address the subset of PLZF+ innate T cells that induce the expression of Eomes in innate T cells. The fourth chapter will further characterize and explore the development of itk-/- CD4+ PLZF+ MAIT-like T cells. The fifth chapter will examine the role of Eomes + innate CD8+ T cells in protective memory responses. Chapters three through five will display work that is in preparation to be submitted to a peer-reviewed journal. The sixth chapter will discuss the results of this thesis and their implications.
8
Dubois, Natasha. "Caractérisation de la réponse immune induite par un adjuvant comprenant un agoniste du TLR4 dans des modèles murins." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS131/document.
Full textAbstract:
En 2014 la Tuberculose (TB) à dépassé le VIH comme la principale cause de décès par maladie infectieuse dans le monde soulignant le besoin urgent de développer un vaccin plus efficace contre cette maladie. Le candidat vaccin contre la TB, ID93/GLA-SE, dévéloppé à l’Infectious Disease Research Institute (IDRI), est aujourd’hui en essai clinique de phase IIa et a montré des résultats pré-cliniques et cliniques promettants. Dans de modèle murin de TB, ce vaccin induit une forte réponse TH1, considérée comme centrale dans la protection contre la TB, et la production d’IgG2 par les lymphocytes B. Néanmoins, les mécanismes d’action de GLA-SE sont encore peu connus.L’objectif principal de cette thèse est donc d’élucider les méchanismes clés qui relient les réponses innées et adaptatives induites par cet adjuvant dans le modèle murin. Un objectif secondaire est d’établir un modèle murin de rechute de TB après traitement et d’évaluer l’utilisation d’ID93/GLA-SE en tant que vaccin immuno-thérapeutique et sa capacité à réduire les taux de rechute dans ce modèle. L‘ensemble de ce travail nous a permis de mieux comprendre les mécanismes impliqués dans la réponse immunitaire adaptative induite par GLA- SE et de montrer la capacité de ID93/GLA- SE a être utilisé comme un vaccin thérapeutique contre la tuberculose dans le but de réduire les taux de rechute post-thérapeutiquesIn 2014 tuberculosis (TB) surpassed HIV as the leading cause of death by an infectious disease worldwide emphasizing the urgent need to develop a more effective vaccine against this airborne disease. The Infectious Disease Research Institute (IDRI) TB candidate vaccine ID93/GLA-SE is currently undergoing a Phase IIa clinical trial and has shown promising preclinical and clinical results. In murine models of TB this vaccine drives a strong CD4 TH1 response, which is thought to be important for protection against TB, and an IgG2c skewed B cell response. However, little is known about the cellular and molecular events that drive GLA-SE adjuvanticity.To that end, the main objective of my thesis was to elucidate the key mechanisms that connect innate and adaptive immune responses elicited by this adjuvant in the murine model. A secondary objective was to evaluate the possibility of using ID93/GLA-SE as adjunct therapy to existing antibiotic treatments to reduce relapse rates after TB treatment.Collectively the results obtained during this research project and thesis broaden our knowledge and our current understanding of the mechanisms involved in the adaptive immune response induced by GLA-SE and show the capacity of ID93/GLA-SE to be used as a therapeutic vaccine against TB to reduce post-therapeutic relapse rates
9
Felices, Martin. "The Role of TEC Family Kinases in Innate T Cell Development and Function: a Dissertation." eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/373.
Full textAbstract:
The Tec family kinases Itk and Rlk have been previously shown to have an important role in signaling downstream of the T cell receptor [TCR]. Almost all of the work done in the past on these two kinases looked at their role in conventional αβ T cells, specifically CD4+ T cells. These studies demonstrated functions for Itk [primarily] and Rlk in T cell development, activation, and differentiation. However, despite the wealth of knowledge on conventional CD4+ T cells, prior to the work presented here little to no studies addressed the role of Tec family kinases on CD8+ or innate T cell development. My studies show a clear role for Itk [and in some cases Rlk] in innate T cell development; whether it be deprecating, in the case of innate CD8+ T cells or some subsets of γδ T cells, or beneficial, in the case of NKT cells. I show that Itk has a crucial role in conventional CD8+ T cell development, as absence of Itk [or Itk and Rlk] causes strongly reduced numbers of conventional CD8+ T cells and a vigorous enhancement of an innate-like CD8+ T cell population. In NKT cells, my work demonstrates that Itk [and to a lesser extent Rlk] is required for terminal maturation, survival, and cytokine secretion. Finally, on γδ T cells Itk is important in maintaining the Th1 cytokine secretion profile usually associated with these cells, and regulating the development of CD4+ or NK1.1+ γδ T cells. Taken together, this work clearly illustrates an important role for Tec family kinases in innate T cell development and function.
10
Verrier, Thomas. "Function and plasticity of NKp46 expressing innate lymphoid cells." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCC173/document.
Full textAbstract:
Les cellules lymphoïdes innées de groupe 3 (ILC3) contribuent activement à l’homéostasie intestinale par leur production d’Interleukin-22 (IL-22). Ces ILC3 regroupent 2 sous-populations majeures, les LTi (« Lymphoid Tissue inducer »), caractérisées par l’expression du récepteur au chimiokine CCR6, et les ILC3 exprimant le facteur de transcription (FT) T-bet, qui comprennent une population positive pour le marqueur de surface NKp46, récepteur originalement utilisé pour identifier les ILC de groupe 1 (ILC1). Les ILC1 jouent un rôle prépondérant dans la réponse aux pathogènes intracellulaires et anti-tumorale. Jusqu’à présent, trois populations majeures composent les ILC1 : les lymphocytes cytotoxiques Natural Killer (NK ou ILC1b), qui dépendent largement du FT Eomes et expriment l’intégrine CD49b ; les ILC1 hépatiques et intestinaux, qui dépendent du FT T-bet et expriment CD49a (ILC1a) ; et une population CD49a+ et DX5+ indépendante du FT Nfil3 localisée dans les glandes salivaires ou l’utérus (ILC1ab). Mes travaux visent à comprendre la biologie des ILC exprimant NKp46, ainsi que les facteurs impliqués dans leur développement, leur maturation et leur fonction. La majeure partie de ma thèse se concentre sur les NKp46+ ILC3. Premièrement, nous démontrons un rôle majeur pour le récepteur aux chimiokine CXCR6 dans la localisation des NKp46+ ILC3 dans les villi de la lamina propria intestinale (Satoh-Takayama et al. 2014). Deuxièmement, j’ai mis en évidence que NKp46+ ILC3 pouvait perdre l’expression de NKp46 (Verrier et al. 2016). Déclenchée par le TGFβ, cette perte d’expression est associée à une plus forte capacité à produire de l’IL-22, mais aussi à l’acquisition de marqueurs identifiant les LTi (CCR6, MHC-II), démontrant ainsi la plasticité des NKp46+ ILC3. Enfin, en collaboration avec le groupe de Rachel Golub, nous avons confirmé le rôle présumé de la molécule Notch dans cette plasticité (Chea et al. 2016). Dans ce manuscrit, je discuterai du développement et de l’hétérogénéité des ILC3, ILC1a, ILC1b et ILC1ab. L’ensemble de mes résultats soutient une vision dynamique de la biologie des ILC reflétant l’adaptation de ces cellules effectrices face à leur environnement. En caractérisant les différents acteurs impliqués dans ce processus dynamique, mes travaux pourront servir au développement de thérapies visant à contrôler l’équilibre entre ces différentes populations dans divers pathologies comme le cancer, les infections virales, ou encore les maladies intestinalesGroup 3 Innate Lymphoid cells (ILC3) actively maintain mucosal homeostasis through the production of Interleukin-22 (IL-22). ILC3 encompass 2 major populations, LTi (« Lymphoid Tissue inducer »), characterized by the expression of the chemokine receptor CCR6, and ILC3 that express the transcription factor T-bet, which include a population expressing the surface marker NKp46, a receptor originally used to identify group 1 ILC (ILC1). ILC1 plays a major role in the defense against intracellular pathogens and anti-tumoral responses. Three major ILC1 populations have been identified: the cytotoxic lymphocytes « Natural Killer » (NK or ILC1b), which largely rely for on the transcription factor Eomes their generation and express the integrin CD49b; hepatic and intestinal ILC1 that depends on the T-bet transcription factor and express CD49a (ILC1a); and a population that expresses CD49a and CD49b (ILC1ab) and populates the salivary gland and the uterus, which is independent of the transcription factor Nfil3. My work aimed to understand the biology of NKp46 expressing ILC, as well as factor involved in their development, maturation and function. The major part of my work focuses on NKp46+ ILC3. First, we demonstrate a major role for the chemokine receptor CXCR6 in their localisation in the lamina propria villi (Satoh-Takayama et al. 2014). Second, I showed that NKp46+ ILC3 could lose NKp46 expression (Verrier et al. 2016). Induced by TGFβ, this loss of expression was associated with higher IL-22 production and by the acquisition of markers identifying LTi (CCR6, MHC-II), demonstrating NKp46+ ILC3 plasticity. Finally, in collaboration with Rachel Golub’s group, we confirmed a putative role for Notch-signaling in this plasticity (Chea et al. 2016). In this manuscript, I will discuss the development and the heterogeneity of ILC3, ILC1a, ILC1b and ILC1ab. All the results I generated support a dynamic vision of ILC biology, which reflects how they adapt in response to environmental cues. By characterizing the different actors involved in this dynamic process, my work could be used to design therapies aiming at controlling the equilibrium between these different populations in diverse pathologies such as cancer, viral infection, or intestinal diseases
Books on the topic "Innate lymphocyte cells"
1
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.
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.
2
Piccio, Laura, and Anne H. Cross. Immunology of Multiple Sclerosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199341016.003.0004.
Full textAbstract:
Multiple sclerosis (MS) is considered to be an autoimmune disease of the central nervous system that targets myelin but affects both white matter and gray matter. Multiple sclerosis is thought to be mediated by cells of the adaptive and innate immune systems. CD4+ T lymphocytes of the Th1 and Th17 subtypes are believed to be critical for the initiation of multiple sclerosis. Treatment with monoclonal antibodies that deplete B lymphocytes has proven that B cells are critical to relapse development in multiple sclerosis. While immunopathophysiology is clearly important in MS, whether multiple sclerosis is truly an autoimmune disorder and the target or targets of the autoimmunity remain unknown.
3
Lalvani, Ajit, and Katrina Pollock. Defences against infection. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0303.
Full textAbstract:
The immune system is classified into a series of component parts, each specialized to defend the host against infection. Cells of the innate immune system are distributed throughout the body, in the tissues, and in the circulation, to defend against the first signs of danger, combining the acute inflammatory response with the ability to kill and remove invading pathogens. Monocytes, macrophages, and neutrophils phagocytose and kill exogenous and endogenous targets, using both oxygen-dependent and oxygen-independent mechanisms. The adaptive immune system creates a structurally specific and prolonged response, mediated by lymphocytes to clear infection and generate immunological memory. In this chapter, the functions of the innate and adaptive immune system are reviewed, together with the clinical features and investigation of acquired and inherited immune deficiencies.
Book chapters on the topic "Innate lymphocyte cells"
1
Bonavida, Benjamin. "Tumor Cell Resistance to Apoptosis by Infi ltrating Cytotoxic Lymphocytes." In Innate and Adaptive Immunity in the Tumor Microenvironment, 121–37. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6750-1_6.
Full text
2
Wohn, C. T., S. Pantelyushin, J. L. Ober-Blöbaum, and B. E. Clausen. "Aldara-Induced Psoriasis-Like Skin Inflammation: Isolation and Characterization of Cutaneous Dendritic Cells and Innate Lymphocytes." In Methods in Molecular Biology, 171–85. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1212-4_16.
Full text
3
Eken, Ahmet, and Hamiyet Donmez‐Altuntas. "Innate Lymphoid Cells (Non‐NK ILCs)." In Lymphocyte Updates - Cancer, Autoimmunity and Infection. InTech, 2017. http://dx.doi.org/10.5772/intechopen.68893.
Full text
4
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.
5
Panahi, Elina, Danielle I. Stanisic, Christopher S. Peacock, and Lara J. Herrero. "Protective and Pathogenic Immune Responses to Cutaneous Leishmaniasis." In Leishmaniasis - General Aspects of a Stigmatized Disease. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.101160.
Full textAbstract:
Leishmania (Kinetoplastida: Trypanosomatidae) parasites are known to cause a broad spectrum of clinical diseases in humans, collectively known as the leishmaniases. Cutaneous leishmaniasis is the most common clinical presentation with varying degrees of severity largely driven by host immune responses, specifically the interplay between innate and adaptive immune response. The establishment of a T lymphocyte driven cell-mediated immune response, leading to activated phagocytic cells, leading to Leishmania parasite killing and control of infection. Alternatively, the Leishmania parasite manipulates the host immune system, enabling parasite proliferation and clinical disease. Here we review how the cumulative interactions of different aspects of the host immune response determines disease outcome, severity, and immunity to re-infection.
6
Darmadi, Darmadi, and Riska Habriel Ruslie. "Immunology of Helicobacter pylori Infection." In Immunology of the GI Tract [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.104592.
Full textAbstract:
Helicobacter pylori (H. pylori) is the most common infecting microorganism in humans. H. pylori had coexisted with humans for 30,000 years ago and developed extensive survival adaptations. The infection is both active and chronic and leads to several disorders from chronic gastritis to gastric adenocarcinoma. The prevalence of H. pylori infection is still high in developing countries. The burden of disease due to infection is also heavy. The persistence of infection is the basis of diseases. H. infection activates innate and adaptive immune responses but the immune response fails to eradicate the infection. H. pylori is able to evade both innate and adaptive immune responses. It can neutralize gastric acid, elicit autoimmunity toward parietal cells, prevent phagocytosis, induce apoptosis of immune cells, inhibit lymphocyte proliferation, disrupt imbalance between humoral and cellular adaptive immune responses, promote regulatory T cell activity, and trigger genetic rearrangement. Host factor is involved in the incidence of H. pylori infection and its complications. Reinfection after eradication is common. Multiple drug resistance has also emerged. Vaccination is a promising management approach to eradicate H. pylori and prevent diseases it caused. The development of the vaccine itself needs to consider the immune escape mechanism of H. pylori.
7
Sobolev, Vladimir, Elizaveta Bystritskaya, and Oxana Svitich. "Epigenetic Studies of Atopic Dermatitis." In Atopic Dermatitis [Working Title]. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.94092.
Full textAbstract:
Since the pathogenesis of atopic dermatitis could not be explained only by a population genetic and phenotypic profiles, epigenetic regulator factors have been considered. Epigenetics is the study of inherited changes in gene expression that are not related to changes in its nucleotide sequence. One of the main classical regulatory mechanisms in human cells is DNA methylation. It is not clear how permanent modifications caused by this process are and whether it is possible to affect them by changing the activity of enzymes that trigger remodeling reactions. In this chapter we analyze all recent studies in this field. We focus more on methylation of innate and adaptive immune factors, with an emphasis on T-lymphocyte genes such as CD3, CD4, and CD8.
8
Huber, S. A. "Innate Lymphocyte Effectors (Natural Killer, Natural Killer T and γδ T Cells) in Infection and Myocarditis." In Myocarditis. InTech, 2011. http://dx.doi.org/10.5772/20773.
Full text
9
"Innate Cell-mediated Immunity." In Killer Lymphocytes, 125–57. Dordrecht: Springer Netherlands, 2007. http://dx.doi.org/10.1007/978-1-4020-3270-7_6.
Full text
10
Singh Chauhan, Vikram. "Vitamin D and the Immune System." In Vitamin D. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97300.
Full textAbstract:
In the past few decades, various novel actions of vitamin D have been discovered. The mechanism of action of calcitriol or vitamin D is mediated by the Vitamin D receptor (VDR), a subfamily of nuclear receptors, which acts as a transcription factor in the target cells after formation of a heterodimer with the retinoid X receptor (RXR). As the VDR has been found in virtually all cell types, vitamin D exerts multiple actions on different tissues. Vitamin D has important immunomodulatory actions, which includes enhancement of the innate immune system and inhibition of the adaptative immune responses. These actions are associated with an increase in production of interleukin (IL)-4 by T helper (Th)-2 lymphocytes and the up-regulation of regulatory T lymphocytes. Vitamin D can regulate the immune responses in secondary lymphoid organs as well as in target organs through a number of mechanisms. Vitamin D inhibits the expression of APC cytokines, such as interleukin-1 (IL-1), IL-6, IL-12, and tissue necrosis factor- α (TNF-α) and decreases the expression of a set of major histocompatibility complex (MCH) class II cell surface proteins in macrophages. Vitamin D also inhibits B cell differentiation and antibody production. These actions reflect an important role of Vitamin D in balancing the immune system.
Conference papers on the topic "Innate lymphocyte cells"
1
Rovere-Querini, Patrizia. "SP0103 T LYMPHOCYTES AND INNATE IMMUNE CELLS BALANCE MUSCLE REGENERATION AND AUTOIMMUNITY." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.8577.
Full text
2
Martinu, Tereza, Christine V. Kinnier, Kymberly Gowdy, Francine L. Kelly, Michael L. Gunn, and Scott M. Palmer. "Pulmonary Innate Immune Activation In Allotransplantation Induces A Distinct Antigen Presenting Cell Profile Followed By Lymphocytic Inflammation." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1083.
Full text