Top PDF Suppression of a Natural Killer Cell Response by Simian Immunodeficiency Virus Peptides.

Suppression of a Natural Killer Cell Response by Simian Immunodeficiency Virus Peptides.

Suppression of a Natural Killer Cell Response by Simian Immunodeficiency Virus Peptides.

tions 6 and 7 also resulted in partial (YY9 G6A and G6W), or a nearly complete (YY9 I7W), loss of inhibition, suggesting that these residues may also contribute to interactions with Mamu- KIR3DL05. Similar to Gag GY9 and Nef YY9, a valine-to-tryptophan substitution in the penul- timate position of Env RY8, in this case position 7 (RY8 V7W), completely abrogated inhibition (Fig 3E and 3F). A significant increase in cytolyic activity was also observed for a tryptophan substitution at position 6 (RY8 R6W) (Fig 3E and 3F). Yet neither alanine nor tryptophan sub- stitutions at position 5 had a detectable effect on Mamu-KIR3DL05 + NK cell responses to any of these peptides (Fig 3A–3F). In the case of Vif IW9, single amino acid substitutions were not suf- ficient to change this disinhibitory peptide into an inhibitory variant. However, a combination of substitutions at positions 8 and 9 (IW9 F8A W9Y) resulted in significant inhibition of Mamu-KIR3DL05 + NK cells (Fig 3G and 3H), demonstrating that it is also possible to convert a peptide that permits a cytolytic response into one that suppresses this activity with only a couple of amino acid changes. Taken together, these results reveal a prominent role for residues at the penultimate position of Mamu-A1  002-bound peptides, with additional contributions of the
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The antiviral efficacy of simian immunodeficiency virus-specific CD8(+) T cells is unrelated to epitope specificity and is abrogated by viral escape

The antiviral efficacy of simian immunodeficiency virus-specific CD8(+) T cells is unrelated to epitope specificity and is abrogated by viral escape

T-cell lines (Fig. 2B and C). The Gag variant peptide displayed cross-reactivity at a pep- tide concentration range of 10,000 nM to 100 nM, while the Tat escape variant was only weakly recognized at the highest peptide concentration (Fig. 2B and C). To confirm these results, we then tested the recognition of the variant pep- tides in ex vivo IFN-␥ ELISPOT assays using freshly isolated PBMC. At a peptide concentration of 100 nM, the Gag escape variant induced cytokine secretion (Fig. 2D). Re- sponses to the wild-type and variant Gag peptides were equal in magnitude at the highest peptide concentration. In contrast, the Tat escape variant showed minimal cytokine reactivity and only at the highest peptide concentration (Fig. 2E). The responses to variant peptides in IFN-␥ ELISPOT were likely due to recognition of the variant peptide (cross- reactivity) and not the stimulation of a de novo response against the mutant peptides. When both peptides were tested in the same well, the number of SFC/10 6
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Unusual natural killer cell responses to HIV-1 peptides are associated with protection against maternal-infant transmission of HIV-1

Unusual natural killer cell responses to HIV-1 peptides are associated with protection against maternal-infant transmission of HIV-1

It is devoted to cover mother-to-child transmission and pediatric viral infections, such as Human Cytomegalovirus, Hepatitis C Virus and Human Immunodeficiency Virus, and also other chronic infectious agents, close to Dominique Dormont's wide interest.The topics of the sessions selected by the organizing committee span from basic research to prevention and therapy. Attention is given to viral and host determinants of mother-to-child transmission, as well as means of prevention and control of transmission and disease in children, with drugs, immunotherapy and vaccine. Emphasis is also on the immunological development of host defences at the maternal-fetal interface and, in the newborn, basic concepts to understand pathogenesis and clinical outcome.The interaction between basic scientists and clinicians interested in different pathogens is intended to encourage the exchange of knowledge and foster new collaborations.
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Mapping the small RNA content of simian immunodeficiency virions (SIV).

Mapping the small RNA content of simian immunodeficiency virions (SIV).

While our approach aimed at identifying virion-enriched small RNAs, we also detected small RNAs that were more abundant in supernatants from mock-infected cells, which appears puzzling at first sight. As described above, the RNA content of supernatants from mock-infected cells should be enriched in exosomes that are released into the cell culture medium by the used human T-cell line C8166. Accordingly, sequence reads derived from the mock-sample mirror the content of small RNAs that reside in these exosomes. In comparison, supernatants from SIV-infected cells should harbour virions, but also contain exosomes. Thus, the lower abundance of a small RNA in the SIV-virion containing sample can be explained either by a lower amount of co-isolated exosomes or by alterations of the exosomal content. Accumulating evidence indicates that exosomes play pivotal roles in physiological and pathological settings, including antigen presentation and the transport of infectious agents [61]. Cell recognition molecules on the exosomal surface enable selective targeting of recipient cells. Furthermore, exosome-embedded mRNAs and miRNAs can be shuttled into recipient cells and modulate their function [62-64]. Regarding the immune system, it has been found that T-cells can unidirectionally transfer exosomal information to antigen presenting cells [65]. Furthermore, an exosome- mediated transfer of Epstein-Barr virus (EBV)-encoded miRNAs leads to repression of EBV target genes in recipient B- cells [66]. Thus it appears that exosomes can convey RNA- encoded information systemically, which has gained broad interest over the past couple of years.
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Influence of In Vitro IL-2 or IL-15 Alone or in Combination with Hsp 70 Derived 14-Mer Peptide (TKD) on the Expression of NK Cell Activatory and Inhibitory Receptors on Peripheral Blood T Cells, B Cells and NKT Cells.

Influence of In Vitro IL-2 or IL-15 Alone or in Combination with Hsp 70 Derived 14-Mer Peptide (TKD) on the Expression of NK Cell Activatory and Inhibitory Receptors on Peripheral Blood T Cells, B Cells and NKT Cells.

CD16, a low affinity IgG receptor, has been already reported to be expressed on monocytes, macrophages, neutrophils, mast cells and besides on NK cells, CD8+ T cells, and peripheral blood NKT-like cells [21, 22], which we confirmed in this independent study. Our data are in agreement with the data of Romero et al. [23] who found that CD4+ resting peripheral blood lymphocytes did not express surface CD94, while CD8+ lymphocytes and NKT-like cells may be positive for CD94 [23, 24, 25]. As expected, we confirmed the presence of NKG2D receptor on unstimulated CD8+ T lymphocytes and NKT cells [26] and the absence of NKG2D receptor on unstimulated CD4+ T lymphocytes derived from healthy individuals [27, 28]. However, we observed a certain expression of NKG2D on unstimulated B lymphocytes as well. We were also able to identify NKG2C positivity on unstimulated NKT cells. Similarly, Lin et al. [29] who used α-GalCer stimulation as a method to obtain large numbers of NKT cells from human peripheral blood, showed the expression of NKG2C on purified NKT cells. DNAM-1/CD226 is constitutively expressed by most NK cells, T helper and cytotoxic T cells and a subset of B cells [30, 31]. These data are in compliance with our current findings. Nevertheless, we also observed a high expression of DNAM-1 on unstimulated NKT cells. In conformity with Kang N et al. and Kuylenstierna et al. we found no expression of KIR2DL2/L3 in unstimulated T cells and B cells [32, 33] and low expression in unstimulated NKT cells [34].
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Dynamics of simian immunodeficiency virus two-long-terminal-repeat circles in the presence and absence of CD8+ Cells

Dynamics of simian immunodeficiency virus two-long-terminal-repeat circles in the presence and absence of CD8+ Cells

Long-term administration of antiretroviral (ARV) therapy (ART) to HIV-infected indi- viduals results in virus suppression for the duration of treatment (25). ART interruption is followed by a rapid virus rebound to virtually pretreatment levels, confirming the persistence of a latent reservoir that cannot be eradicated by ART alone (26–28). The mechanism of reservoir formation involves integration of the linear reverse-transcribed proviral DNA genome into the host genome. However, due to the poor efficiency of this process, the viral genome is not always able to integrate, leading to the production of extrachromosomal elements (29, 30). An increase in these extrachromosomal products also occurs when HIV-infected subjects receive ARV regimens containing integrase inhibitors (INT) (31–33). These viral isoforms represent viral genomes circularized by host DNA repair enzymes or by undergoing recombination with themselves and are represented by 2-LTR and 1-LTR circles, respectively. These episomes, particularly the 2-LTR circles, have been reported to be useful surrogate markers of viral replication (34). However, this aspect is still under debate, as some have suggested that 2-LTR circles have a short half-life while other studies have shown that 2-LTR circles can still be detected by quantitative PCR (qPCR) when plasma viral loads (pVLs) are undetectable (35–37). Further, 2-LTR circles have been shown to act as the substrates for integration by cleavage of the palindromic site at the LTR-LTR junction by the viral integrase protein, resulting in a linear viral cDNA genome that can be effectively integrated and produce infectious virions (38, 39).
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Decreased memory T-cell response and function in human immunodeficiency virus-infected patients with tegumentary leishmaniasis

Decreased memory T-cell response and function in human immunodeficiency virus-infected patients with tegumentary leishmaniasis

Human immunodeficiency virus (HIV) type 1 is a human retrovirus that infects roughly 34 million people worldwide and is responsible for the majority of the ac- quired immune deficiency syndrome (AIDS) epidemic. The most severely affected areas are in Sub-Saharan Africa, the Caribbean, Eastern Europe and Central Asia (UNAIDS 2012). Leishmania have been recognised as opportunistic pathogens in immunocompromised in- dividuals, including those infected with HIV (Badaro 1997, Cruz et al. 2006). Over the past decades, the HIV epidemic has spread from urban areas to suburban and rural areas, where leishmaniasis is found. In particular, Leishmania and HIV infection overlap in several sub- tropical and tropical regions around the world (Karp & Auwaerter 2007). In northern India, Sudan and Ethiopia, visceral leishmaniasis has been a major scourge in pa- tients infected with HIV (Wolday et al. 2001, Mathur et al. 2006, ter Horst et al. 2008). In Brazil, cutaneous dis- ease is also a common presentation of leishmaniasis in HIV-coinfected patients (Rabello et al. 2003, Carranza- Tamayo et al. 2009, Lindoso et al. 2009). These patients often present with multiple skin ulcers, disseminated le-
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Lymphocyte subsets in human immunodeficiency virus-unexposed Brazilian individuals from birth to adulthood

Lymphocyte subsets in human immunodeficiency virus-unexposed Brazilian individuals from birth to adulthood

The peculiar CD38 expression in the Brazilian co- hort was probably the most striking of our results, be- cause lower levels persisted until adulthood in compari- son with Shearer et al. (2003). CD38 is a multifunctional ectoenzyme that uses nicotinamide adenine dinucleotide (NAD) as a substrate to generate second messengers. It was identified as one of the main cellular NADases in mammalian tissues and appears to regulate cellular levels of NAD in multiple tissues and cells. NAD par- ticipates in multiple physiological processes, such as in- sulin secretion, control of energy metabolism, neuronal and cardiac cell survival, airway constriction, asthma, aging and longevity (Chini 2009). CD38 is a powerful disease marker for human leukaemias and myelomas, is directly involved in the pathogenesis and outcome of chronic lymphocytic leukaemia (Malavasi et al. 2008) and is a marker of immune activation in HIV infection (Zaccarelli-Filho et al. 2007).
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Inhibitory receptor MHC I molecule Activating ligand Healthy cell

Inhibitory receptor MHC I molecule Activating ligand Healthy cell

appearance of symptoms or the totally asymptomatic nature of HBV infection, studies of the early immune events in HBV- infected people are rare. A study of two blood donors who were identified by accident to have seroconverted with the appearance of hepatitis B surface antigen (HBsAg) and sub- sequent rise of HBV viremia without alanine aminotransferse (ALT) elevation, have shown that NK cells are able to mount an early and efficient response to HBV, and that the innate immune system is able to recognize HBV from the beginning of the infection, which probably contributes to the timely induc- tion of adaptive responses. 30 In acute hepatitis B, activation
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Targeting natural killer cell reactivity by employing antibody to NKp46: implications for type 1 diabetes.

Targeting natural killer cell reactivity by employing antibody to NKp46: implications for type 1 diabetes.

We have previously shown that beta cells specifically express the ligand for the NK-activating receptor NKp46/Ncr1 and that NK cells kill beta cells in an NKp46/Ncr1-dependent manner [10,33]. Furthermore, we have shown that anti-mNKp46/Ncr1 antibodies generated through active immunization inhibit T1D development [10]. To recapitulate these observations, we in- vestigated the effect of repeated NCR1.15 treatments in C57BL/6 mice. WT mice were treated with NCR1.15 every other day for two weeks and both PBMCs and splenocytes were tested 3 days following the last injection. Our results were very similar to those observed for one NCR1.15 inoculation (Figs. 2, 3). The fraction of NK cells in PBMCs and the spleen did not change between NCR1.15- and mock-treated mice (Fig. 5A). We also employed the protocol of prolonged multiple injections of NCR1.15 to Ncr1 gfp/+ mice and tested for the fraction of GFP- positive cells indicating NK fraction [20] and for GFP intensity indicating Ncr1 gene promoter activity. Neither the numbers of GFP + nor the GFP intensity was different between NCR1.15- and mock-treated mice (Fig. 5B). In contrast, membrane-associated NKp46 expression was sig- nificantly reduced in PBMCs and in splenocytes harvested from mice that had undergone pro- longed multiple NCR1.15 treatments compared to mock-treated mice (Fig. 5C, D). As with the single NCR1.15 injection, this reduction was not due to reduced Ncr1 gene promoter activity as deduced from qRT-PCR levels of the Ncr1 transcript (Fig. 5E) and from the Ncr1-encoded GFP levels (Fig. 5B). Since treatment lasted for two weeks and mice were tested 3 days later, we could investigate whether NCR1.15 treatment conferred changes in NK subsets representing developmental NK stages. Antibodies to CD3, NK1.1, CD27, and CD11b were used to define CD3 - NK1.1 + CD11b low CD27 + , CD3 - NK1.1 + CD11b + CD27 + and CD3 - NK1.1 + CD11b + CD27 low NK developmental stages. No significant difference was observed between NCR1.15- and mock- treatment for cell numbers among the NK developmental stages. In contrast, mem- brane-associated NKp46 levels were significantly reduced in NCR1.15-treated mice in all stud- ied NK developmental stages as shown in S1 Fig.
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CLÍNICA E EFEITOS DO FÁRMACO A LONGO TERMO

CLÍNICA E EFEITOS DO FÁRMACO A LONGO TERMO

256. Torti C, Quiros-Roldan E, Regazzi M, De Luca A, Mazzotta F, Antinori A, Ladisa N, Micheli V, Orani A, Patroni A, Villani P, Lo Caputo S, Moretti F, Di Giambenedetto S, Castelnuovo F, Maggi P, Tinelli C, Carosi G; RADAR-MASTER Study Group. A randomized controlled trial to evaluate antiretroviral salvage therapy guided by rules-based or phenotype-driven HIV-1 genotypic drug-resistance interpretation with or without concentration-controlled intervention: the Resistance and Dosage Adapted Regimens (RADAR) study. Clin Infect Dis. 2005; 40: 1828-36.

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Circulating natural killer and γδ T cells decrease soon after infection of rhesus macaques with lymphocytic choriomeningitis virus

Circulating natural killer and γδ T cells decrease soon after infection of rhesus macaques with lymphocytic choriomeningitis virus

Evidence that NK cells have little influence on vi- rus loads in murine LCMV infections first came from the Welsh laboratory. They have reported that (i) virus titers were unperturbed during the early stages of infec- tion in mice depleted of NK cells by cyclophosphamide (Biron et al. 1996); (ii) Beige mice (NK deficient) syn- thesized normal levels of virus (Roder & Duwe 1979); (iii) adoptive transfer of NK cells into 5-day-old mice with low NK cell activity did not confer LCMV resis- tance even though it conferred resistance to murine CMV (Bukowski et al. 1985) and (iv) depletion of NK cells (using antibody to asialo-GM1) had no effect on the synthesis of LCMV-WE or LCMV-ARM in acute or persistent infections (Bukowski et al. 1983, Welsh et al. 1984). Although NK cells have little impact on LCMV titers, they are purported to play a role in con- trolling viral dissemination (Welsh et al. 1984) and in modulating T cell responses during infection (Su et al. 2001). NK cells produce IFNγ, which induces the ex- pression of major histocompatibility complex class I on antigen-presenting cells, thereby stimulating CD8 +
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Re-mapping the molecular features of the human immunodeficiency virus type 1 and human T-cell lymphotropic virus type 1 Brazilian sequences using a bioinformatics unit established in Salvador, Bahia, Brazil, to give support to the viral epidemiology studi

Re-mapping the molecular features of the human immunodeficiency virus type 1 and human T-cell lymphotropic virus type 1 Brazilian sequences using a bioinformatics unit established in Salvador, Bahia, Brazil, to give support to the viral epidemiology studi

In conclusion, to facilitate the effective use of all available HIV-1 and HTLV-I genetic data and to train lo- cal expertise, we have developed a specialized viral bioinformatics unit at the Advanced Public Health Labo- ratory of the Gonçalo Moniz Research Center-Oswaldo Cruz Foundation. The work of this unit will enable the analysis of all Brazilian viral sequences deposited in public database through the constructing of new datasets and make use of all molecular biology programs avail- able. Furthermore, this unit could provide important in- formation to be used in HIV-1 evolutionary studies, vac- cine and antiretroviral treatment design, as well as fa-
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Probing natural killer cell education by Ly49 receptor expression analysis and computational modelling in single MHC class I mice.

Probing natural killer cell education by Ly49 receptor expression analysis and computational modelling in single MHC class I mice.

Murine natural killer (NK) cells express inhibitory Ly49 receptors for MHC class I molecules, which allows for ‘‘missing self’’ recognition of cells that downregulate MHC class I expression. During murine NK cell development, host MHC class I molecules impose an ‘‘educating impact’’ on the NK cell pool. As a result, mice with different MHC class I expression display different frequency distributions of Ly49 receptor combinations on NK cells. Two models have been put forward to explain this impact. The two-step selection model proposes a stochastic Ly49 receptor expression followed by selection for NK cells expressing appropriate receptor combinations. The sequential model, on the other hand, proposes that each NK cell sequentially expresses Ly49 receptors until an interaction of sufficient magnitude with self-class I MHC is reached for the NK cell to mature. With the aim to clarify which one of these models is most likely to reflect the actual biological process, we simulated the two educational schemes by mathematical modelling, and fitted the results to Ly49 expression patterns, which were analyzed in mice expressing single MHC class I molecules. Our results favour the two-step selection model over the sequential model. Furthermore, the MHC class I environment favoured maturation of NK cells expressing one or a few self receptors, suggesting a possible step of positive selection in NK cell education. Based on the predicted Ly49 binding preferences revealed by the model, we also propose, that Ly49 receptors are more promiscuous than previously thought in their interactions with MHC class I molecules, which was supported by functional studies of NK cell subsets expressing individual Ly49 receptors.
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Immunopathogenic aspects of infection by the human immunodeficiency virus in Venezuela

Immunopathogenic aspects of infection by the human immunodeficiency virus in Venezuela

The most important findings were depletion of the CD4 cells in HIV-infected individuals, including asymptomatic carriers; significant reduction of the CD3; CD16+ la[r]

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Impact of antiretroviral therapy on intestinal lymphoid tissues in HIV infection.

Impact of antiretroviral therapy on intestinal lymphoid tissues in HIV infection.

in patients on ART, suggesting that the major battle against HIV occurs in sequestered mucosal tissue sites. This important observation suggests a number of potential therapeutic strategies for further research; for example, the investigation of drugs with better intestinal tissue distribution and perhaps the exploration of mechanisms to reduce immune activation in mucosal tissues to more effectively combat HIV infection. 

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Serial killing of tumor cells by human natural killer cells--enhancement by therapeutic antibodies.

Serial killing of tumor cells by human natural killer cells--enhancement by therapeutic antibodies.

To explore the maximal killing potential of NK cells, we first identified a tumor target most susceptible to NK cell lysis. We therefore tested several target cell lines against IL-2 activated NK cells and found that MHC-I negative 722.221 cells showed better lysis that K562 targets and were most susceptible to NK cell killing (data not shown). As effector cells we chose to use primary human NK cells from healthy donors, which had been expanded in IL-2 for two weeks, as these cells showed maximal cytotoxic activity. To determine the number of targets killed per individual NK cell, we used a 51 Cr release assay with an excess of target cells. This way each NK cell has access to a large number of targets, making it possible to estimate the maximal killing activity. We performed standard 4 h and also 16 h 51 Cr release assays to determine the full potential of NK cell activity. Killing activity of NK cells was assessed in terms of % specific lysis and the amount of target cells lysed per NK cell (killing frequency) was determined by dividing the number of killed targets by the number of effector cells (Fig. 1). Killing frequency was inversely proportional to % specific lysis and increased from higher to lower effector to target ratios. This is probably be due to a greater possibility for an individual NK cell to form contacts with target cells at lower effector to target ratios. Analysis of the killing frequency of NK cells from multiple donors demonstrates that on an average two or four targets are killed by an NK cell after 4 or 16 hours, respectively (Fig. 1C). This suggests that IL-2 activated NK cells are capable of making multiple contacts and can kill multiple targets. To visualize the process of serial killing, we employed time lapse video microscopy (Fig. 2). Dye labeled NK cells were incubated with unlabeled 221 target cells and observed under 16 hour time lapse microscopy. Sytox dye was used to visualize dead cells. These data confirm that a single NK cell can make serial contacts with multiple targets and finally kill them. Most of the contact formations observed resulted in killing (Fig. 2B). However, all NK cells were not equally active in forming contacts and killing targets but few ‘hyperactive’ NK
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Epidemiology and genetic variability of HHV-8/KSHV in Pygmy and Bantu populations in Cameroon.

Epidemiology and genetic variability of HHV-8/KSHV in Pygmy and Bantu populations in Cameroon.

This study was carried out in rural areas of Cameroon (figure 1). The present study was performed on a large population of Bantus and Pygmies, living in remote rural villages or settlements of the rain forest area of South and East Cameroon. Study populations were sequentially sampled over different time periods. Samples from the South were mostly collected from 1994 through 2000. A complementary series was collected from 2006 through 2010. Samples from the Centre and the East areas were collected from 2004 through 2010. Populations and collection procedures have been previously described [51,52] and comprise diverse Bantu groups from the three study areas and two Pygmy groups. The Baka Pygmies, by far the most important Pygmy group in Cameroon is found in Eastern and Southern Cameroon. The Bakolas are the second most important group and have their settlements exclusively in the Southern part of the country and the Bedzams are the less numerically important and less accessible. This group was not included in the current work. A systematic approach for the enrolment was carried out in all reachable villages and settlements, scattered alongside roads and tracks across the forest. A standardized questionnaire was used to collect personal demographic data. Collected data included the name, age, sex, location, ethnicity, family links. A 5 to 10 ml whole blood sample was collected in EDTA K2 vacuum tubes, from all consenting individuals meeting the inclusion criteria. Plasma and buffy-coat were obtained 48 to 72 hours after sampling and kept frozen at 280uC.
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Dynamics and kinetics of natural killer cell cytotoxicity in human malaria as evaluated by a novel stepwise cytotoxicity assay

Dynamics and kinetics of natural killer cell cytotoxicity in human malaria as evaluated by a novel stepwise cytotoxicity assay

The evaluation of the dynamics of NK cell activity leads to heterogeneous results, particularly in P. falciparum -infected individuals. Although it seems to be difficult to define a pattern of dynamics, we observed that some individuals presented high fluctuations in the frequency of binding or lytic cells during the incubation time (we call this high dynamic profile as A profile), while some other presented less fluctuation in those frequencies (we call this low dynamic profile as B profile). Concerning the binding capacity of effector cells, no predominant profile was detected. However, in relation to the frequency of lytic cells, the A profile was predominant in all groups, particularly in malaria patients. The binding dynamics was comparable in patients and controls, but P. vivax -infected individuals showed a slower detachment of effector cells from target cells. The detachment of bound effector cells had a peak after 15min of incubation, followed by a reduction till 60min. Only activated NK cells present these early lytic events, as also reported by others 14 27 29 .
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Repositório Institucional da UFPA: Prevalência dos Vírus linfotrópico de células T humanas 1 e 2 (HTLV-1 e HTLV-2), Herpesvírus humano 5 (Citomegalovírus) e Vírus da hepatite B (VHB) em mulheres grávidas portadoras do Vírus da imunodeficiência humana 1 (H

Repositório Institucional da UFPA: Prevalência dos Vírus linfotrópico de células T humanas 1 e 2 (HTLV-1 e HTLV-2), Herpesvírus humano 5 (Citomegalovírus) e Vírus da hepatite B (VHB) em mulheres grávidas portadoras do Vírus da imunodeficiência humana 1 (H

Durante a infecção natural, o CMV replica produtivamente em células epiteliais, endoteliais, células dos músculos da boca, células mesenquimais, hepatócitos, granulócitos e monócitos derivados de macrófagos (Plachter et al., 1996; Sinzger et al.,1996; Sinzger & Jahn, 1996; Kahl et al., 2000; Bissinger et al., 2002). O DNA viral latente, então, pode ser detectado em progenitores da medula óssea macrófago- granulócito e em monócitos periféricos (Kondo et al., 1994; Soderberg-Naucler et al., 1997). O contrário, in vitro, de maneira que as únicas células completamente permissivas para a replicação de cepas de laboratório são de pele humana ou fibroblastos de pulmão, enquanto os isolados clínicos replicam preferencialmente em culturas de células endoteliais (Landolfo et al., 2003).
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