Immunological Features (immunological + feature)

Distribution by Scientific Domains

Selected Abstracts


E. Nobile-Orazio
Multifocal motor neuropathy (MMN) is characterized by progressive asymmetric limb weakness usually predominant in the upper limbs associated with conduction block (CB) in motor but not sensory nerves. There are, however, occasional patients with clinically typical MMN in whom no CB can be detected. Whether these patients differ from patients with MMN and CB remains unclear. Since 1991, we have observed 24 patients with the typical clinical features of MMN. In 20 of them (14 men and 6 women), electrophysiological studies disclosed the presence of CB in at least one motor nerve. In four (all women), no evidence of CB could be detected in examined nerves even if three had some features of demyelination, including asymmetric reduction of motor conduction velocities (1 patient) or prolonged or absent F wave latencies (3 patients). Three of them had markedly reduced or absent proximal and distal CMAP amplitudes in some nerves. The mean age of onset of MMN was similar in patients with (41.5 years, range 21,70) and without CB (41.5 years, range 24,57). The mean duration of the disease at the time of our first visit was longer in patients without CB (18.5 years, range 13,25) than in those with CB (6.3 years, 3 months,25 years); only 3 patients with CB had a duration of the disease longer than 10 years. All patients without CB had a predominant or exclusive impairment of upper limbs compared with 18 (90%) of those with CB. The mean Rankin score before therapy was slightly worse in patients without (2.5) than with (2.2) CB. Anti-ganglioside antibodies were found in 1 patient without CB (25%) and in 8 (40%) with CB. All but 2 patients with CB (90%) consistently improved with IVIg. All patients without CB also improved with IVIg, but only one did so consistently. In conclusion, patients with the typical clinical presentation of MMN but no overt CB are clinically and immunologically indistinguishable from those with MMN and CB. The longer duration of the disease and frequent axonal impairment in patients without CB may explain the lower efficacy of IVIg in these patients than in those with CB. [source]

Cytomegalovirus hyperimmunoglobulin: mechanisms in allo-immune response in vitro

K. Hoetzenecker
Abstract Background Cytomegalovirus hyperimmunoglobulin (CMVIg) containing drugs are routinely administered in cardiac transplantation for prophylaxis against CMV disease. Yet little is known about their influence on transplant relevant immune functions. The aim of this study was to evaluate the effect of CMVIg on cellular immunity in in vitro experiments and to define their role in tolerance inducing mechanisms. Materials and methods/results CMVIg reduces proliferation in mixed lymphocyte reactions and anti-CD3 blastogenesis assays and is related to decreased production of immune modulating cytokines interleukin (IL)-2, interferonr (IFN,), IL-10. This antiproliferative effect is associated with a cell-cycle arrest in the G0/G1 phase and induction of apoptosis in CD8+ and natural killer cells. Co-incubation with CMVIg causes down-regulation of cell bound immunoglobulin and Fc,RIII surface expression on natural killer cells and leads to attenuation of antibody dependent cellular cytotoxicity effector functions. Conclusions We conclude that CMVIg induces immunological features on leukocytes in vitro that are known to be related to tolerance induction. Our observations extend the current concept of CMVIg as passive CMV prophylaxis to a therapeutic drug compound capable of reducing allogeneic immune response. [source]

Induction of neutralizing antibodies in mice immunized with an amino-terminal polypeptide of Streptococcus mutans P1 protein produced by a recombinant Bacillus subtilis strain

Milene B. Tavares
Abstract The oral pathogen Streptococcus mutans expresses a surface protein, P1, which interacts with the salivary pellicle on the tooth surface or with fluid-phase saliva, resulting in bacterial adhesion or aggregation, respectively. P1 is a target of protective immunity. Its N-terminal region has been associated with adhesion and aggregation functions and contains epitopes recognized by efficacious antibodies. In this study, we used Bacillus subtilis, a gram-positive expression host, to produce a recombinant N-terminal polypeptide of P1 (P139,512) derived from the S. mutans strain UA159. Purified P139,512 reacted with an anti-full-length P1 antiserum as well as one raised against intact S. mutans cells, indicating preserved antigenicity. Immunization of mice with soluble and heat-denatured P139,512 induced antibodies that reacted specifically with native P1 on the surface of S. mutans cells. The anti-P139,512 antiserum was as effective at blocking saliva-mediated aggregation of S. mutans cells and better at blocking bacterial adhesion to saliva-coated plastic surfaces compared with the anti-full-length P1 antiserum. In addition, adsorption of the anti-P1 antiserum with P139,512 eliminated its ability to block the adhesion of S. mutans cells to abiotic surfaces. The present results indicate that P139,512, expressed and purified from a recombinant B. subtilis strain, maintains important immunological features of the native protein and represents an additional tool for the development of anticaries vaccines. [source]

Mutations in severe combined immune deficiency (SCID) due to JAK3 deficiency

HUMAN MUTATION, Issue 4 2001
Luigi D. Notarangelo
Abstract During the last 10 years, an increasing number of genes have been identified whose abnormalities account for primary immunodeficiencies, with defects in development and/or function of the immune system. Among them is the JAK3 -gene, encoding for a tyrosine kinase that is functionally coupled to cytokine receptors which share the common gamma chain. Defects of this gene cause an autosomal recessive form of severe combined immunodeficiency with almost absent T-cells and functionally defective B-cells (T,B+ SCID). Herewith, we present molecular information on the first 27 unique mutations identified in the JAK3 gene, including clinical data on all of the 23 affected patients reported so far. A variety of mutations scattered throughout all seven functional domains of the protein, and with different functional effects, have been identified. Availability of a molecular screening test, based on amplification of genomic DNA, facilitates the diagnostic approach, and has permitted recognition that JAK3 deficiency may also be associated with atypical clinical and immunological features. Development of a structural model of the JAK3 kinase domain has allowed characterization of the functional effects of the various mutations. Most importantly, molecular analysis at the JAK3 locus results in improved genetic counseling, allows early prenatal diagnosis, and prompts appropriate treatment (currently based on hematopoietic stem cell transplantation) in affected families. Hum Mutat 18:255,263, 2001. © 2001 Wiley-Liss, Inc. [source]

Conserved regions from Plasmodium falciparum MSP11 specifically interact with host cells and have a potential role during merozoite invasion of red blood cells

Ana Zuleima Obando-Martinez
Abstract Despite significant global efforts, a completely effective vaccine against Plasmodium falciparum, the species responsible for the most serious form of malaria, has not been yet obtained. One of the most promising approaches consists in combining chemically synthesized minimal subunits of parasite proteins involved in host cell invasion, which has led to the identification of peptides with high binding activity (named HABPs) to hepatocyte and red blood cell (RBC) surface receptors in a large number of sporozoite and merozoite proteins, respectively. Among these proteins is the merozoite surface protein 11 (MSP11), which shares important structural and immunological features with the antimalarial vaccine candidates MSP1, MSP3, and MSP6. In this study, 20-mer-long synthetic peptides spanning the complete sequence of MSP11 were assessed for their ability to bind specifically to RBCs. Two HABPs with high ability to inhibit invasion of RBCs in vitro were identified (namely HABPs 33595 and 33606). HABP-RBC bindings were characterized by means of saturation assays and Hill analysis, finding cooperative interactions of high affinity for both HABPs (nH of 1.5 and 1.2, Kd of 800 and 600,nM for HABPs 33595 and 33606, respectively). The nature of the possible RBC receptors for MSP11 HABPs was studied in binding assays to enzyme-treated RBCs and cross-linking assays, finding that both HABPs use mainly a sialic acid-dependent receptor. An analysis of the immunological, structural and polymorphic characteristics of MSP11 HABPs supports including these peptides in further studies with the aim of designing a fully effective protection-inducing vaccine against malaria. J. Cell. Biochem. 110: 882,892, 2010. © 2010 Wiley-Liss, Inc. [source]

Some local and systemic immunological features of prepubertal periodontitis

T. Berglundh
Abstract Objectives: The aim of the present investigation was to study local (gingival) and systemic host defense characteristics in a sample of children exhibiting local prepubertal periodontitis (LPP). Material and methods: 2 groups of subjects were included in the present study. One group consisted of 11 children (9.5±2.0 years) with signs of periodontal disease (LPP group). A 2nd group comprised 21 adults (48.1±5.8 years) with advanced periodontal disease: adult periodontitis (AP) group. Gingival biopsies and a sample of peripheral blood were obtained in each individual of the AP group and in 7 out of the 11 subjects in the LPP group. The biopsies were prepared for morphometrical and immunohistochemical analysis and the blood samples prepared for immunohistochemical analysis. Results: The cellular infiltrates in the biopsies of the LPP group contained a larger proportion of lymphocytes and, in particular B cells, than was the case in the AP group. The TCR V,/V, gene expression in the lesions in the AP group was dominated by V, 17 and in the LPP group by V, 2. The content in peripheral blood of various lymphocyte sub-populations and TCR V,/V, gene expression in the 2 groups was almost similar. Conclusion: It is suggested that (i) the systemic host response in children with prepubertal periodontitis has many features in common with that seen in adult patients but that (ii) local defense mechanisms in the periodontitis lesion of LPP differ from those in adult periodontitis. [source]

Virological and immunological features of active cytomegalovirus infection in nonimmunosuppressed patients in a surgical and trauma intensive care unit,

Marifina Chilet
Abstract Cytomegalovirus (CMV) reactivation occurs frequently in critically ill patients. The natural course of CMV infection and the interaction between CMV and the adaptive immune system in this setting remain poorly defined. Fifty-three CMV-seropositive patients in a surgical and trauma intensive care unit were included in this study. The CMV DNA load in tracheal aspirates (TA) and plasma (PL) was monitored by qPCR. CMV-specific T-cell immunity was assessed by intracellular cytokine staining. Plasma TNF-, levels were determined by ELISA. CMV reactivation occurred in 39.7% of patients (23% had CMV DNA detected only in TA). The analysis of TA allowed an earlier diagnosis in 28% of patients. Clearance of CMV DNAemia preceded that of CMV DNA in TA in some episodes. Peak CMV DNA levels were significantly higher in TA than in PL (P,=,0.02). CMV reactivation developed in the presence of CMV-specific T cells. Termination of CMV reactivation was associated with an expansion of functional CMV-specific T cells. Plasma levels of TNF-, did not allow for the prediction of the occurrence of CMV reactivation. CMV-specific T-cell immunity is preserved in most critically ill patients experiencing CMV reactivation. Analysis of respiratory specimens is imperative for an optimal monitoring of CMV reactivation in this setting. J. Med. Virol. 82:1384,1391, 2010. © 2010 Wiley-Liss, Inc. [source]

Bullous pemphigoid in Liguria: A 2-year survey

E Cozzani
Abstract Background The epidemiology of bullous pemphigoid (BP) is not clear because of the heterogeneity of the disease, and its possible association with internal malignancies has been under debate for many years. We report the findings of a 2-year study on incident BP cases in the Liguria region of Italy. Subjects and methods Thirty-two patients with BP were collected over the 2-year period. Diagnosis was made based on clinical findings and confirmed by histology, direct immunofluorescence (DIF) and indirect immunofluorescence (IIF) with salt-split skin and monkey oesophagus, and immunoblotting (IB). All patients were thoroughly investigated for possible malignancies and all were followed up for 6 months to monitor the response to treatment. Results DIF showed linear deposits at the dermoepidermal junction in all but one patient. IIF gave positive findings for 15 sera tested with monkey oesophagus and 20 tested with salt-split skin. IB gave positive findings in 19 cases. There was a malignancy in six cases, but no clinical or immunological features that could be considered to predict this occurrence. Conclusions The findings of this study are in accordance with most of the data found in the literature, including the fact that IgG serum levels did not predict the course of the disease. Contrary to previous indications, IgE levels were not indicative of disease course either. Mucosal lesions, erythema multiform-like lesions, negative IIF findings and antibodies to AgPB2 were not a prediction for the development of malignancy. [source]

Number III Mucous membrane pemphigoid

ORAL DISEASES, Issue 4 2005
J Bagan
Mucous membrane pemphigoid (MMP) is a sub-epithelial vesiculobullous disorder. It is now quite evident that a number of sub-epithelial vesiculobullous disorders may produce similar clinical pictures, and also that a range of variants of MMP exist, with antibodies directed against various hemidesmosomal components or components of the epithelial basement membrane. The term immune-mediated sub-epithelial blistering diseases (IMSEBD) has therefore been used. Immunological differences may account for the significant differences in their clinical presentation and responses to therapy, but unfortunately data on this are few. The diagnosis and management of IMSEBD on clinical grounds alone is impossible and a full history, general, and oral examination, and biopsy with immunostaining are now invariably required, sometimes supplemented with other investigations. No single treatment regimen reliably controls all these disorders, and it is not known if the specific subsets of MMP will respond to different drugs. Currently, apart from improving oral hygiene, immunomodulatory,especially immunosuppressive,therapy is typically used to control oral lesions. The present paper reviews pemphigoid, describing the present understanding of this fascinating clinical phenotype, summarising the increasing number of subsets with sometimes-different natural histories and immunological features, and outlining current clinical practice. [source]

Clinical impact of altered immunoglobulin levels in Henoch,Schönlein purpura

Andrew Fretzayas
Abstract Background:, The aim of the present study was the identification of immunological features, present at the time of diagnosis, that would predict the severity of Henoch,Schönlein purpura and its outcome. Methods:, A cohort study was carried out in a tertiary pediatric hospital of 69 children with Henoch,Schönlein purpura, in whom serum complement components C3, C4 and IgA, IgM, IgG were repeatedly determined. Results:, During the acute phase of the disease in 54/69 patients (78.3%) immunological imbalances were observed. In 24/54 cases (44.4%) certain complications involving the kidneys and the gastrointestinal tract were noted as opposed to in 3/15 children (20%) without immunologic abnormalities. In 50/69 children (72.5%), elevated serum IgA was detected and 16 of them (32%) developed renal involvement while only 1/19 children (5.3%) with normal IgA concentration had renal involvement. Considering separately the group of 9/69 children (13%) with increased IgM and those with normal IgM levels (53/69; 76.8%), irrespective of IgA and IgG concentration, we found a comparable percentage of children who had both renal and intestinal involvement without, however, developing severe complications, which were exclusively seen in patients with increased IgA (5/7 children) and reduced IgM levels. Serum C3 fraction was elevated in 26 children (37.7%) and in 73% of cases it was associated with increased serum IgA values. Conclusion:, Renal involvement was seen in 32% of children with increased IgA values. Most importantly, elevated IgA concentration along with reduced IgM levels was associated with higher prevalence of severe complications. [source]

AMPA receptor antibodies in limbic encephalitis alter synaptic receptor location,

Meizan Lai MD
Objective To report the clinical and immunological features of a novel autoantigen related to limbic encephalitis (LE) and the effect of patients' antibodies on neuronal cultures. Methods We conducted clinical analyses of 10 patients with LE. Immunoprecipitation and mass spectrometry were used to identify the antigens. Human embryonic kidney 293 cells expressing the antigens were used in immunocytochemistry and enzyme-linked immunoabsorption assay. The effect of patients' antibodies on cultures of live rat hippocampal neurons was determined with confocal microscopy. Results Median age was 60 (38,87) years; 9 were women. Seven had tumors of the lung, breast, or thymus. Nine patients responded to immunotherapy or oncological therapy, but neurological relapses, without tumor recurrence, were frequent and influenced the long-term outcome. One untreated patient died of LE. All patients had antibodies against neuronal cell surface antigens that by immunoprecipitation were found to be the glutamate receptor 1 (GluR1) and GluR2 subunits of the ,-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR). Human embryonic kidney 293 cells expressing GluR1/2 reacted with all patients' sera or cerebrospinal fluid, providing a diagnostic test for the disorder. Application of antibodies to cultures of neurons significantly decreased the number of GluR2-containing AMPAR clusters at synapses with a smaller decrease in overall AMPAR cluster density; these effects were reversed after antibody removal. Interpretation Antibodies to GluR1/2 associate with LE that is often paraneoplastic, treatment responsive, and has a tendency to relapse. Our findings support an antibody-mediated pathogenesis in which patients' antibodies alter the synaptic localization and number of AMPARs. Ann Neurol 2009;65:424,434 [source]