The influence of human immunodeficiency virus-1 on hematopoiesis.
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Acquired Immunodeficiency Syndrome↗
Biomedical subjects
J Nelson
Publications and source records attributed to J Nelson.
Influence of bromodeoxyuridine radiosensitization on malignant glioma patient survival: a retrospective comparison of survival data from the Northern California Oncology Group (NCOG) and Radiation Therapy Oncology Group trials (RTOG) for glioblastoma multiforme and anaplastic astrocytoma.
PURPOSE: To examine the effect of treatment using Bromodeoxyuridine (BrdU) during radiation therapy on malignant glioma patient survival by comparing historical survival data from several large clinical trials. METHODS: A retrospective analysis of patient data from Radiation Therapy Oncology Group (RTOG) trials 74-01, 79-18, and 83-02 and the Northern California Oncology Group (NCOG) study 6G-82-1 was conducted. Patient data was supplied by both groups, and analyzed by the RTOG. Pretreatment characteristics including age, extent of surgery, Karnofsky Performance Status (KPS), and histopathology were collected; the only treatment variable evaluated was the use of BrdU during radiation therapy. Radiation dose, dose-fractionation schedule, use of chemotherapy, and/or type of chemotherapy was not controlled for in the analyses. Univariate and multivariate analyses were conducted to examine the potential treatment effect of BrdU on patient survival. RESULTS: Data from 334 patients treated with BrdU on NCOG 6G-82-1 and 1743 patients treated without BrdU on 3 RTOG studies was received. Patients were excluded from the review if confirmation of eligibility could not be obtained, if the patient was ineligible for the study they entered, if central pathology review was not done, or if radiotherapy data was not available. Patients treated according to the RTOG studies had to start radiotherapy within 4 weeks of surgery; no such restriction existed for the NCOG studies. To ensure comparability between the studies, patients from the NCOG studies who began treatment longer than 40 days from surgery were also excluded. The final data set included 296 cases from the NCOG studies (89%) and 1478 cases from the RTOG studies (85%). For patients with glioblastoma multiforme (GBM) the median survival was 9.8 months in the RTOG studies and 13.0 months in the NCOG trial (p < 0.0001). For patients with AA the median survival was 35.1 months for the RTOG studies and 42.8 months in the NCOG trial (p = 0.126). Univariate results showed consistent results favoring BrdU among patients over 30 years of age, across the extent of surgery, and for GBM patients. A proportional hazards regression model that included treatment, histopathology, KPS, age, and extent of surgery demonstrated that treatment with BrdU was included in the best model only for the GBM group of patients (risk ratio 0.83). CONCLUSIONS: Because of the heterogeneity of the treatment groups, including potentially important differences in pathology reviewers assessment of nonglioblastoma cases, differences in radiation dose and schedules, and chemotherapy during or after radiation, these analyses cannot provide the definitive answer as to whether BrdU given during radiation therapy improves survival in patients with malignant glioma. There does appear to be a favorable treatment effect seen in patients with GBM, with a lesser effect in patients with AA.
Adolescent↗
Long-term stabilization after bone marrow transplantation in juvenile metachromatic leukodystrophy.
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Adolescent↗
Molecular heterogeneity in mucopolysaccharidosis IVA in Australia and Northern Ireland: nine novel mutations including T312S, a common allele that confers a mild phenotype.
Mucopolysaccharidosis IVA (MPS IVA) is an autosomal recessive lysosomal storage disorder caused by a genetic defect in N-acetylgalactosamine-6-sulfate sulfatase (GALNS). Previous studies of patients from a British-Irish population showed that the I113F mutation is the most common single mutation among MPS IVA patients and produces a severe clinical phenotype. We studied mutations in the GALNS gene from 23 additional MPS IVA patients (15 from Australia, 8 from Northern Ireland), with various clinical phenotypes (severe, 16 cases; intermediate, 4 cases; mild, 3 cases). We found two common mutations that together accounted for 32% of the 44 unrelated alleles in these patients. One is the T312S mutation, a novel mutation found exclusively in milder patients. The other is the previously described I113F that produces a severe phenotype. The I113F and T312S mutations accounted for 8 (18%) and 6 (14%) of 44 unrelated alleles, respectively. The relatively high residual GALNS activity seen when the T312S mutant cDNA is overexpressed in mutant cells provides an explanation for the mild phenotype in patients with this mutation. The distribution and relative frequencies of the I113F and T312S mutations in Australia corresponded to those observed in Northern Ireland and are unique to these two populations, suggesting that both mutations were probably introduced to Australia by Irish migrants during the 19th century. Haplotype analysis using 6 RFLPs provides additional data that the I113F mutation originated from a common ancestor. The other 9 novel mutations identified in these 23 patients were each limited to a single family. These data provide further evidence for extensive allelic heterogeneity in MPS IVA in British-Irish patients and provide evidence for their transmission to Australia by British-Irish migrants.
Australia↗
Cloning, expression, purification, and characterization of the 6-phosphogluconate dehydrogenase from sheep liver.
The mRNA encoding the 51-kDa subunit of 6-phosphogluconate dehydrogenase (6PGDH) from sheep liver was reverse-transcribed and amplified. The resulting cDNA was reamplified in N-terminal and C-terminal segments and spliced to generate a full-length clone, and an internal cDNA fragment was also amplified. The full-length clone containing the complete coding sequence of the 6PGDH cDNA was sequenced and found to contain two mutations and two deletions in the internal region and two mutations outside of the internal region, an A to G point mutation at position 1407 that resulted in the amino acid change Gln 445 to Arg and a silent mutation at position 1426. The internal clone was sequenced and shown to be free of any mutations; therefore the internal piece was used to replace the same region in the full-length clone to correct the mutations in this region. The mutation at position 1407 which was outside of the internal region was corrected using site-directed mutagenesis. The cDNA with the correct codon was then subcloned into the bacterial expression vector pQE-30 and overproduced in Escherichia coli strain M15. A protein with a subunit molecular weight of 51,000 was expressed at a level of about 4.5% of the total soluble protein in M15 as judged by SDS/PAGE. Cloning into pQE-30 adds six histidines and a short linker to the N-terminus of the enzyme. The recombinant 6PGDH with His-tag was purified using the Ni-NTA affinity column supplied by Qiagen. The purification procedure resulted in a homogeneous protein by SDS/PAGE with 22.4-fold purification with an overall yield of 61%. The recombinant enzyme exhibits kinetic parameters within error identical to those measured for native sheep liver enzyme.
Animals↗
Visual complexity in letter-by-letter reading: "pure" alexia is not pure.
Standard accounts of pure alexia have favoured the view that this acquired disorder of reading arises from damage to a left posterior occipital cortex mechanism dedicated to the processing of alphanumeric symbols. We challenge these accounts in two experiments and demonstrate that patients with this reading deficit are also impaired at object identification. In the first experiment, we show that a single subject, EL, who shows all the hallmark features of pure alexia, is impaired at picture identification across a large set of stimuli. As the visual complexity of pictures increases, so EL's reaction time to identify the stimuli increases disproportionately relative to the control subjects. In the second experiment, we confirm these findings with a larger group of five pure alexic patients using a selected subset of high- and low-visual complexity pictures. These findings suggest that the deficit giving rise to pure alexia is not restricted to orthographic symbols per se but, rather, is a consequence of damage to a more general-purpose visual processing mechanism.
Adult↗
Alopecia areata and cytomegalovirus infection in twins: genes versus environment?
BACKGROUND: Alopecia areata (AA) is hypothesized to be an organ-specific autoimmune disease mediated by T cells directed to the hair follicle. Genetic susceptibility may be conferred by HLA, and an environmental trigger, such as a viral infection, is suspected. The incidence of AA in the population is estimated to be 1.7%, with an average of one in four patients having a positive family history. OBJECTIVE: Our purpose was to examine the concordance rate of AA among identical versus fraternal twins and the correlation between stress, cytomegalovirus (CMV) infection, and disease. METHODS: Families with AA were solicited from dermatologists in the United States and through a Website on the Internet. HLA class 2 typing and identification of CMV early and late genes were performed by polymerase chain reaction (PCR) on genomic peripheral blood DNA. Serum antibodies for CMV were determined by enzyme-linked immunosorbent assay. RESULTS: From 114 families, we identified 11 sets of monozygotic twins and 3 sets of dizygotic twins. The concordance rate was 55% for monozygotic twins and 0% for fraternal twins. Most identical twins were male. The severity of the AA phenotype varied and appeared most severe in the first affected twin. Five of 24 twins were CMV seropositive but CMV DNA was not detected in blood lymphocytes of any of the subjects when studied after the onset of AA. The presence of AA in twins was not correlated with evidence of CMV. CONCLUSION: A 55% concordance rate in identical twins and AA occurring in families support a genetic component as well as possible environmental triggers that remain unknown.
Adolescent↗
Solving a real-world problem using an evolving heuristically driven schedule builder.
This work addresses the real-life scheduling problem of a Scottish company that must produce daily schedules for the catching and transportation of large numbers of live chickens. The problem is complex and highly constrained. We show that it can be successfully solved by division into two subproblems and solving each using a separate genetic algorithm (GA). We address the problem of whether this produces locally optimal solutions and how to overcome this. We extend the traditional approach of evolving a "permutation + schedule builder" by concentrating on evolving the schedule builder itself. This results in a unique schedule builder being built for each daily scheduling problem, each individually tailored to deal with the particular features of that problem. This results in a robust, fast, and flexible system that can cope with most of the circumstances imaginable at the factory. We also compare the performance of a GA approach to several other evolutionary methods and show that population-based methods are superior to both hill-climbing and simulated annealing in the quality of solutions produced. Population-based methods also have the distinct advantage of producing multiple, equally fit solutions, which is of particular importance when considering the practical aspects of the problem.
Algorithms↗
Comparable engraftment kinetics following peripheral-blood stem-cell infusion mobilized with granulocyte colony-stimulating factor with or without cyclophosphamide in multiple myeloma.
PURPOSE: To compare, in the setting of tandem autotransplantations for multiple myeloma (MM), two established methods of peripheral-blood stem-cell (PBSC) procurement with chemotherapy or hematopoietic growth factor alone. PATIENTS AND METHODS: Between June 1994 and July 1995, 44 patients with MM were randomized to PBSC mobilization with either granulocyte colony-stimulating factor (G-CSF) 16 microg/kg (group 1; n = 22) or high-dose cyclophosphamide (HDCTX) 6 g/m2 plus G-CSF 5 microg/kg (group 2; n = 22). All 44 patients received melphalan 200 mg/m2 with their first autograft and 32 patients proceeded to a second transplantation. RESULTS: Group 2 required a significantly longer time interval for completion of PBSC collection than group 1 (median, 22 v 8 days; P = .0001), greater frequency of hospitalization (100% v 32%; P = .0001), and increased transfusion of platelets (86% v 18%; P = .0001) and packed RBCs (86% v 55%; P = .02). Likewise, the incidence of fever and pneumonia/sepsis were higher in group 2 (P = .02 and P = .04, respectively). Surprisingly, despite greater CD34 cell quantities infused in group 2, median recovery times of granulocytes (both > 500/microL and 2,500/microL) and platelets (both > 50,000/microL and > 100,000/microL) were similar (all P > .7). Posttransplant toxicities were also similar. CONCLUSION: Compared with HDCTX plus G-CSF, high-dose G-CSF alone is associated with lower morbidity, shorter duration of PBSC mobilization, and comparable hematopoietic recovery after transplantation, which should result in significant cost reduction. Considering the relatively limited antitumor activity of HDCTX (10% with > or = 50% tumor cytoreduction), PBSC mobilization with HDCTX should be limited to selected patients with persistent MM despite induction chemotherapy.
Antineoplastic Combined Chemotherapy Protocols↗
Collection of more hematopoietic progenitor cells with large volume leukapheresis in patients with multiple myeloma.
Reinfusion of mobilized peripheral blood stem cells (PBSC) after high dose chemotherapy accelerates hematopoietic recovery. Because of the relatively low content of hematopoietic progenitors in the peripheral blood even after mobilization, multiple leukapheresis procedures are necessary to reach the required target number of CD34 cells to ensure prompt engraftment post-transplantation. Our previous studies have shown that the highest proportions of hematopoietic progenitors cells (CD34) are collected during the first three days of apheresis, whereas peak levels of myeloma cells are observed during subsequent days. Therefore, large volume leukapheresis (LVL), defined as processing of greater than 3 blood volumes or a total of at least 15 liters, was explored in 23 myeloma patients, undergoing 91 procedures; 14 patients were mobilized with high dose cyclophosphamide (6g/m2) and hematopoietic growth factors and 9 with G-CSF only. CD34 yields were measured separately for the first and last two hours of collection. We observed no decrease in CD34 cells/kg during the last two hours of collection and when the LVL collections were compared to historical matched controls, mobilized with the same regimen, the median quantity of CD34 cells/kg/liter collected remained equivalent during all days of apheresis. When compared to G-CSF only, mobilization with high dose cyclophosphamide appeared to result in superior hematopoietic stem cell collections. Interestingly, the G-CSF group experienced a progressive decrease in platelets during consecutive days of LVL, while the opposite was seen in the cyclophosphamide group. LVL procedures were not associated with a higher complication rate than standard volume apheresis. We conclude that LVL procedures allow collection of more CD34 cell per session while not jeopardizing progenitor cell collections during subsequent sessions. Since more CD34 cells are collected, fewer days are required to attain the optimal target of progenitor cells. This should result in PBSC grafts with less tumor contamination.
Antineoplastic Agents, Alkylating↗
The 67-kd laminin receptor is preferentially expressed by proliferating retinal vessels in a murine model of ischemic retinopathy.
Endothelial cell association with vascular basement membranes is complex and plays a critical role in regulation of cell adhesion and proliferation. The interaction between the membrane-associated 67-kd receptor (67LR) and the basement membrane protein laminin has been studied in several cell systems where it was shown to be crucial for adhesion and attachment during angiogenesis. As angiogenesis in the pathological setting of proliferative retinopathy is a major cause of blindness in the Western world we examined the expression of 67LR in a murine model of hyperoxia-induced retinopathy that exhibits retinal neovascularization. Mice exposed to hyperoxia for 5 days starting at postnatal day 7 (P7) and returned to room air (at P12) showed closure of the central retinal vasculature. In response to the ensuing retinal ischemia, there was consistent preretinal neovascularization starting around P17, which persisted until P21, after which the new vessels regressed. Immunohistochemistry was performed on these retinas using an antibody specific for 67LR. At P12, immunoreactivity for 67LR was absent in the retina, but by P17 it was observed in preretinal proliferating vessels and also within the adjacent intraretinal vasculature. Intraretinal 67LR immunoreactivity diminished beyond P17 until by P21 immunoreactivity was almost completely absent, although it persisted in the preretinal vasculature. Control P17 mice (not exposed to hyperoxia) failed to demonstrate any 67LR immunoreactivity in their retinas. Parallel in situ hybridization studies demonstrated 67LR gene expression in the retinal ganglion cells of control and hyperoxia-exposed mice. In addition, the neovascular intra- and preretinal vessels of hyperoxia-treated P17 and P21 mice labeled strongly for 67LR mRNA. This study has characterized 67LR immunolocalization and gene expression in a murine model of ischemic retinopathy. Results suggest that, although the 67LR gene is expressed at high levels in the retinal ganglion cells, the mature receptor protein is preferentially localized to the proliferating retinal vasculature and is almost completely absent from quiescent vessels. The differential expression of 67LR between proliferating and quiescent retinal vessels suggests that this laminin receptor is an important and novel target for future chemotherapeutic intervention during proliferative vasculopathies.
Animals↗
Gillespie syndrome: a report of two further cases.
We describe two unrelated patients with Gillespie syndrome (partial aniridia, cerebellar ataxia, and mental retardation). The typical presentation is the discovery of fixed dilated pupils in a hypotonic infant. The iris abnormality is specific and seems pathognomonic of Gillespie syndrome. It can be distinguished clinically from other forms of aniridia and a presumptive diagnosis of Gillespie syndrome can be made in the first months of life on the basis of the ocular findings. Neurological involvement includes marked motor delay, hypotonia, disabling ataxia, and usually mental retardation. Cerebral and cerebellar atrophy with white matter changes on MRI scan were present in our second patient suggesting that patients with Gillespie syndrome may have more extensive CNS involvement than previously described. The parents of this child were first cousins; thus Gillespie syndrome may be heterogeneous with autosomal recessive and autosomal dominant forms.
Aniridia↗
Porcine and bovine cartilage transplants in cynomolgus monkey: I. A model for chronic xenograft rejection.
Transplantation of discordant xenograft tissues usually results in antibody-mediated hyperacute rejection response. It has been speculated that because cartilage has a limited vascular, neural, and lymphatic supply, it might be immunologically privileged and may not undergo hyperacute or chronic rejection. Moreover, porcine and bovine cartilage were found to express very low amounts of alpha-galactosyl epitopes (Gal alpha1-3Gal beta1-4GlcNAc-R). To evaluate animal cartilage for possible human transplantation, xenograft meniscal cartilage was transplanted from pigs and cows into the suprapatellar pouches of six cynomolgus monkeys (group 1). In a second group of six monkeys (group 2), porcine meniscal cartilage and porcine articular cartilage plugs were evaluated. During the 2-month evaluation period in group 1, all monkeys displayed an extensive humoral response to the xenograft, as indicated by the increase in production of antibodies against bovine and porcine cartilage. Upon explant, all meniscal cartilage samples in this group demonstrated histological evidence of chronic rejection, including fibroplasia, encapsulation, mononuclear infiltrates, foreign body giant cells, and eosinophilic infiltrates. There was no difference between the response seen in untreated tissues and that seen in tissues treated with UV irradiation or ozone oxidation. In group 2, the menisci explanted after 1 month displayed extensive infiltration of eosinophils alone or eosinophils mixed with mononuclear cells. The mononuclear infiltrates consisted primarily of CD4+ and CD8+ T cells and of macrophages. The articular cartilage plugs demonstrated only a small area of fibrous encapsulation and leukocyte infiltration at the periphery. This study suggests that xenograft cartilage tissue does not appear to be immunoprivileged and is unsuitable for human implantation due to a chronic rejection mechanism, which is evident already within 1 month after transplantation. In addition, this study may serve as a general model for the primate immune response against xenografts in the absence of hyperacute rejection.
Animals↗
Childhood-onset schizophrenia. Progressive ventricular change during adolescence.
BACKGROUND: There is controversy about progression in brain abnormalities in later-onset schizophrenia. This study looked for more striking progression in brain abnormalities during adolescence in a chronically ill, treatment-refractory sample of patients with childhood-onset schizophrenia who had had more prepsychotic developmental disturbance, but clinical and neurobiological characteristics similar to those of patients with treatment-refractory adult-onset schizophrenia who have poor outcome. METHODS: Anatomic brain magnetic resonance images were obtained for 16 children and adolescents with onset of schizophrenia by 12 years of age and 24 temporally yoked, age- and sex-matched healthy controls. Subjects were scanned on initial admission and rescanned after 2 years with the identical equipment and measurement methods. RESULTS: Childhood schizophrenics showed a significantly greater increase in ventricular volume than did controls, for whom ventricles did not increase significantly (analysis of variance, diagnosis x time, F = 16.1, P < .001). A significant decrease in midsagittal thalamic area was also seen for the schizophrenics (P = .03), which was unchanged at rescan for controls. These differential brain changes correlated significantly with each other and tended to be predicted by both prepsychotic developmental abnormality (Premorbid Assessment Scale, P = .06) and Brief Psychiatric Rating Scale at follow-up (P = .07). CONCLUSIONS: More consistent progressive ventricular enlargement was seen during adolescence for this childhood-onset sample than has been reported for adult-onset populations. The brain imaging results support other clinical data showing both early and late deviations in brain development for at least this rare subgroup of treatment-refractory, very-early-onset schizophrenic patients.
Adolescent↗
Pharmacokinetics and dose proportionality of beclomethasone from three strengths of a CFC-free beclomethasone dipropionate metered-dose inhaler.
As part of a development program to offer alternatives to chlorofluorocarbon (CFC) containing metered-dose inhalers, beclomethasone dipropionate has been formulated in a CFC-free system at three strengths: 50, 100, and 200 micrograms/actuation ex valve. To measure serum levels and dose proportionality of the beclomethasone derived from beclomethasone dipropionate, 13 mild to moderate asthmatic patients received a single dose of eight inhalations from each strength according to a double-blind crossover design. Seven patients were studied over 4 h and six patients over 12 h. For the total doses of 400, 800, and 1600 micrograms studied over 12 h, Cmax and AUC increased in a ratio of 1:1.8:3.1. A good correlation was seen between the fine-particle mass delivered and the in vivo performance of the three strengths. From a clinical point of view, the predictable increases in serum levels with an increase in dose will permit the clinician to effectively titrate a patient with this product.
Administration, Inhalation↗
Incidence of the mucopolysaccharidoses in Northern Ireland.
An epidemiological study of the mucopolysaccharidoses (MPS) in Northern Ireland using multiple ascertainment sources was carried out and the incidence rate for the period 1958-1985 was estimated. An incidence of approximately 1 in 76,000 live births was obtained for MPS 1H (Hurler phenotype); 1 in 280,000 for MPS 1 H/S (Hurler/Scheie phenotype); 1 in 140,000 live births (1 in 72,000 male live births) for MPS II (Hunter syndrome); 1 in 280,000 for MPS III (Sanfilippo syndrome) and 1 in 76,000 for MPS IV A (Morquio syndrome type A). No cases of MPS IS (Scheie phenotype), MPS IV B (Morquio syndrome type B) or MPS VI (Maroteaux-Lamy syndrome) were ascertained during the study period. Three cases of non-immune hydrops fetalis born to consanguineous parents were thought to be due to beta-glucuronidase deficiency (MPS VII) on the basis of placental histology and enzyme studies on both parents but no living cases of MPS VII were ascertained. The overall incidence for all types of mucopolysaccharidosis was approximately 1 in 25,000 live births. A comparison is made with incidence estimates obtained from other published studies.
Humans↗
Results of a phase I clinical trial of a T-cell receptor peptide vaccine in patients with multiple sclerosis. I. Analysis of T-cell receptor utilization in CSF cell populations.
To identify a panel of multiple sclerosis patients (MS) for a phase I clinical trial of a T-cell receptor (TCR) peptide vaccine we characterized the T-cell populations present in the cerebrospinal fluids (CSF) of a large group of patients with respect to surface phenotype and state of activation, TCR beta chain utilization, features of the CDR3 junctional region, the extent of clonality and persistence of selected clonotypes over time. These CSF cell populations consist of approximately 60% CD4+ T-cells, half of which bear IL-2 receptors, indicating these activated T-cells may be part of the pathogenic process in MS. When these activated CD4+ T-cells were selectively expanded in IL-2/IL-4 supplemented cultures, an over-representation of several TCRV beta families was noted in 39/47 patients, the most frequent being V beta 6.5, V beta 6.7, V beta 2, V beta 5 and V beta 4. Biased expression of various members of the V beta 6 family was seen in 21 of this group of 39 patients. Clonal analysis of TCR beta 6 CDR3 sequences, revealed two notable features: clonal dominance and clonal persistence. CSF cells from two-thirds of MS patients contained a dominant clone comprising 50% or more of sequences and the same patient-specific clone could be shown to persist for up to 18 months. This clonal prevalence and over representation of V beta 6+TCR raises the possibility that immunization with a V beta 6 peptide vaccine may produce a regulatory immune response leading to a clinical benefit.
Adult↗
Results of a phase I clinical trial of a T-cell receptor vaccine in patients with multiple sclerosis. II. Comparative analysis of TCR utilization in CSF T-cell populations before and after vaccination with a TCRV beta 6 CDR2 peptide.
We report here the results of a phase I trial of a T-cell receptor (TCR) V beta 6 CDR2 region peptide vaccine in 10 patients with multiple sclerosis who showed biased over-representations of V beta 6 mRNA among T-cells in their cerebrospinal fluids (CSF). One group of 5 patients was immunized twice during a four week period with 100 micrograms of the TCRV beta 6 peptide 39-LGQGPEF LTYFQNEAQLEKS-58 emulsified in incomplete Freund's adjuvant (IFA); the second group of 5 MS patients received 300 micrograms of the same peptide in IFA over a similar time period. Patients were monitored for adverse events, immunogenicity of the peptide and changes in their CSF T-cell populations. The results indicate that this peptide was immunogenic (T-cell proliferation assays and recall DTH responses) in some of the patients, although none of the immunized patients produced detectable anti-peptide antibodies. More importantly, we show that the 5 patients treated with higher doses of the vaccine displayed a slight decrease in CSF cellularity, a lack of growth of CSF cells in cytokine supplemented expansion cultures that implies a significant absence of a subset of activated CD4 T-cells and a marked diminution in V beta 6 mRNA levels among T-cells in these cultures. By comparison, in 5 patients receiving the lower dosage of the vaccine, CSF cellularity was the same or slightly increased over pre-vaccination levels, CSF cells from 1 patient failed to grow in expansion cultures and cultured CSF cells from 2 patients underwent a change from an oligoclonal V beta 6 pattern to one that was more polyclonal. These results justify a more through exploration of the use of TCR peptide vaccines as a possible therapeutic treatment for MS.
Adult↗