No description available.

Stereotypy is one of the defining characteristics of autism spectrum disorders (ASD) and can significantly interfere with an individual's development and acquisition of knowledge and skills as well as distract from and disrupt educational environments. Numerous behavioral interventions have been implemented by researchers in an attempt to reduce or eliminate such behaviors, including antecedent aerobic exercise. Research studies conducted on using antecedent aerobic exercise as an effective intervention to decrease stereotypy have been spread out over several years, and many of the studies are methodologically weak according to today's standards and guidelines for evidence-based practices. This study was conducted to replicate and extend previous research by examining the effect of aerobic exercise in the form of vigorous jogging for 10 consecutive minutes on the percentage of time two elementary-school-aged children with autism engaged in stereotypic behaviors during instructional activities in the morning (immediately following the aerobic exercise), with a secondary analysis evaluating potential residual effects later in the school day. A six-phase reversal (ABABAB) design was used to determine the presence of a functional relation between jogging and stereotypy. Upon visual analysis of graphed data, functional relations were apparent for both participants. Allison spent 12% less time engaging in stereotypic behavior immediately following the jogging sessions as compared to baseline, and Boyd’s stereotypic behavior decreased by 10.7% overall. There was no significant carryover effect to the instructional sessions two hours after the intervention. Measures of social validity confirmed that the intervention was easy to implement and perceived as beneficial. Implications for future research and practice are discussed.

O processo de diferenciação e ativação de osteoclastos, essencial para a manutenção da homeostasia do tecido ósseo e também envolvido na patogênese de diversas patologias caracterizadas pela atividade osteolítica, depende de um sistema central de controle que envolve a ligação das moléculas RANK/RANKL. Além do sistema RANK/RANKL, moléculas co-estimulatórias de osteoclastos, tais como os complexos DAP-12, TREM-2 e SIRP1, e FcR, OSCAR e PIR-A, também apresentam um papel importante na geração e ativação de osteoclastos. Entretanto, a possível contribuição de tais moléculas para a progressão da doença periodontal (DP) permanece desconhecida, assim como o possível impacto de citocinas na modulação de sua expressão no microambiente periodontal. Nosso objetivo foi investigar, por RealTimePCR, o padrão de expressão de moléculas co-estimulatórias de osteoclastos (DAP-12, TREM-2 e SIRP1, e FcR, OSCAR e PIR-A) na periodontite crônica em humanos, além de avaliar a cinética de expressão destas moléculas e a sua modulação por citocinas (TNF-, IFN-, IL-17 e IL-10) ao longo do curso da DP em camundongos em camundongos C57Bl/6 wild-type (WT) e geneticamente modificados (TNFp55KO, IFNKO, IL17KO, IL10KO. Nossos resultados demonstram que nas lesões periodontais crônicas a expressão de todas as moléculas co-estimulatórias de osteoclastos apresentaram-se significativamente aumentadas quando comparadas às amostras controle. Com relação à periodontite experimental, verificamos que todas as moléculas co-estimulatórias alvo apresentavam aumento em sua expressão após a indução de doença quando comparado aos controles. Nos camundongos para TNFp55KO, IFNKO e IL17KO, observamos uma redução na severidade da DP (reabsorção óssea e quantidade de células inflamatórias) e na expressão de moléculas co-estimulatórias, ao contrário do observado nos camundongos IL10KO. Entretanto, ao normalizarmos os níveis de expressão das moléculas co-estimulatórias de osteoclastos pelo número de células inflamatórias, verificamos que TNF- e IL-17 se mostram associados a uma maior expressão de moléculas co-estimulatórias, enquanto IFN- e IL-10 parecem regular negativamente a expressão de tais moléculas. Em termos gerais, demonstramos que a expressão de moléculas co-estimulatórias de osteoclastos se mostra aumentada na DP humana e experimental, e que citocinas parecem modular sua expressão por mecanismos diretos e indiretos, tais como a migração de células inflamatórias para os sítios de doença periodontal. / The osteoclast differentiation and activation are essential to bone tissue homeostasis and in the development of bone pathologies, which RANK/RANKL signaling molecules are the major osteoclastogenic factor. However, osteoclast co-stimulatory molecules, such as DAP-12, TREM-2, SIRP1, FcR, OSCAR and PIR-A, also present an important role in the osteoclastogenesis. However, the exact role and regulation of these molecules in human and mice periodontal diseases (PD) development have not completely known. Our aim was to investigate the pattern of osteoclast co-stimulatory expression (DAP-12, TREM-2, SIRP1, FcR, OSCAR and PIR-A) in human chronic periodontitis (CP), apart from analyze the kinetic of these molecules and their regulation by cytokines (TNF-, IFN-, IL-17 and IL-10) in the development of experimental periodontal disease in mice C57Bl/6 and knockout. Our results demonstrated that all osteoclast co-stimulatory molecules presented highly expressed in CP patients when compared with control. Similar results are presented about experimental PD, where all co-stimulatory molecules was presented highly expressed in infected mice when compared with control mice. We observed in TNFp55KO, IFNKO and IL17KO mice a decrease in PD scores and co-stimulatory molecules expression, the opposite of IL10KO mice. However, when we standardized the co-stimulatory molecules levels by the number of inflammatory cells, we found that TNF- and IL-17 are associated with increased expression of co-stimulatory molecules, while IFN- and IL-10 appear to negatively regulate the expression of such molecules. In conclusion, we demonstrated that osteoclast co-stimulatory molecules shown increased in human and experimental PD, and cytokines appear to modulate their expression by direct and indirect mechanisms, such as inflammatory cells migration to the PD infected tissue.

O processo de diferenciação e ativação de osteoclastos, essencial para a manutenção da homeostasia do tecido ósseo e também envolvido na patogênese de diversas patologias caracterizadas pela atividade osteolítica, depende de um sistema central de controle que envolve a ligação das moléculas RANK/RANKL. Além do sistema RANK/RANKL, moléculas co-estimulatórias de osteoclastos, tais como os complexos DAP-12, TREM-2 e SIRP1, e FcR, OSCAR e PIR-A, também apresentam um papel importante na geração e ativação de osteoclastos. Entretanto, a possível contribuição de tais moléculas para a progressão da doença periodontal (DP) permanece desconhecida, assim como o possível impacto de citocinas na modulação de sua expressão no microambiente periodontal. Nosso objetivo foi investigar, por RealTimePCR, o padrão de expressão de moléculas co-estimulatórias de osteoclastos (DAP-12, TREM-2 e SIRP1, e FcR, OSCAR e PIR-A) na periodontite crônica em humanos, além de avaliar a cinética de expressão destas moléculas e a sua modulação por citocinas (TNF-, IFN-, IL-17 e IL-10) ao longo do curso da DP em camundongos em camundongos C57Bl/6 wild-type (WT) e geneticamente modificados (TNFp55KO, IFNKO, IL17KO, IL10KO. Nossos resultados demonstram que nas lesões periodontais crônicas a expressão de todas as moléculas co-estimulatórias de osteoclastos apresentaram-se significativamente aumentadas quando comparadas às amostras controle. Com relação à periodontite experimental, verificamos que todas as moléculas co-estimulatórias alvo apresentavam aumento em sua expressão após a indução de doença quando comparado aos controles. Nos camundongos para TNFp55KO, IFNKO e IL17KO, observamos uma redução na severidade da DP (reabsorção óssea e quantidade de células inflamatórias) e na expressão de moléculas co-estimulatórias, ao contrário do observado nos camundongos IL10KO. Entretanto, ao normalizarmos os níveis de expressão das moléculas co-estimulatórias de osteoclastos pelo número de células inflamatórias, verificamos que TNF- e IL-17 se mostram associados a uma maior expressão de moléculas co-estimulatórias, enquanto IFN- e IL-10 parecem regular negativamente a expressão de tais moléculas. Em termos gerais, demonstramos que a expressão de moléculas co-estimulatórias de osteoclastos se mostra aumentada na DP humana e experimental, e que citocinas parecem modular sua expressão por mecanismos diretos e indiretos, tais como a migração de células inflamatórias para os sítios de doença periodontal. / The osteoclast differentiation and activation are essential to bone tissue homeostasis and in the development of bone pathologies, which RANK/RANKL signaling molecules are the major osteoclastogenic factor. However, osteoclast co-stimulatory molecules, such as DAP-12, TREM-2, SIRP1, FcR, OSCAR and PIR-A, also present an important role in the osteoclastogenesis. However, the exact role and regulation of these molecules in human and mice periodontal diseases (PD) development have not completely known. Our aim was to investigate the pattern of osteoclast co-stimulatory expression (DAP-12, TREM-2, SIRP1, FcR, OSCAR and PIR-A) in human chronic periodontitis (CP), apart from analyze the kinetic of these molecules and their regulation by cytokines (TNF-, IFN-, IL-17 and IL-10) in the development of experimental periodontal disease in mice C57Bl/6 and knockout. Our results demonstrated that all osteoclast co-stimulatory molecules presented highly expressed in CP patients when compared with control. Similar results are presented about experimental PD, where all co-stimulatory molecules was presented highly expressed in infected mice when compared with control mice. We observed in TNFp55KO, IFNKO and IL17KO mice a decrease in PD scores and co-stimulatory molecules expression, the opposite of IL10KO mice. However, when we standardized the co-stimulatory molecules levels by the number of inflammatory cells, we found that TNF- and IL-17 are associated with increased expression of co-stimulatory molecules, while IFN- and IL-10 appear to negatively regulate the expression of such molecules. In conclusion, we demonstrated that osteoclast co-stimulatory molecules shown increased in human and experimental PD, and cytokines appear to modulate their expression by direct and indirect mechanisms, such as inflammatory cells migration to the PD infected tissue.

No description available.

Student Number : 9402348T - MSc(Med) dissertation - School of Medicine - Faculty of Health Sciences / My previous investigations have indicated that a connection exists between the state of health of specific internal organs and the electrical characteristics of related, although sometimes remote, skin areas. These skin areas are referred to as organ projection areas (OPA) and include acupuncture points. Pathology of a particular organ causes a related OPA to rectify electrical currents, once the resistance ‘breakthrough effect’ has been induced in the skin. The ‘breakthrough effect’ is a rapid reversible decrease in skin resistance which takes place under certain electrical stimulatory conditions. Only after it occurs, the skin resistance measured by means of a positively polarised point electrode is significantly higher for diseased organs’ projection areas, when compared to the resistance for the same but negatively polarised measuring electrode (rectification / diode phenomenon). For healthy organs’ projection areas, this phenomenon is not observed. The pathology of an internal organ also increases the impedance of the corresponding OPA. The location of the skin zone, where a high degree of rectification and increased impedance is observed, indicates which particular organ is diseased. The degree of rectification or difference in impedance indicates the extent of the pathological process within the organ. These findings created the basis for a new non-invasive diagnostic method – organ electrodermal diagnostics (OED). Although the electrical phenomena of the skin described above have been confirmed clinically, the resistance and impedance values involved have not been characterized statistically. Therefore, in order to determine the accuracy of OED, optimization of OED parameters was undertaken. Evaluation of electrical characteristics revealed that for AC measurements, low frequency and high amplitude were most suitable. Therefore 250Hz was selected as the measurement frequency, since lower frequencies produced uncomfortable sensations under the measuring electrode. Measuring current amplitude was chosen to be 25uA (peak) since it was observed to be below the perception threshold. For DC measurements, the highest amplitude of the measurement stimulus that does not cause uncomfortable sensations was the most suitable. Since the skin resistance is very low after the ‘breakthrough effect’, 25uA was chosen as optimal. According to these parameters the OED device ‘Diagnotronics’ was built. The device specifies the actual condition of the organ related to the investigated skin area as 'HEALTHY', 'WITHIN NORMAL LIMITS', ‘SUBACUTE’ and ‘ACUTE’. A special display graded according to percentage of the disease intensity, makes it possible to specify accurately the activity of organ pathology. The locations of skin areas corresponding to the examined organs and final results are displayed on a screen. A double-blind comparative study of OED results and clinical diagnoses, as a criterion standard, was performed on a group of 200 inpatients at Helen Joseph Hospital's surgical department. The study was restricted to the following organs: oesophagus, stomach, gall bladder, pancreas, colon, kidneys, urinary bladder and prostate. These organs are relatively easy to access clinically, and their pathologies represent a variety of aetiological and pathogenetic factors e.g. infections, inflammation, neoplasms, immunological and metabolic disorders. In total 630 true OED results were obtained from the 714 subjects considered: detection rate 88.2% (85,6-90,5%). Established OED sensitivity was 89.5% (85,2-92,8%) and OED specificity equaled 87.5% (84,0-90,4%). The predictive value for positive OED results was 81.7% (76,9-85,9%) and for negative OED results 93.0% (90,1-95,2%). There were no significant differences in the results obtained from various internal organs. Healthy organs usually display the OED result 'HEALTHY' or 'WITHIN NORMAL LIMITS’, while subacute pathology displays 'SUBACUTE' and acute pathology as an 'ACUTE'. The OED results were affected neither by the type nor the aetiology of disease i.e. OED estimates the actual extent of the pathological process activity within a particular organ but does not explain the direct cause of the pathology. The OED results were not influenced by a patient's muscle tension, emotional state, skin humidity, environmental temperature or by procedure duration. The pressure of the measuring electrode had a limited influence (up to 5%) on the OED results and did not affect the final diagnoses. No side-effects of the OED examinations were observed. The study confirmed the existence of OPA on the skin surface and proved that OED is a reliable bioelectronic method of non-invasive medical diagnostic testing, with high rates of sensitivity, specificity and predictive values. OED may detect diseased organs and estimate the activity of the pathological process.

Das Ergebnis einer T-Zellmediierten Immunantwort ist von der Signalvermittlung durch kostimulatorische Moleküle abhängig. Diese kostimulatorischen Moleküle sind - neben dem spezifischen Antigen - notwendig für eine vollständige T-Zellaktivierung, die es der T-Zelle erlaubt zu proliferieren, neue Oberflächenantigene zu exprimieren und Zytokine zu sezernieren. Ohne das kostimulatorische Signal wird die T-Zelle anerg oder sogar apoptotisch, eine effektive Immunantwort ist dann nicht möglich. Die vorliegende Dissertationsschrift enthält die initiale Beschreibung eines neuen kostimulatorischen Moleküls, eine umfangreiche Charakterisierung seiner Expression in vitro, sowie seiner Funktion. Das Molekül "ICOS" (ICOS steht für inducible costimulator) ist ein T-Zellspezifisches Molekül und weist eine große Homologie zu dem Prototyp eines kostimulatorischen Moleküls, dem CD28 Molekül auf. Die Experimente, die zur Charakterisierung der Induktionsbedingungen des ICOS Moleküls durchgeführt wurden, zeigen, daß die Expression des ICOS Moleküls sehr schnell nach T-Zellaktivierung induziert wird, die Expressionsstärke innerhalb von Stunden stark heraufreguliert wird und die Expression lange (mindestens 96h) auf der T-Zelloberfläche zu detektieren ist. Ein Vergleich mit anderen aktivierungsabhängigen T-Zelloberflächenmolekülen zeigt eine ICOS-spezifische Zeitkinetik der Expression, die durch verschiedene T-Zellstimuli zu induzieren ist. Eine optimale Expression des Moleküls ist zwei-signalabhängig und durch Cyclosporin A blockierbar. Bezüglich der Funktion von ICOS wurde die Wirkung der Kostimulation via ICOS auf eine Reihe von kritischen Parametern der T-Zellaktivierung analysiert. Durch die Kostimulation mit einem ICOS-spezifischen Antikörper wird konzentrationsabhängig die T-Zellproliferation induziert, unabhängig davon, ob das ersten Signal via CD3 oder via einen löslichen Stimulus, wie PHA erfolgte. Die ICOS Kostimulation bewirkt die Hochregulation von typischen T-Zellaktivierungsantigenen und sie induziert oder verstärkt die Sekretion zahlreicher Lymphokine. Die verstärkende Wirkung auf alle diese Parameter der T-Zellaktivierung führt schließlich dazu, daß die über ICOS kostimulierten Zellen in der Lage sind T-Zellhilfe für B-Zellen zu leisten, so daß diese Immunglobuline sezernieren. Wurde versucht, die direkte Interaktion des ICOS Moleküls mit seinem potentiellen Liganden bei der T-Zellinduzierten Immunglobulinsekretion durch den mAk F44 zu blockieren, so zeigte sich kein Effekt. Bei Langzeitkostimulation via ICOS zeigte sich allerdings, daß die Kostimulation durch das ICOS Molekül auch in der Lage ist, die T-Zellaktivierung negativ zu beeinflussen: Die Langzeitstimulation via ICOS erzeugt eine deutliche Proliferationsdepression und einen Viabilitätsverlust der T-Zellen. Insgesamt lassen diese Ergebnisse den vorsichtigen Schluß zu, daß das ICOS Molekül eine wichtige Rolle an der Schnittstelle zwischen Expansion und Effektorfunktion einerseits und Depression der T-Zellen andererseits spielt. / The outcome of T-cell resonses after T-cell encounter with specific antigens is modulated by co-stimulatory signals, which are required for both lymphocyte activation and development of adaptive immunity. Here I report the initial characterization of a novel co-stimulatory molecule which enhances all basic T-cell functions and displays a unique induction and expression pattern. ICOS (for inducible co-stimulator) is a T-cellspecific activation antigen with high homology to CD28, the prototype of a co-stimulatory molecule. Analysis of induction requirements for ICOS expression revealed a two-signal dependency and cyclosporine A sensitivity. ICOS' expression kinetics are unique when compared with other early T-cell activation antigens. ICOS is induced very quickly on the T-cell surface and is rapidly upregulated following T-cell activation. The surface expression of ICOS is surprisingly prolonged - lasting at least 96 hours - considering its rapid induction kinetics. Stimulation via an ICOS-specific monoclonal antibody enhances all basic T-cell functions such as proliferation, upregulation of molecules that medicate cell-cell interaction, secretion of lymphokines and effective help for antibody secreting B-cells. Costimulation via ICOS is effective regardless of the route of action of the first signal (immobilized or soluble). Blockade of the ICOS interaction with its presumed ligand on B-cells does not inhibit immunoglobulin production by these B-cells, though. Finally long-term stimulation experiments reveal a possible negative role for ICOS in regulating T-cell responses. These results indicate that ICOS is a major regulator of the adaptive immune system determining the healthy balance of negative and positive signaling during T-cell activation and differentiation.

Infection is a leading cause of death in hemodialysis patients, partly due to dysfunctional immunity. Frequent dialysis therapy improves patient outcomes and quality of life. We hypothesize that extended home hemodialysis (EHHD) also improves immune function compared to conventional in-hospital hemodialysis (CHD); therefore, we designed a prospective matching-cohort clinical study to assess serum inflammatory markers and the functional capacity of monocyte-derived dendritic cells (MDDCs) and T-lymphocytes. Serum CRP was decreased in EHHD patients suggesting that extended dialysis may decrease inflammatory solute/cytokine levels. Compared to controls, MDDCs from hemodialysis patients had similar endocytic capacity, expression of co-stimulatory molecules, and T-cell activation capacity. However, CHD was associated with the highest expression of CD83 and CD40. Activated T-cells in CHD patients also produced significantly more immunosuppressive IL-10 compared to EHHD patients and controls. Therefore, EHHD may improve immune function by decreasing inflammation, MDDC pre-activation, and synthesis of immunosuppressive cytokines.

Submitted by Renata Lopes (renatasil82@gmail.com) on 2016-10-13T14:14:46Z No. of bitstreams: 1 michellealvesvicentini.pdf: 761505 bytes, checksum: 2f59d68ce4001875ae7881a93f5e4930 (MD5) / Approved for entry into archive by Adriana Oliveira (adriana.oliveira@ufjf.edu.br) on 2016-10-22T12:56:30Z (GMT) No. of bitstreams: 1 michellealvesvicentini.pdf: 761505 bytes, checksum: 2f59d68ce4001875ae7881a93f5e4930 (MD5) / Made available in DSpace on 2016-10-22T12:56:30Z (GMT). No. of bitstreams: 1 michellealvesvicentini.pdf: 761505 bytes, checksum: 2f59d68ce4001875ae7881a93f5e4930 (MD5) Previous issue date: 2008-03-05 / FAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Gerais / As parasitoses intestinais representam um importante problema médico-sanitário, tendo em vista o grande número de pessoas acometidas e as inúmeras alterações orgânicas que podem provocar no hospedeiro. Infecções provocadas por Strongyloides venezuelensis apresentam uma resposta imune local tanto nos pulmões quanto no intestino, predominantemente do tipo Th2, caracterizada pela produção das citocinas IL-4, IL-5, IL-13 e IL-10, resultando em eosinofilia, aumento da produção de muco, mastocitose e altas concentrações de IgE. Por outro lado, infecções provocadas por micobactérias estimulam uma imunidade predominantemente do tipo Th1 caracterizada pela produção de IFN-, IL-12, TNF- e óxido nítrico. A tuberculose, causada pelo patógeno intracelular Mycobacterium tuberculosis, é uma das doenças infecciosas mais importantes, sendo responsável por aproximadamente 2,9 milhões de óbitos e 8 milhões de novos casos por ano. Ainda são escassos os trabalhos envolvendo co-infecções, e devido às complexas relações existentes entre parasitos e entre eles e seu hospedeiro, faz-se necessário observações criteriosas. No presente trabalho avaliou-se o efeito modulatório que o Mycobacterium bovis virulento exerce sobre a resposta imune de camundongos co-infectados com S. venezuelensis. Os resultados demonstraram que o perfil de resposta imune durante a infecção por S. venezuelensis parece ser diretamente influenciado pela presença do M. bovis, uma vez que o perfil de resposta Th2, específico ao verme, esteve diminuído nos animais co-infectados. Tal diminuição pôde ser constatada pelo aumento do número de ovos e vermes nos animais co-infectados quando comparado com os animais infectados somente com S. venezuelensis; assim como a diminuição dos níveis de IgE específica à larva L3 do verme detectada em diferentes pontos da infecção; diminuição dos níveis de IL-10 produzida por células de baço estimuladas in vitro com antígeno da larva L3 do verme; diminuição dos níveis de IL-4, IL-5 e IL-13 no intestino; diminuição da expressão de CD80, CD86 e CD25 em células de baço e linfonodo e aumento da expressão de CD28 em células de linfonodos mesentéricos. Em conjunto, esses resultados sugerem que a infecção por M. bovis, e a conseqüente ativação do perfil de resposta imune do tipo Th1, foi capaz de modular o desenvolvimento do perfil de resposta imune do tipo Th2 contra S. venezuelensis nos animais co-infectados, deixando-os mais susceptíveis à infecção com S. venezuelensis. Esse trabalho é o primeiro a avaliar os mecanismos imunoregulatórios envolvidos na co-infecção S. venezuelensis versus M. bovis. / The intestinal parasites are a major medical-health problem, in view of the large number of people involved and the numerous organizational changes which may result in the host. Infections caused by Strongyloides venezuelensis have a local immune response in both lungs as in the intestine, predominantly from the Th2 type, characterized by the production of cytokines IL-4, IL-5, IL-13 and IL-10, resulting in eosinophilia, increased production of mucus, mastocytosis and high levels of IgE. In addition, infections caused by mycobacteria stimulate predominantly an Th1-type immune response characterized by the production of IFN-, IL-12, TNF- and nitric oxide. Tuberculosis, caused by intracellular pathogen Mycobacterium tuberculosis, is one of the most important infectious diseases, accounting for approximately 2.9 million deaths and 8 million new cases per year. Are still scarce papers involving co-infections, and because of the complex relationship between parasites and between them and their host, it is necessary criterious evaluations. This study evaluated the modulatory effect that the virulent Mycobacterium bovis has on the immune response of mice co-infected with S. venezuelensis. The results showed that the profile of immune response during infection with S. venezuelensis seems to be directly influenced by the presence of M. bovis, because the profile of Th2 response, specific to the worm, was reduced in co-infected animals. This decline could be observed by increasing the number of eggs and worms in animals co-infected when compared with animals infected only with S. venezuelensis, as well as decreased levels of IgE specific to the L3 larvae of the worm detected at different points of infection, decreased levels of IL-10 produced by spleen cells stimulated in vitro with L3 larvae antigen; decreased levels of IL-4, IL-5 and IL-13 in the intestine, reducing the expression of CD80, CD86 and CD25 cells in the spleen and lymph nodes and increased expression of CD28 cells in mesenteric lymph nodes. Together, these results suggest that infection with M. bovis, and the consequent activation of the profile of Th1-type immune response, was able to modulate the development of the profile of Th2 type of immune response against S. venezuelensis in co-infected animals, leaving them more susceptible to infection with S. venezuelensis. This work is the first to evaluate the mechanisms involved in imunoregulatory mechanisms involved in co-infection S. venezuelensis versus M. bovis.

Infection is a leading cause of death in hemodialysis patients, partly due to dysfunctional immunity. Frequent dialysis therapy improves patient outcomes and quality of life. We hypothesize that extended home hemodialysis (EHHD) also improves immune function compared to conventional in-hospital hemodialysis (CHD); therefore, we designed a prospective matching-cohort clinical study to assess serum inflammatory markers and the functional capacity of monocyte-derived dendritic cells (MDDCs) and T-lymphocytes. Serum CRP was decreased in EHHD patients suggesting that extended dialysis may decrease inflammatory solute/cytokine levels. Compared to controls, MDDCs from hemodialysis patients had similar endocytic capacity, expression of co-stimulatory molecules, and T-cell activation capacity. However, CHD was associated with the highest expression of CD83 and CD40. Activated T-cells in CHD patients also produced significantly more immunosuppressive IL-10 compared to EHHD patients and controls. Therefore, EHHD may improve immune function by decreasing inflammation, MDDC pre-activation, and synthesis of immunosuppressive cytokines.