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PubMed2005

Frequency, proliferation, and activation of human memory T cells induced by a nonhuman adenovirus.

Multiple human adenovirus (HAd) infections during childhood generate a memory T-cell (T(M)) response, which is the primary defense against HAd-induced morbidity. This cellular memory creates a conundrum for the potential clinical use of HAd-derived vectors: vector-mediated gene transfer is efficient in immunologically naïve mammals but will be compromised by memory immunity when using vectors derived from ubiquitous human pathogens. The potential lack of cellular and humoral memory is one reason we developed vectors from canine adenovirus serotype 2 (CAV-2). Here, we assayed human peripheral blood mononuclear cells for a T(M) response that could be stimulated by CAV-2 virion and individual capsid proteins. We found that less than half of the donors harbored a proliferating T(M) response directed against the CAV-2 virion (versus >85% against HAd5) in spite of a conserved antigenic Adenoviridae epitope in the CAV-2 hexon. When CAV-2 induced proliferation, it was 2.3- to >10-fold lower than HAd5 depending on the assay. The primary proliferating cells appeared to be memory (CD45RO+) CD4+ lymphocytes, differentiated into Th1 gamma interferon-producing cells, with a frequency that was up to 66-fold lower than that obtained for HAd5. We also compared CAV-2 to prototype HAd from five of the six human species and found that CAV-2-induced cellular proliferation was similar to that found with rare HAd serotypes. Individual CAV-2 capsid proteins also induced less proliferation than their HAd5 homologues. Our data suggest that CAV-2 vectors may be safer (i.e., less immunogenic) for gene transfer but are not without a theoretical risk in a subset of potential patients.

Adenoviridae↗
PubMed2000

Criteria for solvent-induced chronic toxic encephalopathy: a systematic review.

In 1985, a WHO Working Group presented diagnostic criteria and a classification for solvent-induced chronic toxic encephalopathy (CTE). In the same year, the "Workshop on neurobehavioral effects of solvents" in Raleigh, N.C., USA introduced a somewhat different classification for CTE. The objective of this review is to study the diagnostic procedures that are used to establish the diagnosis of CTE, and the extent to which the diagnostic criteria and classification of the WHO, and the classification of the Raleigh Working Group, are applied. A systematic search of studies on CTE was performed, and the diagnostic criteria and use of the WHO and Raleigh classifications were listed. We retrieved 30 original articles published in English from 1985 to 1998, in which CTE was diagnosed. Only two articles did not report the duration of solvent exposure. The type of solvent(s) involved was described in detail in four articles, poorly in 17 articles, and not at all in nine articles. Tests of general intelligence were used in 19 articles, and tests of both attention and mental flexibility and of learning and memory were used in 18 articles. Exclusion, by interview, of potentially confounding conditions, such as somatic diseases with central nervous effects and psychiatric diseases, was reported in 21 and 16 articles, respectively. In only six of the articles were both the WHO diagnostic criteria and the WHO or Raleigh classifications used. In the future, parameters of exposure, psychological test results, and use of medication that possibly affects psychological test results should always be described. We list some advantages and disadvantages of the Raleigh and WHO classifications. To aid inter-study comparisons, the diagnosis of CTE should be categorized and reported according to an internationally accepted classification.

Brain Damage, Chronic↗
PubMed2001

The topography of tactile learning in humans.

The spatial distribution of learned information within a sensory system can shed light on the brain mechanisms of sensory-perceptual learning. It has been argued that tactile memories are stored within a somatotopic framework in monkeys and rats but within a widely distributed network in humans. We have performed experiments to reexamine the spread of tactile learning across the fingertips. In all experiments, subjects were trained to use one fingertip to discriminate between two stimuli. Experiment 1 required identification of vibration frequency, experiment 2 punctate pressure, and experiment 3 surface roughness. After learning to identify the stimuli reliably, subjects were tested with the trained fingertip, its first and second neighbors on the same hand, and the three corresponding fingertips on the opposite hand. As expected, for all stimulus types, subjects showed retention of learning with the trained fingertip. However, the transfer beyond the trained fingertip varied according to the stimulus type. For vibration, learning did not transfer to other fingertips. For both pressure and roughness stimuli, there was limited transfer, dictated by topographic distance; subjects performed well with the first neighbor of the trained finger and with the finger symmetrically opposite the trained one. These results indicate that tactile learning is organized within a somatotopic framework, reconciling the findings in humans with those in other species. The differential distribution of tactile memory according to stimulus type suggests that the information is stored in stimulus-specific somatosensory cortical fields, each characterized by a unique receptive field organization, feature selectivity, and callosal connectivity.

Adult↗
PubMed2004

A novel human homologue of Drosophila polycomblike gene is up-regulated in multiple cancers.

Polycomb group (PcG) proteins function to maintain the stable epigenetic repression of homeotic genes and other important developmental and cell cycle regulatory genes. Such maintenance establishes a form of cellular memory for its identity or state of differentiation. Accumulating evidence indicates that perturbation of this transcriptional memory may be required for tumor progression and may represent a hallmark of cancer. We have identified a novel gene encoding a human homologue of the Drosophila polycomblike protein, hPCL3. Through alternative polyadenylation and/or splicing, the gene encodes two nuclear proteins, hPCL3S and hPCL3L. Both proteins repressed transcription upon recruitment to the proximity of an HSV-tk promoter by a Gal4 DNA binding domain. Interestingly, the products of the hPCL3 gene, particularly the short form, hPCL3S, are markedly overexpressed in many types of cancers, including colon, skin, lung, rectal, cervical, uterus, and liver cancers. This increase in expression correlated with tumor progression. Both hPCL3S and hPCL3L messages were increased dramatically in most cell lines derived from various stages of melanoma and glioma tumor progression. Thus, our data link PcG deregulation to the progression of multiple cancers and may have important implications for unraveling the mechanisms of tumor progression.

Amino Acid Sequence↗
PubMed2002

The diagnosis and differential diagnosis of dementia.

The initial approach to the patient with memory complaints should consist of a focused history, mental status examination, and functional assessment. Patients with MCI should be monitored every 6 to 12 months for conversion to dementia. Delirium, depression, amnestic disorders, and aphasias should be considered in the differential diagnosis of memory impairment. Once a diagnosis of dementia is made, patients should have a brain CT or MRI scan and laboratory tests to assist with determining the cause. It is crucial that dementia be recognized and evaluated at the earliest stage so as to begin appropriate therapy and allow the patient to have a role in management decisions. In the future, therapies for MCI may prevent conversion to dementia. The need for early recognition makes the development of diagnostic tools, such as quantitative or functional neuroimaging, and genetic or clinical biologic markers essential.

Aged↗
PubMed2003

Definition of the HLA-A2 restricted peptides recognized by human CD8+ effector T cells by flow-assisted sorting of the CD8+ CD45RA+ CD28- T cell subpopulation.

In response to antigenic stimulation, naive MHC-class I restricted and antigen-specific CD8+ CD45RA+ CD28+ T cells undergo clonal expansion, differentiate into CD8+ CD45RO+ memory T cells and convert to CD8+ CD45RA+ CD28- T cells displaying potent immune effector functions upon re-encounter with the nominal antigen. We show that the effector CD8+ CD45RA+ CD28- T cell subset is expanded in peripheral blood lymphocytes (PBL) from patients with human papilloma virus (HPV)+ cervical lesions as well as in PBL from patients with pulmonary tuberculosis. Flow-cytometric cell sorted CD8+ CD45RA+ CD28- and CD8+ CD45RA+ CD28- T cells were tested for recognition of HLA-A2 restricted peptides derived either from the human papillomavirus (HPV)16-E7 gene product, or from M. tuberculosis antigens. Mostly CD8+ CD45+ CD28- T cells define antigen/peptide-specific and MHC-restricted responses. These data were confirmed in PBL from patients with tuberculosis using HLA-A2 tetramer-complexes loaded with a peptide from the M. tuberculosis Ag85b antigen by flow cytometry. The sorting of this T cell subset enables to determine the fine specificity of CD8+ effector T cells without the need for in vitro manipulation.

Antigen-Antibody Reactions↗
PubMed2003

Maintenance and attrition of T-cell memory.

After antigenic stimulation in the context of "danger signals," naive T cells embark on a programmed, intense expansion phase to counteract the rapid proliferation of pathogens. During the first week of infection, responding T cells undergo > 1000-fold expansion, resulting in the development of large numbers of cells exhibiting potent effector function. As the pathogen (antigen) burden dwindles, a majority of the effectors generated are eliminated by apoptosis, resulting in the survival and maintenance of a small population of antigen-specific cells as long-term memory T cells. Depending on the infection studied, CD8+ T cells appear to differentiate through multiple pathways into resting and effector memory subsets, and require multiple cytokines and cell surface molecules for survival and proliferation. Once generated, the repertoire of memory T cells remains highly vulnerable to attrition during heterologous infections, where homeostatic forces drive deletions in T-cell memory pools to accommodate the entry of new memory T cells. This review will primarily focus on the factors that influence the generation, maintenance, and attrition of memory CD8+ T cells.

Animals↗
PubMed2004

Telomere erosion in memory T cells induced by telomerase inhibition at the site of antigenic challenge in vivo.

The extent of human memory T cell proliferation, differentiation, and telomere erosion that occurs after a single episode of immune challenge in vivo is unclear. To investigate this, we injected tuberculin purified protein derivative (PPD) into the skin of immune individuals and isolated responsive T cells from the site of antigenic challenge at different times. PPD-specific CD4+ T cells proliferated and differentiated extensively in the skin during this secondary response. Furthermore, significant telomere erosion occurred in specific T cells that respond in the skin, but not in those that are found in the blood from the same individuals. Tissue fluid obtained from the site of PPD challenge in the skin inhibited the induction of the enzyme telomerase in T cells in vitro. Antibody inhibition studies indicated that type I interferon (IFN), which was identified at high levels in the tissue fluid and by immunohistology, was responsible in part for the telomerase inhibition. Furthermore, the addition of IFN-alpha to PPD-stimulated CD4+ T cells directly inhibited telomerase activity in vitro. Therefore, these results suggest that the rate of telomere erosion in proliferating, antigen-specific CD4+ T cells may be accelerated by type I IFN during a secondary response in vivo.

BCG Vaccine↗
PubMed1983

The dementias.

The dementias have been examined from the viewpoint of representing a primary memory system deficit leading to an array of cortical function impairments, behavioral alterations, and mood disturbances. Although several classification systems to categorize the dementias exist, a useful system to guide the planning of nursing care is to categorize the dementia according to the lobe of the hemispheres that is most seriously affected. From this approach, clinical manifestations and appropriate nursing interventions are more easily identifiable. Emphasis has been placed on the importance of evaluating a person who is evidencing the presence of a dementing process to determine if the etiology of the disorder is from a treatable cause, making it possible to halt the dementing process or to reverse the process. When cortical deficits persist in spite of treatment or when the dementing process is a progressive, nonreversible one, nursing's therapeutic approach is aimed at maintaining and maximizing use of remaining mental capacities, restoring cortical functions that may not be permanently lost, and minimizing the need for those abilities that are permanently lost. Often the family must be assisted to carry out the therapeutic approach in the home situation. Ongoing nursing assessment is required as is ongoing evaluation of the effectiveness of the therapeutic approach.

Dementia↗
PubMedDate not supplied

[Evaluating the simulation of memory problems within the legal and forensic fields].

The present article is a theoretic review of the techniques used to assess the malingering of memory problems in the forensic and legal context. The necessity of instruments to facilitate the detection of malingerers is confirmed. This phenomenon is more relevant in the memory pathology context because their exaggeration or false performance is very common. The reason of this preference is the ease of the simulation of these very well known symptoms. The consequences, economics primarily, of the confirmation of brain damage sequels have produced that malingerers are well informed about the characteristics of this syndrome. This review is focus on, both tests assessing different components of memory, such as the Wechsler Memory Scale III and the California Verbal Learning Test, and tests designed specifically to detect malingering. We also differentiate tests assessing explicit and implicit memory. Likewise, future lines of research are proposed in this important legal context.

Brain Injuries↗
PubMed2006

Phenotypical and functional analysis of memory and effector human CD8 T cells specific for mycobacterial antigens.

Mycobacterium tuberculosis infects one-third of the global population and claims two million lives every year. Because memory CD8 T cells exhibit a high heterogeneity in terms of phenotype and functional characteristic, we investigated the frequency, phenotype, and functional properties of Ag85A epitope-specific HLA-A*0201 CD8 T cells in children affected by tuberculosis (TB) before and 4 mo after chemotherapy and healthy contact children. Using Ag85A peptide/HLA-A*0201 pentamer, we found a low frequency of blood peptide-specific CD8 T cells in tuberculous children before therapy, which consistently increased after therapy to levels detected in healthy contacts. Ex vivo analysis of the expression of CD45RA and CCR7 surface markers indicated a skewed representation of Ag85A epitope-specific CD8 T cells during active TB, with a predominance of T central memory cells and a decrease of terminally differentiated T cells, which was reversed after therapy. Accordingly, pentamer-specific CD8 T cells from tuberculous patients produced low levels of IFN-gamma and had low expression of perforin, which recovered after therapy. The finding of an elevated frequency of pentamer-specific CD8 T cells with T effector memory and terminally differentiated phenotypes in the cerebrospinal fluid of a child with tuberculous meningitis strongly indicates compartmentalization of such CD8 effectors at the site of disease. Our study represents the first characterization of Ag-specific memory and effector CD8 T cells during TB and may help to understand the type of immune response that vaccine candidates should stimulate to achieve protection.

Antigens, Bacterial↗
PubMed2003

Establishment of memory for IL-10 expression in developing T helper 2 cells requires repetitive IL-4 costimulation and does not impair proliferation.

T helper (Th) lymphocytes can develop memory for the expression of particular cytokines, like IL-4 or IL-10, in that reexpression of those cytokines is independent of the original costimulatory signal IL-4 and depends only on T cell receptor stimulation. Here, we show that in the course of Th2 cell differentiation in vitro, IL-4 memory is established during primary activation of naïve Th cells, whereas the establishment of IL-10 memory requires repetitive stimulation of the Th cell with IL-4 and T cell receptor. Likewise, established IL-10 memory, maintained in the absence of further IL-4 signals, was observed in individual IL-10-producing cells generated from in vivo antigen-experienced CD62L(low) Th cells and isolated by using the newly developed cytometric cytokine secretion assay for IL-10. In naïve Th cells undergoing primary activation, the induction of both IL-4 and IL-10 memory requires DNA synthesis, but reexpression of the cytokine genes can occur throughout cell cycle. In in vitro polarized Th2 cell populations, Th cells with IL-4 or IL-10 memory do not differ in proliferative behavior. Populations of Th cells isolated from polarized Th2 cultures according to expression of IL-4 or IL-10 also do not differ in proliferative behavior. Their proliferation mainly depends on IL-2. Thus, effector memory Th lymphocytes with memory for IL-4 or IL-10 expression are not intrinsically impaired in their proliferative potential and can play an essential role in reactive immunological memory and its regulation.

Animals↗
PubMed2000

[Age-related cognitive decline: evaluation and prevention strategy].

The age-related decline of cognitive functions generally refers to a mild deterioration in memory performance, executive functions, and speed of cognitive processing. The terms "age-related cognitive decline" (ARCD) and "aging-associated cognitive decline" have been proposed recently to indicate an objective decline in cognitive functioning associated to the ageing process but within normal limits given the person's age. Whether ARCD is expression of a normal ageing process or represents a distinct clinical entity or, eventually, is a continuum with dementia is, at present, difficult to establish. The causes of ARCD are unknown, but some studies have suggested that it may be prevented. Avoidance of cardiovascular and other chronic diseases, high educational level, and maintenance of vision and hearing have been identified as protective factors from ARCD. On the contrary, hypertension, effects of altered metabolism of steroid hormones, smoking, low-complexity occupation, higher density of persons/bedroom in home, and low level of physical activity have been identified as risk factors for ARCD. Recent findings suggest a possible role of diet in the ARCD. In fact, in an elderly population of Southern Italy with a typical Mediterranean diet, high monounsaturated fatty acids energy intake appeared to be associated with a high protection against cognitive decline. Dietary antioxidants, specific macronutrients, estrogens, and anti-inflammatory drugs, may act synergistically with other protective factors, opening new therapeutic interventions for cognitive decline.

Age Factors↗
PubMed2003

Either IL-2 or IL-12 is sufficient to direct Th1 differentiation by nonobese diabetic T cells.

Th cell differentiation from naive precursors is a tightly controlled process; the most critical differentiation factor is the action of the driving cytokine: IL-12 for Th1 development, IL-4 for Th2 development. We found that CD4(+) T cells from nonobese diabetic mice spontaneously differentiate into IFN-gamma-producing Th1 cells in response to polyclonal TCR stimulation in the absence of IL-12 and IFN-gamma. Instead, IL-2 was necessary and sufficient to direct T cell differentiation to the Th1 lineage by nonobese diabetic CD4(+) T cells. Its ability to direct Th1 differentiation of both naive and memory CD4(+) T cells was clearly uncoupled from its ability to stimulate cell division. Autocrine IL-2-driven Th1 differentiation of nonobese diabetic T cells may represent a genetic liability that favors development of IFN-gamma-producing autoreactive T cells.

Animals↗
PubMed1989

Parental adjustment to intrapartum and delivery room loss. The role of a hospital-based support program.

Perinatal loss prompts a unique bereavement for parents and their families that is unlike the mourning process experienced at the death of other loved ones. The Support Center For Perinatal and Childhood Death has developed a comprehensive program to provide support, counseling, and information to families who experience miscarriage, stillbirth, fetal anomalies, and therapeutic abortion for genetic or congenital abnormalities. The impact of perinatal loss is felt not only in the real loss of the wished-for child but also in the loss of self-esteem, the role of parent, and the loss of confidence in the ability to produce a healthy child. The emotional experience of miscarriage or stillbirth creates an atmosphere of despair and confusion for families anticipating a joyous event. The presence of a support counselor and medical caregivers at this time can help parents to navigate the crisis surrounding the loss in ways that promote a healthy grieving process and avert pathologic adaptations. Prenatal, intrapartum, and postpartum counseling opportunities are afforded to families as the situation and parental needs dictate. Services also are extended to other family members, with particular attention to surviving siblings who might be vulnerable to the consequences of unresolved or unacknowledged grief. Grief is experienced as a long-term process, which frequently emerges fully after discharge from the hospital and lasts well beyond the interest and stamina of supportive family members and friends. Support groups, which meet the specific needs of families who experience perinatal loss, contemplate subsequent pregnancy, or face the prenatal decision to terminate a genetically or congenitally compromised pregnancy, have been run successfully for a period of several years. Beyond the experience of intrapartum loss in the delivery room, the experience comes full circle for families who enter the delivery room again with a subsequent child. The expressed need for support in acknowledging the rekindled memories of prior loss at this poignant time are matched only by parents' needs to find reassuring ways of differentiating healthy newborns from the memory of those who died. It is often at the time of the subsequent birth that the memory of the lost child can take its proper place in the family. Stein expresses the essence of grief work and resolve: Mourning is not just feeling sad. It is the specific psychological process by which human beings become able to give up some of the feelings they have invested in a person who no longer exists, and extend their love to the living. Mourning is hard, emotional work.(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Psychological↗
PubMed1983

Dexamethasone-sensitive and -insensitive responses during in vitro differentiation of Friend erythroleukemia cells.

We have investigated the mechanism(s) by which dexamethasone inhibit DMSO-induced Friend erythroleukemia cell differentiation in vitro. In particular, we examined the effects of dexamethasone on (a) the early events of differentiation such as cell volume alterations and 'memory response' and (b) the onset of biochemical events associated with terminal erythroid cell differentiation. By analysing kinetics of commitment of Friend cells to terminal erythroid differentiation on a clonal basis, we have observed that dexamethasone inhibited the completion of the latent period (time elapsed prior to commitment) and impaired "memory" (ability to inducer-treated cells to continue differentiation after a discontinuous exposure to inducer). Treatment of Friend cells with dexamethasone did not prevent the occurrence of DMSO-induced alterations in cell volume. However, dexamethasone treatment prevented a series of biochemical events associated with terminal Friend cell differentiation. These include the decrease in the rate of both cytoplasmic and nuclear RNA synthesis as well as the induction of cytidine deaminase activity and hemoglobin synthesis. These data indicate that the dexamethasone-sensitive process(es) operate during the early stages of Friend cell differentiation and that they are responsible for the inhibition of terminal erythroid maturation. These dexamethasone-sensitive processes, however, appear to be different from those regulating cell volume alterations during the early steps of DMSO-induced Friend cell differentiation.

Animals↗
PubMed1997

Germinal center development.

Using a set of surface markers including IgD and CD38, human tonsillar B cells were classified into discrete subpopulations. Molecular and functional analysis allowed us to identify: i) two sets of naive B cells (Bm1 and Bm2); ii) germinal center founder cells (Bm2'); iii) an obscure population of germinal center B cells, displaying a high load of somatic mutations in IgV genes, C mu to C delta switch and preferential Ig lambda light chain usage: these cells may represent the precursors of normal and malignant IgD-secreting plasma cells; iv) the centroblasts (Bm3) in which somatic mutation machinery is activated; v) the centrocytes (Bm4) in which isotype switch occurs; vi) the memory B cells. The characterization of these subpopulations showed that: i) programmed cell death is set before somatic mutations, possibly providing an efficient way for affinity maturation; ii) only high affinity centrocytes are allowed to switch isotype; iii) CD40-ligation inhibits plasmacytic differentiation of mature B lymphocytes; iv) memory B cells preferentially differentiate into plasma cells; v) IgD isotype switch occurs in normal B cells; vi) receptor editing may be induced by somatic mutations in germinal centers. We also characterized two types of antigen-presenting cells in germinal centers: follicular dendritic cells that select high affinity B cells, and a new subset of germinal center dendritic cells that activate germinal center T cells.

Animals↗
PubMed2006

Impaired memory CD8 T cell development in the absence of methyl-CpG-binding domain protein 2.

Intracellular differentiation events that determine which cells develop into memory CD8 T cells are currently incompletely understood. Methyl-CpG-binding domain protein 2 (MBD2) is a transcriptional repressor that binds to methylated DNA and mediates the biological consequences of epigenetic gene methylation. The role of MBD2 during the differentiation of naive CD8 T cells into effector and memory cells was determined following acute infection of MBD2-deficient mice with lymphocytic choriomeningitis virus. Despite rapid viral clearance and an efficient primary effector CD8 T cell response, reduced numbers of Ag-specific memory CD8 T cells were observed. Importantly, the appearance of precursor memory cells (IL-7Ralphahigh) was delayed. The remaining MBD2(-/-) memory cells were not fully protective during rechallenge, and memory cell characteristics were altered with regard to surface markers (IL-7Ralpha, KLRG-1, CD27, and others) and cytokine production. The defect was CD8 T cell intrinsic, because memory cell development was also delayed when MBD2(-/-) CD8 T cells were adoptively transferred into SCID mice. These data demonstrate that MBD2 is a previously unrecognized intracellular factor required for the efficient generation of protective memory CD8 T cells.

Animals↗