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Dissertations / Theses on the topic 'Langerhans'

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Published: 4 June 2021
Last updated: 19 February 2022

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1

Chorro, Laurent. "Inside Langerhans cells." Paris 5, 2010. http://www.theses.fr/2010PA05T050.

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Les cellules de Langerhans (CLs) sont des cellules myéloïdes de l’épiderme, actuellement considérées en Immunologie comme des cellules dendritiques (CDs) originaires de la moelle osseuse. Contrairement aux autres cellules myéloïdes, comme les monocytes ou les CDs conventionnelles qui dérivent et se renouvellent à partir de cellules souches hématopoïétiques (SCHs), l’origine et les mécanismes de renouvellement des CLs restent encore aujourd’hui mal connus. Mon travail de thèse a pour but (i) de déterminer l’origine des CLs et (ii) de comprendre les mécanismes contrôlant leur homéostasie chez l’adulte en conditions normales ou inflammatoires. Mes résultats montrent que les CLs se développent à partir de précurseurs extra embryonnaires originaires du sac vitellin. Peu avant la naissance, ces précurseurs colonisent l’épiderme avant de se différentier en CLs et de proliférer. Chez l’adulte et en conditions normales, les CLs se maintiennent indépendamment des SCHs. Elles sont leurs propres précurseurs et s’auto renouvellent dans l’épiderme pour maintenir leur nombre. Dans un modèle murin de Dermatite atopique, le nombre des CLs est dramatiquement augmenté suite à la multiplication des ces cellules dans l’épiderme. Nous trouvons que la prolifération des CLs est contrôlée par un signal moléculaire produit par les kératinocytes de l’épiderme mais qui restent encore à identifier. Associés à de récents travaux sur la microglie du cerveau, mes résultats suggèrent que certaines populations de cellules myéloïdes, situées dans des tissues où le recrutement de leucocytes est limité ou délétère, suivent un modèle différent de développement chez l’embryon et d’homéostasie chez l’adulte
Langerhans Cells (LCs) are myeloid cells of the epidermis, currently featured in immunology textbooks as bone marrow-derived dendritic cells (DC). Unlike other myeloid cells such as monocytes and classical DCs that derive and continuously renew from haematopoietic stem cell (HSC) precursors, the exact origin and homeostasis of LCs remained unclear. My work aimed at (i) determining the origin of LCs and (ii) defining the mechanisms of LC homeostasis in adult during steady and inflammatory conditions. My results showed that LCs developed from an extra-embryonic precursor originating from the yolk sac, and not from HSC precursors, that colonize the epidermis during late embryogenesis and further acquire features of adult LCs during the neonatal period. In adult and under steady state conditions, the LC network is maintained independently from HSC precursors. Differentiated LCs are their own precursors and can self-renew in the epidermis to maintain their number in vivo. In a model of skin Atopic Dermatitis, LCs can increase their number by local proliferation and not by the recruitment of HSC precursors. We also found that proliferation of LCs is controlled by a yet unknown molecular signal derived from neighbouring keratinocytes. My results on LCs, together with recent works on brain microglia, suggest that selected populations of myeloid cells, located in tissues where leukocyte recruitment may be limited or deleterious, follow a different pathway of development in embryos and homeostasis in adult, where extra-embryonic precursors are recruited during development and maintained by self-renewal via molecular cues from surrounding cells
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2

Misery, Laurent. "Précurseurs des cellules de Langerhans." Lyon 1, 1995. http://www.theses.fr/1995LYO1T020.

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3

Alam, Sam Mohammad Kutubul. "Pathogenesis of Langerhans Cell Histiocytosis." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487289.

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The Langerhans cell (LC) is a histiocytic cell that represents a resident immigrant population in the epidermis and functions as a professional antigen presenting cell (APC). Langerhans cell histiocytosis (LCH) is a rare disorder that can affect both adults and children and can involve various organs. Clinically the disease ranges from a solitary lytic bone lesion, which may resolve following curettage, to a disseminated leukaemia-like disease with multiple organ involvement, which can be fatal. Despite considerable advances in our understanding of the disease, the aetiology ofLCH remains obscure. The aim of this study is to identify differentially expressed genes in LCH cell as compared to normal LC to gain novel insight into potential pathologic mechanisms involved in this disease. This has been carried out by using immunoaffinity cell purification against the LC marker CDla, a technique developed in our laboratory, together with a suppressive subtractive cDNA hybridisation (SSH) technique. Because of the limited LCH RNA material, an initial study was carried out to optimise conditions for SSH using HeLa cells and YCI cells, a derivative of HeLa in which CDla is constitutively expressed. By doing these experiments, it was found that the inclusion of an additional step to the subtraction protocol, namely size fractionation and purification of subtracted cDNA, allowed efficient recovery ofcDNA clones for the differentially expressed CDla gene. Using this optimised protocol, gene expression between normal LC and LCH cells obtained from bronchial alveolar lavage from one patient with LCH have been compared. A total of 291 differentially expressed clones were identified by differential screening and sequenced. The resulting sequences were used to search DNA sequence databases and the results used to classify sequences into three groups: (i) sequences that matched known human gene sequences, (ii) sequences that were found to originate from the pathogen Mycoplasma hyorhinis (M hyorhinis) and (iii) gene sequences of unknown origin. Using RT-PCR I have evaluated the expression of these in other LCH samples and have demonstrated one of the known human genes, argininosuccinate synthetase to be differentially expressed exclusively in 18 LCH-involved tissues from 17 LCH involved patients examined to date. Further, using RT-PCR, M hyorhinis sequences were also confirmed in six out of six additional LCH samples derived from bronchial alveolar lavage and two additional LCH samples involving gum. Taken together, these findings suggest that a discrete set of genes are differentially expressed in LCH, which may be important in the pathogenesis of this disease. Further, my data suggest the possible involvement of a novel infectious agent in the disease.
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4

Reis, e. Sousa Caetano Maria Pacheco Pais dos. "Phagocytosis of antigens by Langerhans cells." Thesis, University of Oxford, 1992. http://ora.ox.ac.uk/objects/uuid:1f69e0f0-1d08-4c2f-aa02-216231100f14.

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Mature dendritic cells (DC) isolated from lymphoid tissues initiate antigen-specific T-dependent responses even though they are non-phagocytic and weakly pinocytic, whereas Langerhans cells (LC; immature DC) can process protein antigens but are poorly immunostimulatory. Thus antigens may be acquired by cells of this lineage at an immature stage but, to our knowledge, there have been no studies on the phagocytic capacity of these cells in vitro. Using a newly-developed flow cytometric assay to measure the association between fluorescent markers and LC in epidermal cell cultures, and light and electron microscopy, we have observed phagocytosis of a variety of particles by freshly-isolated LC. The cells readily phagocytosed zymosan, heat-killed S. cerevisiae, bacteria (S. aureus and C. parvum) and fluorescent latex beads, but were unable to take up IgG- or complement-coated sheep erythrocytes, as opposed to MØ. Similarly, many freshly-isolated splenic DC had some phagocytic activity. However, the capacity of both LC and splenic DC to phagocytose zymosan, bacteria and fluorescent latex beads was markedly decreased after maturation in culture, consistently with the fact that mature DC are poorly phagocytic. Zymosan binding and uptake were much greater in fresh LC from C57BL/6 compared to BALB/c mice, and the loss of phagocytic capacity for zymosan during maturation followed different kinetics in the two strains. Two receptors mediating uptake of zymosan in LC were identified based on the effect of different inhibitors. Both of these receptors, recognising mannose and β-glucan residues, appear to be differentially regulated in the two mouse strains and during culture of LC. Our findings support the notion that DC are capable of acquiring particulate antigens for presentation at an immature stage, through recognition units for carbohydrate determinants common to a variety of potentially pathogenic organisms.
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5

Calming, Ulrika. "Langerhans cell histiocytosis : detection, monitoring and pathophysiology /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-180-2.

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6

Vedel, Jean. "Cellules de Langerhans humaines et molécules d'adhésion." Bordeaux 2, 1990. http://www.theses.fr/1990BOR23108.

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7

Ar'Rajab, Aamer. "Islet transplantation in the treatment of diabetes number of islets, functional regulation and metabolic control /." Lund : Dept. of Surgery, Lund University, 1991. http://catalog.hathitrust.org/api/volumes/oclc/38187937.html.

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8

Westerlund, Johanna. "Pulsatile insulin release from single islets of Langerhans." Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2000. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-494.

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Insulin release from single islets of Langerhans is pulsatile. The secretory activities of the islets in the pancreas are coordinated resulting in plasma insulin oscillations. Nutrients amplitude-regulate the insulin pulses without influencing their frequency. Diabetic patients show an abnormal plasma insulin pattern, but the cause of the disturbance remains to be elucidated. Ithe present thesis the influence of the cytoplasmic calcium concentratio([Ca2+]i) and cell metabolism on pulsatile insulin release was examined in single islets of Langerhans from ob/ob-mice. Glucose stimulation of insulin release involves closure of ATP-sensitive K+ channels (KATP channels), depolarization, and Ca2+ influx in β-cells. In the presence of 11 mM glucose, pulsatile insulin secretion occurs in synchrony with oscillations i[Ca2+]i. When [Ca2+]i is low and stable, e.g. under basal conditions, low amplitude insulin pulses are still observed. When [Ca2+]i is elevated and non-oscillating, e.g. when the β-cells are depolarized by potassium, high amplitude insulin pulses are observed. The frequency of the insulin pulses under these conditions is similar to that observed when [Ca2+]i oscillations are present. By permanently opening or closing the KATP channels with diazoxide or tolbutamide, respectively, it was investigated if glucose can modulate pulsatile insulin secretion when it does not influence the channel activity. Under these conditions, [Ca2+]i remained stable whereas the amplitude of the insulin pulses increased with sugar stimulation without change in the frequency. Metabolic inhibition blunted but did not prevent the insulin pulses. The results indicate that oscillations in metabolism can generate pulsatile insulin release when [Ca2+]i is stable. However, under physiological conditions, pulsatile secretion is driven by oscillations in metabolism and [Ca2+]i, acting in synergy.

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9

Bernstrand, Cecilia. "Langerhans cell histiocytosis : a clinical and immunological study /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-468-2/.

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10

Dandapat, Shera. "Studies of maturation in human epidermal Langerhans cells." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429394.

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11

Napierala, Hendrik [Verfasser]. "Rebesiedlung dezellularisierter Rattenpankreata mit Langerhans-Inseln / Hendrik Napierala." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2019. http://d-nb.info/1180993888/34.

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12

Barrett, Andrew W. "Immunological studies of human oral mucosal Langerhans cells." Thesis, University of Newcastle Upon Tyne, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333511.

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13

Mikulowska, Anna. "The human langerhans cell in irritant contact dermatitis." Lund : Dept. of Medical Cell Research, Lund University, 1994. http://catalog.hathitrust.org/api/volumes/oclc/39693813.html.

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14

Brugerolle, de Fraissinette Anne de. "Étude des précurseurs de la cellule de Langerhans." Lyon 1, 1989. http://www.theses.fr/1989LYO1T053.

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15

MILLOT, XAVIER. "Isolement et greffe d'ilots de langerhans : resultats preliminaires." Strasbourg 1, 1993. http://www.theses.fr/1993STR15079.

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16

Clayton, Heather Anne. "The encapsulation and transplantation of islets of Langerhans." Thesis, University of Leicester, 1992. http://hdl.handle.net/2381/34306.

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Although several clinical human islet transplants have been performed, allograft rejection has been a major problem. Encapsulation in sodium alginate/poly-l-lysine has been proposed as a method to protect the islets from rejection and autoimmune destruction. The aims of this project were to determine optimum capsule composition and to assess encapsulated islet function following transplantation using the spontaneously diabetic BioBreeding (BB/d) rat as a model of autoimmune insulin-dependent diabetes. The membrane integrity of islets, determined by microfluorometry, was not adversely affected by encapsulation. During perifusion, the stimulation increase of encapsulated islets was decreased relative to controls, but the stimulation index and response time were unaffected. Capsule composition did not affect these results. The biocompatibility of the capsules was related to their composition. The presence of an outer layer of alginate, and the preparation of alginate used, reduced the severity of pericapsular fibrosis. Capsules implanted in the peritoneal cavity provoked a more severe response than those placed in the renal subcapsular space. BB/d rats displayed a marked response to the capsules. Transplantation experiments demonstrated that 3000 non-encapsulated or 5000 encapsulated islets were the minimum number required to reverse streptozotocin-induced diabetes when transplanted into the peritoneal cavity. An intense pericapsular fibrosis led to failure of the encapsulated grafts. Further transplants into the BB/d rat were postponed to allow the cause of fibrosis to be investigated. The alginate was found to be contaminated with protein and this was removed by dialysis. In vitro experiments with the dialysed alginate demonstrated that treatment of the alginate did not affect the viability of encapsulated islets. Biocompatibility studies showed that capsules coated with dialysed alginate remained free from pericapsular fibrosis, even in the BB/d rat, when tested over the time interval which had resulted in the development of severe fibrosis of capsules coated with untreated alginate.
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17

Nikhilanandhan, Ganendra S. "Conformal coating of islets of Langerhans in HEMA-MMA." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0001/MQ45898.pdf.

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18

Barbaroux, Jean-Baptiste Olivier Stephen. "The trance system in langerhans cell and keratinocyte homeostasis." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499092.

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19

Smith, P. A. "Electrophysiology of #beta#-cells form the islets of Langerhans." Thesis, University of East Anglia, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.380117.

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20

Dalle, Stéphane. "Le miniglucagon, nouveau régulateur local de l'îlot de Langerhans." Montpellier 2, 1998. http://www.theses.fr/1998MON20257.

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Grace a l'utilisation de la lignee cellulaire b pancreatique min 6, nous avons etudie la capacite du miniglucagon, fragment c-terminal (19-29) du glucagon, present dans le pancreas, a moduler la secretion d'insuline et analyse son mode d'action cellulaire. Nous montrons qu'a des concentrations allant de 0,1 a 1000 pm, le miniglucagon inhibe la secretion d'insuline de maniere dose-dependante, quelque soit le type de secretagogue utilise (glucose, glucagon, tglp-1 ou sulfonylure). Le miniglucagon est non seulement tres puissant (ed#5#0 = 1 pm), il est aussi tres efficace, car capable de supprimer la quasi-totalite de la secretion stimulee. Le miniglucagon est actif sans modifier les niveaux d'ampc stimules par le glucagon et le tglp-1 et sans intervenir sur la voie phospholipase c. Le miniglucagon montre la meme puissance et la meme efficacite a bloquer l'entree de calcium dans les cellules min 6 qu'a inhiber la secretion d'insuline. La technique de patch-clamp sur cellules min 6 indique que le miniglucagon induit une hyperpolarisation de la cellule b, probablement en provoquant l'ouverture de canaux potassium, ce qui a pour consequence d'abolir les depolarisations declenchees par le glucose. Nous pouvons conclure que le miniglucagon est un inhibiteur puissant et efficace de la secretion d'insuline en provoquant, par hyperpolarisation, la fermeture des canaux calciques voltage-dependants. Ses effets sont bloques par traitement des cellules a la toxine bordetella pertussis, ce qui implique probablement un recepteur original couple a des canaux potassium via une proteine g de type g#i ou g#o. De plus, l'effet inhibiteur du miniglucagon sur la secretion d'insuline stimulee par le glucose et le tglp-1 a ete retrouve en utilisant un autre modele experimental physiologique de pancreas isole perfuse de rat. Le miniglucagon apparait ainsi comme un nouveau regulateur local de la secretion d'insuline.
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21

ESPOSITO-FARES, BEHR-GROSS MARIE-EMMANUELLE. "Connaissances actuelles sur les cellules de langerhans epidermiques humaines." Université Louis Pasteur (Strasbourg) (1971-2008), 1993. http://www.theses.fr/1993STR15057.

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22

Shenkman, Rustin M. "Quadrupole Magnetic Sorting (QMS) of Porcine Islets of Langerhans." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1229640573.

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23

Ogden, Stephanie. "An investigation of Langerhans' cell function in aged skin." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/an-investigation-of-langerhans-cell-function-in-aged-skin(a5d3967f-51bc-49fb-ab05-31e5aad4ae40).html.

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With increasing age, aspects of the innate and adaptive immune systems show functional decline. In the skin this is associated with an increased incidence of epidermal malignancies and infections, a decreased incidence of contact allergy, and the development of autoimmunity. The mechanisms underlying these clinical effects in aged skin are poorly understood. Langerhans’ cells (LCs), which are members of the wider family of dendritic cells (DCs), reside in the epidermis where they act as sentinels of the immune system by processing and presenting antigen and inducing T cell responses. Previous investigations have suggested that the number of epidermal LCs is reduced, and that the motility of LCs is impaired in aged skin. A series of investigations was performed to characterise the mechanistic basis for the reduced frequency and restricted mobility of epidermal LCs in the skin of the elderly. Initially LC-like cells were cultured from circulating monocyte precursors and characterised using flow cytometry. The ability of precursors to differentiate into LC-like cells was not impaired in the aged; furthermore there were no age-associated differences in expression of markers of LC activation at baseline or upon stimulation. The phenotype of epidermal LCs was assessed using flow cytometric analysis of epidermal cell suspensions and did not appear altered in aged individuals. In addition, using the same techniques with dermal cell suspensions the dermal DC population was not altered with age. Langerhans’ cell migration from epidermal explants prepared from the skin of aged individuals was impaired but could be restored with exogenous interleukin (IL)-1β. There was no age-related reduction in the epidermal levels of IL-1β or caspase-1 (IL-1β converting enzyme which converts pro-IL-1β to the active form) or the expression of the IL-1 receptor I (IL-1RI), to account for this observation. However, the amount of IL-1 receptor antagonist was reduced in aged skin suggesting a change in the overall local cytokine balance. Based on previous reports that topical retinoic acid (RA) can increase cutaneous IL-1 production, a 4-day patch test assay was performed using 0.025% all-trans RA cream to explore whether this could restore LC migration in the aged. There was no effect on LC migration from epidermal explants prepared after treatment with RA in the aged.These data demonstrate that changes in LC function in the elderly may not be associated with changes in systemic DC biology. Age related changes in the cutaneous microenvironment are likely to be more relevant.
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24

LUAN, NGUYEN MINH. "PROTECTION OF ISLETS OF LANGERHANS FROM COMPLEMENT MEDIATED CYTOTOXICITY." 京都大学 (Kyoto University), 2011. http://hdl.handle.net/2433/151986.

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25

Moëll, Annika. "Inflammatory Mediators and Enterovirus Infections in Human Islets of Langerhans." Doctoral thesis, Uppsala University, Department of Oncology, Radiology and Clinical Immunology, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8501.

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Type 1 diabetes (T1D) is due to a selective loss of the insulin producing β-cells. However, the process responsible for this loss is still unknown. There is accumulating evidence that enteroviruses (EVs) are involved in T1D. In addition to direct virus-induced cytolysis, EVs could facilitate β-cell destruction by inducing inflammatory cytokines. Induction of such genes has previously been shown in EV-infected islets in vitro. Modulation of inflammatory mediators expressed in the islets could be a possible strategy to reduce β-cell destruction.

In the first paper we screened uninfected isolated human islets for genes with the potential to induce or modulate an immune response. We found that several of the genes expressed in the islets encode proteins with a powerful biological activity, such as IL-1β, IL-8, MIP-2α, MCP-1 and MIF. This indicates that the islets themselves can express several triggers of inflammation, and if expressed in vivo these mediators would probably contribute to β-cell destruction.

The vitamin B3 derivate, nicotinamide (NA), has been shown to modulate expression of factors important for coagulation and inflammatory responses. Addition of NA into isolated islet cultures resulted in a reduced expression of the pro-inflammatory chemokine MCP-1 and the coagulation activator tissue factor, suggesting that NA may have implications for both inflammatory responses and the pro-coagulant activity of islets.

We successfully isolated EVs from three newly diagnosed T1D patients. All isolates showed tropism for human islets and β-cells in vitro and clearly affected islet function. We also found that EV infection induced islet secretion of the chemokines IP-10 and MCP-1and that this induction could be blocked or reduced by addition of NA to the culture medium. Interestingly, NA also reduced viral replication and virus-induced islet destruction.

To conclude, this thesis provides new information about expression and modulation of inflammatory mediators in infected and uninfected human islets that could trigger inflammatory reactions leading to β-cell destruction. Moreover, it further strengthens the causal relationship between EV and T1D.

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26

Paraskevas, Steven. "Pathways signaling apoptosis and survival in isolated islets of Langerhans." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84306.

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The transplantation of islets of Langerhans is a promising procedure which could, if successful, restore normal glucose homeostasis in a recipient with type 1 diabetes, while avoiding the risks associated with whole organ pancreas transplantation.
The studies presented here observed the cellular and subcellular response to the process of islet isolation. The first paper made the primary observation of apoptosis after isolation, as manifested by the appearance of apoptotic bodies, DNA fragmentation, and the activation of the enzyme tissue transglutaminase. Importantly, the fact that cell death in this context is apoptotic, and therefore a programmed response to discrete stimuli, suggests that it could be avoided or minimized by manipulation of the cellular milieu.
The second paper in this thesis examined the changes in activity of signal transduction pathways known to mediate the effects of extracellular stress and to balance growth and death promoting signals. Activation of these intermediates, the MAP kinases JNK, ERK and p38, was seen to fluctuate after isolation, representing perhaps a loss of survival signals and a rise in those promoting apoptosis.
The final three experiments examined ways to improve cell survival after isolation by manipulating the MAP kinase pathways. The first mediator of survival tested was insulin itself, and this was found to reduce apoptotic cell death, and primarily activate p38 and ERK, while inhibiting the response of JNK. The existence of an autocrine signaling loop was proposed to explain this effect.
The insulin-like growth factors also diminished cell death, by signaling primarily through the PI3 kinase/Akt system and also through ERK. Inhibition of any of these pathways was clearly detrimental to cell survival. Finally, the action of the immunosuppressive tacrolimus was shown to protect against cytokine-induced apoptosis, and may inhibit JNK as well as activating survival pathways.
These experiments demonstrated that cell loss through apoptosis is common after islet isolation, and by manipulating the signal transduction pathways governing this process, islet survival can be improved, hopefully leading to the use of higher quality grafts and resulting in improved outcomes. (Abstract shortened by UMI.)
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27

Moëll, Annika. "Inflammatory mediators and enterovirus infections in human islets of Langerhans /." Uppsala : Acta Universitatis Upsaliensis : Universitetsbiblioteket [distributör], 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8501.

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28

Wamhoff, Eike-Christian [Verfasser]. "Glycomimetic Langerin Ligands for Langerhans Cell Targeting / Eike-Christian Wamhoff." Berlin : Freie Universität Berlin, 2018. http://d-nb.info/117663481X/34.

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29

Scheider, Laura. "The regulation of Langerhans' cell function in health and disease." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492883.

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Langerhans' cells (LC) are the dendritic cells (DC) found in the epidermis, where they serve as sentinels of the skin immune system. Langerhans' cells recognise, internalise and process foreign antigen and transport it from skin to the lymph node (LN), where immune responses are initiated. Here, skin biopsies were obtained from volunteers before and 24 h after exposure to the Trier social stressor. Epidermal LC frequencies appeared significantly reduced 24 h after exposure to the stressor, suggesting an important role for LC in the modulation of skin immune responses by acute psychosocial stress. Taken together, these results suggest that LC function plays an important role in the generation and regulation of the skin immune response, and the modulation of LC frequencies and function by environmental and intrinsic factors may have relevance to the natural history of skin inflammatory disease.
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30

Yassin, Fakhir. "Qualitative and quantitative of langerhans cells in health and disease." Thesis, University of Dundee, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.516894.

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31

Bigley, Venetia Hart. "Homeostasis of Langerhans and dendritic cells in health and disease." Thesis, University of Newcastle upon Tyne, 2011. http://hdl.handle.net/10443/1197.

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Dendritic Cells (DC) play a pivotal role in both the initiation of immunity and its regulation through tolerance induction. They represent potential targets or tools of therapy in autoimmunity, allergy, cancer, and transplant medicine. Despite recent progress in mapping tissue DC subsets in human, their ontogeny and mechanisms of homeostasis remain elusive. The conventional view is that maintenance of tissue DC and macrophages is dependent on constant replenishment from circulating monocyte precursors. This concept was derived from in vitro data and mouse models under perturbed conditions. While these observations may reflect events in inflammation, studies in murine steady-state biology have challenged this, with data indicating at least three ways in which DC may persist independently of monocytes: 1, tissue DC are replaced by non-monocyte, blood-borne precursors; 2, embryological cells seed tissues and persist in adulthood; 3, DC, or their immediate precursors, self-renew in tissues. These mechanisms may not be mutually exclusive. Although much has been gained from the study of DC kinetics in human transplant, these conditions are, at least in part, inflammatory. To understand the steady-state homeostasis of DC and epidermal Langerhans cells (LC) in human tissues, a number of approaches were taken. Firstly, a comprehensive ‘DC profile’ of normal human tissues was developed, starting with detailed characterization of DC, monocyte and macrophage populations in human peripheral blood (PB) and skin. This lead to the identification of new DC subsets in peripheral tissue. Cells with DC precursor potential were then sought, through analysis of their growth factor receptor expression and ability to enter into cell cycle. Correlative data was gathered to suggest relationships between potential blood borne DC precursors and skin APC. The CD34+ haematopoietic compartment was examined to identify potential DC progenitors. The granulocyte/macrophage progenitor (GMP) and a more recently described multilymphoid progenitor (MLP) were identified and shown also to be present in PB. CD34+ cells were identified in peripheral tissue. While cell and gene knockout experiments have significantly advanced understanding of murine DC, these experiments are not possible in human. The second approach was therefore to undertake a search for subjects with spontaneous DC or monocyte deficiencies. Two novel syndromes were identified; Dendritic Cell, Monocyte, B and NK Lymphoid (DCML) deficiency (4 subjects) and autosomal recessive IRF8 deficiency (1 subject). In both cases, severe depletion of peripheral blood monocyte and DC subsets was associated with absence of tissue DC but preservation of LC and some tissue macrophages. Examination of CD34+ stem cell compartments revealed distinct stem cell defects resulting in loss of MLP and depletion of GMP in DCML deficiency, but accumulation of these subsets in IRF8 deficiency. As predicted by mouse models, DC deficiency was associated with a reduction in circulating regulatory T cells, in the context of elevated Flt3-ligand. Finally, lesions of Langerhans Cell Histiocytosis (LCH), a histiocytic disorder presenting with pathological accumulation of langerin+ DC in tissues, were studied. Analysis of langerin distribution in normal skin and lung identified a langerin+ DC, independent of LC. In keeping with in vitro culture data, preliminary observations show that langerin may be up-regulated on mDC in inflammatory conditions. These data suggest that langerin expression in LCH lesions may reflect its upregulation, rather than determine the LC origin of LCH cells. A variety of techniques have been used to explore DC in normal tissue, novel syndromes of DC deficiency and Langerhans cell histiocytosis. These studies provide new insights into the ontogeny and homeostasis of human DC and LC.
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32

Lundén, Mattias. "Mathematical modeling of insulin response in encapsulated islets of Langerhans." Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-231163.

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Transplantation of the islets of Langerhans is a promising technique for restoring the impairedinsulin production in brittle type 1 diabetics. The downside is that the patient will have to takeimmunosuppressant drugs in order to protect the islet cells from the immune system. Donorsare also sparse, making the quest of finding sufficient amounts of islets for transplantationhard. Encapsulation of the islets of Langerhans has been proposed as a means of protectingthe cells from the immune system taking away the need for immunosuppresives. The mostcommon encapsulation technique is extravascular capsules, which are categorized into micro-and macrocapsules. The microcapsules hold only one or a small set of islet whereas themacrocapsules hold a large quantity of islets.This thesis investigates the encapsulation impact on the beta-cells rapid insulin response torising plasma glucose levels. This was done by simulating the glucose-insulin system inMATLAB with included encapsulation of the islets. Two current macro-encapsulation set upswere used in the model, Beta-Air and ViaCyte devices, and they were compared against anormal case. The results showed that the Beta-Air device would not be able to restorenormoglycemia in a T1DM patient but rather showed a delay in insulin response, while theViaCyte device could mimic the normal case well.
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Hadjivassiliou, Vicky. "Cytokine inhibitory actions and gene expression in islets of Langerhans." Thesis, University of Sussex, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311334.

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34

Pons, Marie-Laure. "Granulomatose à cellules de Langerhans (Histocytose X) : forme hépatique nodulaire." Montpellier 1, 2001. http://www.theses.fr/2001MON11038.

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35

Marshall, Jonathon J. A. "Regulation of insulin gene expression in rat islets of Langerhans." Thesis, University of Leicester, 1986. http://hdl.handle.net/2381/35103.

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The rate of glucose stimulated in vitro (pro)insulin synthesis in islets of Langerhans isolated from fed male rats was determined. Increases in the glucose concentration of the incubation medium, over the physiological range (2 to 20 mM), stimulated the rates of both (pro)insulin and total protein synthesis during a two hour incubation. This stimulation was preferential for (pro)insulin synthesis and had a sigmoidal dose response curve with a concentration threshold of between 2.5 mM and 5.0 mM and a maximal rate at 20 mM glucose. Inhibition of islet RNA synthesis by.;ctinomycin D depressedthe rate of total protein synthesis within 30 minutes of the application of a 20 mM glucose stimulus. A specific inhibition of (pro)insulin synthesis by actinomycin D, that occured 60 minutes after the application of a 20 mM glucose stimulus, was thought to reflect the inhibition of glucose stimulated preproinsulin mRNA synthesis. The effect of glucose on islet preproinsulin mRNA content during in vitro incubations was also determined. To achieve this a dot blot hybridization assay for preproinsulin mRNA was 3 2 developed which used a P-labeled cloned human insulin gene as the hybridization probe. The assay proved to be sensitive enough to detect preproinsulin mRNA in as few as fifty islets. Incubation of islets, for 2 hours, at 2.5 mM glucose had no effect on islet preproinsulin mRNA content but incubation at 20 mM glucose increased islet preproinsulin mRNA content. Actinomycin D had no effect on this pattern of glucose stimulation and it is suggested that the degradation of preproinsulin mRNA is in some way dependent on RNA synthesis and that its inhibition by glucose plays an important role in the regulation of islet preproinsulin mRNA content.
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36

Koulmanda, Maria. "Transplantation of organ cultured foetal islets of Langerhans in mice." Thesis, University of Leicester, 1997. http://hdl.handle.net/2381/29492.

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Foetal islets are functionally immature but retain their capacity for proliferation if harvested and cultured in an appropriate manner. Graft function was shown to depend largely on the gestational age and conditions of organ culture prior to transplantation. The required period of organ culture for optimal graft function was investigated for foetal mouse pancreas of different gestational ages. The growth of the graft in situ also depended on the diabetic state of the host, and chronic hyperglycaemia appeared to impair graft function. Subsequent studies using NOD recipient mice as a model for IDDM showed that recurrent autoimmune disease was seen in foetal islet isografts but rapid rejection of allografts and foetal pig xenografts also occurred. The striking differences seen between the allo-, and xenograft response was the presence of many eosinophils that dominated the infiltrate at the xenograft site. However, HAR was not a problem in this discordant xenograft and Gal(1-3)Gal expression, the major epitope for xenoreactive Ab, was not present on differentiated cells but was detectable on ductal cells. A brief treatment with a specific anti-CD4 MAb (GK1.5) had a profound effect in the survival of xenografts in NOD mice. There were consistent differences in xenograft survival and in the number of circulating T and B cells in other strains of mice, e.g. CBA, BALB/c, C57BL/6 compared to NOD mice. Prolongation of xenograft survival for up to 12 weeks was achieved with the use of peri-transplant and weekly treatment with anti-CD4 or anti-CD3 MAbs especially when the graft has been "immunomodulated" by using 90% O2 in organ culture. Using this protocol foetal pig xenografts maturing under the kidney capsule of spontaneously diabetic NOD mice reversed hyperglycaemia and appeared also to secrete growth factor(s) that induced regeneration of cells in the host pancreas.
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37

Voisin, Benjamin. "Impact of the hair follicle cycle on Langerhans cell homeostasis." Thesis, Strasbourg, 2014. http://www.theses.fr/2014STRAJ118.

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Le follicule pileux (FP) est un appendice cutané animé par un cycle régénératif dynamique provoquant des modifications de son microenvironnement. Les cellules de Langerhans (CLs), sentinelles de l’épiderme, sont en partie localisées à proximité du FP. Cette association spatiale nous a conduit à explorer le possible impact du cycle pileux sur l’homéostasie des CLs. Durant mon doctorat, nous avons mis en évidence (1) une augmentation de la prolifération des CLs au cours de l’anagène (phase de pousse du poil), (2) le mécanisme moléculaire sous-jacent impliquant une variation d’expression folliculaire de l’IL-34, une cytokine cruciale dans l’homéostasie des CLs et (3) un départ accru des CLs vers les ganglions lymphatiques en catagène (phase de régression du FP) concomitant avec le recrutement de cellules susceptibles d’être des précurseurs des CLs.Par ailleurs, la structure de la peau ainsi que la densité et le type de FP peuvent varier selon la région corporelle considérée. Nous avons émis l’hypothèse de variations locales dans la composition du système immunitaire cutané. Notre étude, focalisée sur les cellules dendritiques cutanées, a démontré l’existence d’une hétérogénéité de ces cellules en fonction de la zone de peau considérée
The hair follicle (HF) is a skin appendage endowed with a dynamic regenerating cycle. This renewal remodels the HF microenvironment. Langerhans cells (LCs) are epidermal immune sentinels, a part of which localizes close to the HF. This spatial association led us to explore whether the HF cycle could impact on LC homeostasis. During my doctorate, we uncovered an anagen (HF growing phase)-associated burst of LC proliferation with dividing cells associated with the HF. Using mouse models of HF loss and hair cycle manipulation, we showed that HFs are dispensable for initial formation of the LC network but critical for the proliferation burst. We correlated it to a cyclic variation of IL-34 expression, a crucial cytokine for LC homeostasis, by a specific subset of HF cells. In addition, catagen (HF regression phase) is characterized by the departure of LCs to draining lymph nodes and the concomitant recruitment of a potential LC precursor.The skin structure as well as the density and type of HFs vary across body areas. This observation led us to assess the possibility of local variations in skin immune cells composition. Our study, focused on cutaneous dendritic cells, highlighted an heterogeneity in those cells according to the skin area considered
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Axcrona, Ulrika Myrsén. "Expression and regulation of neuropeptide Y (NPY) in the Islets of Langerhans." Lund : Dept. of Physiology and Neuroscience, Section for Neuroendocrine Cellbiology, Lund University, 1997. http://books.google.com/books?id=Ew5rAAAAMAAJ.

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André, Isabelle. "Contribution de la cellule de Langerhans dans le système immunitaire cutané." Paris 5, 1994. http://www.theses.fr/1994PA05P261.

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Astier, Anne, and Pierre-André Cazenave. "Etude du mode de production des rfcgamma solubles humains de basse affinite de type ii (rfcgammaiia). Caracterisation biochimique et fonctionnelle." Paris 6, 1994. http://www.theses.fr/1994PA066468.

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Le mecanisme de production des rfcgammaiia solubles humains liberes par les cellules de langerhans, les plaquettes et les lignees megacaryocytaires a ete etudie. Une partie de ces recepteurs solubles sont directement secretes du fait de l'absence de la region transmembranaire due a un mecanisme d'epissage alternatif de l'exon codant pour cette region. Ils ont ete appeles rfcgammaiia2, par opposition a la forme membranaire designee sous le nom de rfcgammaiia1. Alors que les cellules de langerhans secretent des molecules solubles comprenant l'integralite des regions extra- et intra- cellulaires du rfcgammaiia2, les plaquettes et les cellules de la lignee megacaryocytaire dami liberent en majorite des molecules solubles ne possedant plus une partie de l'extremite c- terminale de la region intracytoplasmique, a la suite d'un clivage proteolytique. De telles molecules sont aussi retrouvees dans le serum humain. Le clonage de l'adnc codant pour le rfcgammaiia2 dans des vecteurs d'expression eucaryote ou procaryote nous a permis de montrer que ces molecules sont capables d'entrer en competition avec le recepteur membranaire equivalent pour la fixation d'immunscomplexes. Ils pourraient aussi agir directement sur des lignees cellulaires humaines n'exprimant pas d'igg a leur surface, ce qui suggere l'existence de recepteur(s) autre(s) que les igg membranaires
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41

Procida, Guylaine. "Adénopathies superficielles inaugurales au cours de l'histiocytose à cellules de Langerhans : à propos de deux cas." Montpellier 1, 1993. http://www.theses.fr/1993MON11080.

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42

Aikin, Reid. "Characterization and prevention of cell death in isolated islets of langerhans." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111816.

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A major limitation to the success of islet cell transplantation as a therapy for type I diabetes is the cell loss induced by the islet isolation procedure. The aim of this thesis was to elucidate signal transduction events and related intracellular activities that are implicated in islet cell survival/death following islet isolation in order to develop therapeutic interventions to promote islet survival.
The isolation of pancreatic islets imposes considerable stress on these cells, resulting in significant levels of cell death following isolation which was associated with activation of the stress-activated c-jun NH2-terminal kinase (JNK). However, within 24 hours in culture, JNK activation was greatly reduced concomitant with an increase in AKT activation. Inhibition of phosphatidylinositol 3-kinase (PI3K)/AKT signalling resulted in sustained JNK phosphorylation, while activators of AKT suppressed JNK phosphorylation, indicating that the rise in AKT activity during islet culture suppresses JNK. One of the stimulus of the PI3K/AKT pathway was found to be insulin secreted by the islets themselves, acting in an autocrine manner. The result of this autocrine activation of the prosurvival AKT pathway, and subsequent suppression of JNK, was a decrease in the appearance of apoptotic cells in islets after 72 hours in culture. Caspase inhibition alone was unable to prevent cell death in isolated islets. In addition, the amount of mitochondrial depolarization occurring in isolated islets was unaffected by caspase inhibition, leading to the notion that the commitment to islet cell death could be occurring at the level of, or upstream of, mitochondrial dysfunction. Indeed, inhibition of BAX translocation to the mitochondria, a critical event mediating mitochondrial permeabilization, prevented islet cell death. Inhibition of JNK also prevented mitochondrial permeabilization and cell death.
The current results demonstrate that insulin can act as an autocrine survival signal in isolated human islets. These findings also reveal the interdependence of necrosis and apoptosis in isolated islets, suggesting therapeutic strategies which target early events in cell death signalling in order to prevent multiple forms of islet cell death.
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Sterkers, Adrien. "Evaluation pré-clinique et clinique de l'autogreffe intramusculaire d'îlots de Langerhans." Phd thesis, Université du Droit et de la Santé - Lille II, 2013. http://tel.archives-ouvertes.fr/tel-00951952.

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La transplantation d'îlots permet la restauration d'une insulino-sécrétion endogène chez les patients diabétiques de type 1 par greffe allogénique et limite les conséquences métaboliques d'une pancréatectomie en cas d'autogreffe. Le site de référence intrahépatique présente néanmoins de nombreuses limites. Dans le cadre d'autogreffe, le risque hémorragique accru chez les patients récemment opérés liée à l'injection nécessairement conjointe des îlots et d'héparine en intraportal doit faire privilégier une technique de greffe mini invasive. De nombreux sites d'implantation ont été décrits. L'hypothèse de ce travail de thèse était que la voie intramusculaire offrirait par rapport à la voie portale, l'avantage de simplifier l'acte de transplantation, de réduire le traumatisme pour le patient et d'améliorer la viabilité des îlots en limitant les processus inflammatoires immédiats et en optimisant les processus de néo-vascularisation.Dans une première partie, nous avons pu démontrer, dans un model préclinique, que le site intramusculaire permet la survie, la revascularisation et la sécrétion des îlots autogreffés. Nous avons décrit une technique de greffe permettant d'ameliorer le contrôle glycémique d'animaux autogreffés après pancréatectomie totale. Bien qu'inférieure à la voie intraportale, les tests fonctionnels nous ont permis de valider le site intramusculaire pour la greffe d'îlots autologues. Dans une deuxième partie, nous décrivons un cas clinique original confirmant la possible transposition en clinique de l'autogreffe d'ilots en intramusculaire après pancréatectomie partielle. Ce cas clinique, confirme la faisabilité et suggère son innocuité. Il était cependant difficile dans ce contexte de pancréatectomie partielle d'établir un rapport entre l'absence de développement de diabète et la greffe. Pour ce faire, nous décrivons dans une troisième partie, une étude pilote sur l'évaluation de la fonction des îlots autogreffés dans le muscle chez 8 patients ayant subi une pancréatectomie partielle. Dans ce but nous avons comparé la sécrétion d'insuline après stimulation par l'arginine mesurée simultanément dans le bras greffé et le bras non greffé après l'autogreffe par des tests de stimulation à l'arginine. Malgré une faible quantité d'ilots greffés, nous avons documenté une fonction primaire du greffon chez plus de la moitié des patients, ainsi que sa persistance à plus d'un an. Enfin, nous avons également montré que le gradient d'insulinémie entre le bras greffé et le bras systémique était corrélé avec la masse d'ilots greffés.Le muscle est donc un site phare pour le développement d'un site alternatif lors de greffe d'ilots intramusculaire. Le site intramusculaire permet un formidable site d'évaluation des îlots. Cette procédure, résolument mini-invasive, est particulièrement attractive par son extrême accessibilité aux biopsies, à l'imagerie et aux explantations. Cette accessibilité permet d'élargir les indications de greffe telles que l'autogreffe d'îlots provenant de pancréas tumoraux.
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44

Williams, N. A. "The role of Langerhans cells in infection with herpes simplex virus." Thesis, University of Bristol, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235240.

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Fahy, Gerald Thomas. "Alterations in Langerhans cells in the cornea during herpes simplex keratitis." Thesis, University of Bristol, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240031.

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46

Pisania, Anna. "Development of quantitative methods for quality assessment of islets of Langerhans." Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/38964.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Chemical Engineering, 2007.
Includes bibliographical references (p. 241-257).
Transplantation of isolated islets of Langerhans has promising potential to cure type 1 diabetes by inducing long-term normoglycemia and insulin independence. The feasibility of clinical islet transplantations has been established according to the Edmonton Protocol. However, results are variable, and it is not yet possible to predict transplantation outcome from in vitro measurements with islet preparations. Currently, islet enumeration is based on microscopic visualization after staining with a zinc-specific binding dye (dithizone, DTZ) and manual counting with normalization on the basis of an islet equivalent (IE), an islet with volume equivalent to that of a sphere with a 150 Pm diameter. Islet viability is based on a live/dead staining test with two fluorescent dyes, fluorescein diacetate (FDA) and propidium iodide (PI). These methods are operator- dependent and prone to error due to the variability in islet size and shape and are not predictive of transplantation outcome. We developed quantitative assays that allowed reproducible evaluation of meaningful properties that affect the clinical outcome in impure human islet preparations. For purity estimation, we examined light microscopic (LM) morphological analysis of 1-jm sections to estimate the islet volume fraction and compared the results with those of electron microscopy (EM) ultrastructural analysis on the same preparations.
(cont.) For quantifying the total number of cells in a preparation, we developed an assay based on nuclei counting and compared three different counting methods: (1) visual counting in a hemacytometer and automatic counting by (2) aperture resistance measurements (Coulter Multisizer II) and (3) flow cytometer measurements (Guava PCA). The methods differed in the way nuclei were distinguished from fragments, accuracy, time required and range of linearity. Total amount of tissue was also quantified by DNA measurements. A theoretical framework was developed in order to combine volume fraction data from the LM analysis with the total number of cells in the tissue from nuclei measurements in order to estimate the total number of islets present in impure preparations. To evaluate tissue viability, we used oxygen consumption rate measurements (OCR), an assay of mitochondrial function. We developed a very small stirred chamber system (Micro Oxygen Uptake System, Model FO/SYS210T, Instech Laboratories, Plymouth Meeting, PA) specifically designed for measurements with islets. OCR measurements combined with an assay of total amount of tissue quantification (nuclei counting or DNA analysis) provide a measure of the tissue fractional viability.
(cont.) We used the methods we developed to characterize a large number of islet preparations of different species prior to and following culture. We also studied the transient response of cells and islets to various stresses, as reflected by assays of different type. We found that membrane integrity tests are poor indicators of the fractional viability of a cell sample, while mitochondrial function assays identify cell death at its earlier stages. We examined the predictive capability of the assays we developed through in vivo studies. Ttransplantation experiments were performed with rat islets implanted into mice and high purity fraction of human islets transplanted into mice. We found that OCR measurements combined with a measure of total amount of tissue (nuclei or DNA) are good predictors of the transplantation outcome.
by Anna Pisania.
Ph.D.
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Amaral, Maria Esmeria Corezola do. "Vias de sinalização da prolactina em ilhotas de Langerhans de ratos." [s.n.], 2003. http://repositorio.unicamp.br/jspui/handle/REPOSIP/313940.

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Orientador: Antonio Carlos Boschero
Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: Durante a prenhez, as ilhotas de Langerhans dos mamíferos passam por modificações estruturais e funcionais em resposta a uma demanda maior de insulina. Essas modificações são orquestradas por diferentes hormônios, incluindo GIl, lactogênios placentários e prolactina (pRL). Muitas das alterações observadas durante a prenhez podem ser reproduzidas in vitro, especialmente se forem usadas ilhotas de Langerhans de neonatos como modelo biológico. O tratamento prolongado de ilhotas de ratos neonatos in vitro com prolactina (pRL) aumenta a síntese de insulina, a expressão do GLUT2, a atividade da glicoquinase, o metabolismo da glicose, a formação de ATP, a atividade iônica (representada por maior habilidade da glicose em reter K+ e Ca2+ pelas células insulares) e, finalmente, a secreção de insulina. Desta forma, considerando a ação pleiotrófica da PRL sobre as ilhotas pancreáticas e levando-se em conta que os efeitos da PRL nos tecidos se manifestam predominantemente através da via JAK2/STATs, este trabalho visou estudar outras possíveis vias de estimulação da PRL em ilhotas isoladas de ratos neonatos e de ratas prenhes. Além disso, diante da importância da insulina na manutenção da massa e funcionalidade das células f3 pancreáticas, buscou-se a existência de um possível cross-talk entre as vias de sinalização desses dois hormônios. O tratamento de ilhotas de ratos neonatos com PRL por 7 dias potencializou a secreção de insulina induzida por glicose, sendo este efeito abolido pela wortmannin, um bloqueador da PI 3 quinase. O tratamento com PRL também reduziu a apoptose em ilhotas de ratos neonatos. Este efeito foi acompanhado por aumento da fosforilação da Bad em serina 112 e foi abolido pela wortmannin. O tratamento com PRL não alterou a expressão do mRNA de proteínas apoptóticas tais como Bax, Bad, Bcl-XL. A exemplo do observado para a insulina, a exposição de ilhotas de ratos neonatos à PRL por 5 e 15 mino aumentou, de maneira dose-dependente, a fosforilação do IRS 1/2, a associação destes com a PI 3-quinase e a atividade desta enzima. Contudo, esses efeitos não foram aditivos aos da insulina. A PRL também estimulou a fosforilação da JAK2, SHC e ERK1/2 em ilhotas de neonatos. Em ilhotas isoladas de ratas prenhes (15°-18° dias de prenhez) houve aumento da fosforilação em tiro sina do IRS 1/2, SHC e ERK, em serina da AKT e em serina-treonina da p70 S6-quinase, quando comparado a ilhotas de ratas-controle. A administração nas ratas prenhes de oligonucleotídeo antisense (mas não do sense) para o receptor de PRL (pRLR) reduziu a expressão do PRLR no útero e nas ilhotas, a fosforilação em tiro sina de proteínas insulares com peso molecular entre 250-160, 160-105 e 105-75 kDa, a fosforilação da p70 S6 quinase e, finalmente, a secreção de insulina. Concluindo, esses resultados indicam que a PRL pode estimular as vias da PI 3-quinase e da MAPK em ilhotas de ratos neonatos e que essas vias estão mais ativas nas ilhotas de ratas prenhes. O fato de a PRL ter induzido fosforilação da Bad serina 112, um substrato da via da MAPK, e este efeito ter sido abolido pela wortmannin, sugere a existência de um possível cross-talk entre as cascatas da PI 3-quinase e da MAPK em ilhotas de ratos neonatos
Abstract: During pregnancy, panereatie islets undergo a number of structural and functional changes in response to an increased demand for insulin. These changes are orchestrated by several hormones including GH, plaeental lactogens, and prolactin (pRL). Many ofthe alterations observed during pregnancy ean be reproduced in vitro, especially if one uses neonatal islets as a model. The treatment of neonatal islets with PRL inereases: insulin synthesis, GLUT2 expression, glueokinase activity, glucose metabolism, eAMP metabolism, ATP produetion, ionic activity (represented by higher ability of the glueose in retaining K+ and Ca2+ inside the islet eells), and finally insulin secretion. Thus, taking into aeeount the pleiotropie effects of PRL on panereatie islets and reconsidering that PRL acts mainly via the JAK2/STATs pathways in most of the target tissues, we have studied here if PRL stimulates also the PI 3 kinase and MAPK pathways in islets ITom neonatal and ITom pregnant rats. Sinee insulin is important for the maintenance of the mass and functionality of adult islets, we have also analyzed a possible eross-talk between the signaling pathways of these two hormones. PRL signifieantly potentiated glueose-induced insulin secretion in islets cultured for 7 days. This effect was bloeked by the speeifie PI 3-kinase inhibitor, wortmannin. PRL treatment also reduced apoptosis that was accompanied by an inerease in Bad Ser 112 phosphorylation. These effects were abolished by wortmannin. PRL did not affeet mRNA expression of apoptotie protein sueh as Bad, Bax, and Bcl-XL. Similar to what was observed for insulin, the exposure of neonatal islets for short period of time (5 and 15 min) to PRL inereased, in a dose-dependent manner, IRS 1/2 tyrosine phosphorylation, their association with, and activation of PI 3-kinase. However, these effects were not additive to the effects of insulin. PRL also increased JAK2, SHC, ERK1/2 phosphoryIation in neonatal isIets. In pregnant rats (17th -19th days of pregnancy) higher IeveIs of tyrosine (IRS1, IRS2, SHC, ERK), serine (AKT), and serine-threonine (p70 S6-kinase) phosphorylation were found, compared to controIs. The treatment of pregnant rats with PRL receptor antisense (pRLR), but not sense oligonucIeotides, significantly reduced the expression of PRLR in uterus and islets, the expression of islet tyrosine phosphorylated proteins with molecu1ar masses of 250-160, 160-105 and 105-75 kDa, phosphorylation of the p70 S6-kinase and, finally, the glucose-induced insulin secretion. In conclusion, PRL treatment activates PI 3-kinase and MAPK pathways in neonatal islets. These pathways seem to be more active in islets ITom pregnant than controI rats. Since PRL induced phosphoryIation of Bad Ser 112, a preferential target for MAPK, was abolished by wortmannin, some earIy cross talk between the PI 3-kinase and MAPK cascades may occur during stimulation with PRL
Doutorado
Fisiologia
Doutor em Biologia Funcional e Molecular
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48

Christie, Lesley Jane. "Investigating lesions of Langerhans cells and their role in lymphoproliferative diseases." Thesis, University of Dundee, 2011. https://discovery.dundee.ac.uk/en/studentTheses/747a8238-b026-4774-bc2c-85bf6c2f33d6.

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Abstract:
Langerhan’s cells (LCs) are the immune sentinels of the skin, sampling the cutaneous microenvironment and presenting captured antigen to T cells. A sheet-like proliferation of LCs is termed Langerhan’s cell histiocytosis (LCH), an enigmatic and poorly understood disorder with a widely varied clinical spectrum and disease course. In non-pulmonary LCH all cases reported to date have been monoclonal. Clonality argues for LCH as a neoplastic rather than reactive disorder. After initial investigation of the limitations of formalin fixed paraffin embedded tissues for downstream analysis, lesions of LCH were collected from 4 sites across Scotland. To further define the spectrum of LCH, clonality was assessed using an X inactivation assay based on the polymorphous region of the Human Androgen Receptor. To improve understanding of the assay, a study on post-mortem material was undertaken. This demonstrated a unique insight into patterns of X inactivation across different tissues of the same individual and highlighted potential pitfalls in interpretation. An important question was whether lesions of LCH associated with haematopoietic neoplasms were polyclonal or monoclonal proliferations? For the first time, associations of LCH with B-cutaneous lymphoid hyperplasia (B-CLH), lymphomatoid papulosis (LyP) and mycosis fungoides (MF) are reported. In two female cases, the LCs were polyclonal providing some reassurance that such lesions are reactive in nature and should not be regarded as potential second neoplasms. In a more expanded study a wide variety of primary LCH lesions were assessed for clonality. Significant limitations were posed by the quality of the material available; in 2 cases the lesions were found to be polyclonal. This is the first time such a result has been reported. Monoclonality was identified in 2 other cases including one of pulmonary LCH. The findings reported herein suggest that clonality and hence neoplasia cannot be assumed in all cases of primary non-pulmonary LCH. The possible functions of LCs in cutaneous lymphoma were explored. In T-cell lymphoma 2 cases reported here suggest a role for LCs in disease progression. In contrast, LCs play no significant part in the development or progression of cutaneous B-cell proliferations although other types of dendritic cells probably have an important role. By studying proliferations of LCs in a variety of settings, this work has extended knowledge of the spectrum of LCH. Displaying similar histopathological appearances, lesions of LCH may be best defined by clonality as well as cytokine expression and level of maturation. In future, such markers may be employed as prognostic indicators allowing individualised and targeted management.
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49

HUSLER, ISABELLE. "La cellule de langerhans : caracteristiques et role dans l'allergie de contact." Strasbourg 1, 1987. http://www.theses.fr/1987STR10707.

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50

Schmitt, Bertrand. "Synthese et etude d'hydrogels de polyoxyethylene pour l'immunoprotection d'ilots de langerhans." Université Louis Pasteur (Strasbourg) (1971-2008), 1995. http://www.theses.fr/1995STR13139.

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Le polyoxyethylene est un polymere reconnu pour sa bonne bio- et hemocompatibilite. Dans ce travail, nous avons utilise ce polymere pour l'obtention d'une membrane destinee a l'immunoprotection d'ilots de langerhans, en vue de leur implantation dans un pancreas bioartificiel. Cette membrane a ete preparee sous forme d'hydrogel, a partir de l'homopolymerisation de macromonomeres de polyoxyethylene alpha-omega dimethacryliques. Les proprietes physico-chimiques des reseaux ont ete etudiees en fonction des differents parametres de synthese. L'influence du solvant de preparation a plus particulierement ete etudiee, du fait du caractere associatif de ces macromonomeres dans l'eau. Les coefficients de diffusion de l'insuline et du glucose dans ces membranes ont ete mesures, et la biocompatibilite a ete evaluee in vitro et in vivo
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