bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prevalence of childhood asthma based on questionnaires and methacholine bronchial provocation test in Korea
Authors: KIM Y. Y. , CHO S. H. , KIM W. K. , PARK J. K. , SONG S. H. , KIM Y. K. , JEE Y. K. , HA M. N. , AHN Y. O. , LEE S. I. , MIN K. U. 
Published: November 2003

SummaryBackground
In most epidemiological survey studies, only subjective symptoms and past medical history of asthma have been used as diagnostic criteria. Even though a questionnaire survey can be performed in a large population study at low cost, limitations such as lack of objectivity and poor predictability in non‐specific bronchial hyperresponsiveness cannot be avoided.Objectives
The purpose of this study was to elucidate the prevalence of current asthma based on questionnaires and methacholine bronchial provocation test, and the prevalence of atopy in Korea.Methods
We performed modified ATS respiratory questionnaires and allergen skin‐prick test with 10 common inhalant allergens among 3219 subjects aged 7–19 years in Seoul and a rural part of a small city, Chungju in Korea. Methacholine bronchial provocation tests were also performed among those who had asthma symptoms according to the questionnaire. The criteria of asthma was presence of both asthma symptoms and non‐specific bronchial hyperresponsiveness. Atopy was defined as when an allergen induced weal size is same or larger than that caused by histamine.Results
The prevalence of asthma based on questionnaires and methacholine bronchial provocation tests was 4.6%, while the prevalence of wheeze was 8.2% and 19.3% of total population complained of one or more respiratory symptoms related to asthma on the questionnaires. There was no significant difference according to age, sex and living area. The mean prevalence of atopy was 35.0% and the most common allergens were Dermatophagoides farinae (30.9%), Dermatophagoides pteronyssinus (27.5%), cat fur (20.4%) and cockroach (11.8%). The atopy prevalence in Chungju area was higher than that in Seoul and males showed a higher prevalence than females. The asthma prevalence was higher among atopies (6.8%) than among non‐atopies (2.7%). None of questionnaire items were enough to predict the presence of bronchial hyperresponsiveness in terms of sensitivity, specificity and positive predictive value.Conclusion
The prevalence rate of current asthma in Korea was 4.6% and the prevalence rate of atopy in Korea was 35.0%. Questionnaire‐based surveys are not enough to predict the actual prevalence of asthma.
Loss of nitric oxide release in passively sensitized guinea‐pig aorta with purified immunoglobulin Gl
Authors: JONDET A. , GOGNY M. , VU A. T. , BLIN M. , BIDON J.‐C. 
Published: November 2003

SummaryBackground
Vascular hyperresponsiveness can be reproduced by in vitro passive sensitization of isolated aorta with immunoglobulin G1 (IgGl) taken from ovalbumen‐sensitized BFA guinea‐pig.Objective
The aim of the present work was to investigate the role of nitric oxide in the sensitization‐induced alteration of the contractile and relaxant responses of guinea‐pig aorta to noradrenaline (NA) and acetylcholine (ACh). respectively.Methods
Cumulative concentration‐response curves to NA or ACh were established before and after IgG1 sensitization and then after successive treatments.Results
IgGl in vitro passive sensitization of aorta caused a significant hyperreactivity to NA and completely inhibited the relaxation to ACh. After sensitization. the addition of an intact aortic ring (with endothelium) in the organ chamber restored the maximal response to NA and ACh close to control but was ineffective in the presence of hemoglobin. The restoration of the control reactivity to NA was also inhibited in the presence of L‐NAME or when the added aortic ring was endothelium‐denuded. Moreover. L‐arginine. a nitric oxide (NO) precursor, was able to restore the control reactivity to NA.Conclusion
The present results show that IgG| in vitro sensitization induced a loss of NO release from the vascular endothelium. This loss of NO probably plays a great role in vascular hyperreactivity by increasing the contractile response and decreasing the relaxant response to mediators and would be a component of allergic diseases pathogenesis.
Presence of antibodies to replication protein A in some patients with systemic lupus erythematosus (SLE)
Authors: Garcia-Lozano R , Wichmann I , Garcia A , Sanchez-Roman J , Gonzalez-Escribano F , Nuñez-Roldan A 
Published: November 2003

SUMMARY
Presence of antibodies directed against replication protein A (RPA), a DNA binding protein complex composed of three subunits (RPA-70, RPA-32 and RPA-14) was investigated among patients with SLE and other autoimmune diseases using immunoblot analysis to RPA-70 and RPA-32 recombinant proteins. Anti-RPA antibodies were found in two out of 108 sera from SLE patients, one of them showing reactivity against RPA-32 and RPA-70 and the other reacting only against RPA-32. Sera from 108 patients with other autoimmune disorders as well as from 42 healthy control individuals were negative. Thus, the frequency of these antibodies in SLE is estimated to be 2–3%. The study demonstrates that RPA is one target more of the wide array of autoantigens that elicit an immune response in SLE. The presence of anti-RPA autoantibodies seems to be circumscribed to a small number of patients with SLE.
Human natural killer (NK) cells present staphylococcal enterotoxin B (SEB) to T lymphocytes
Authors: D’Orazio J A , Stein-Streilein J 
Published: November 2003

SUMMARY
Superantigen-mediated T cell activation requires the participation of antigen-presenting cells (APC). Once superantigen has bound class II MHC molecules on the surface of APC, it then can interact with the T cell receptor to induce T cell activation. Superantigen-mediated T lymphocyte activation, along with its consequent cytokine production is thought to be the basis for the pathophysiology of conditions such as toxic shock syndrome, Kawasaki’s disease and possibly rheumatoid arthritis. We examined the role of CD56+ NK lymphocytes in the interaction between superantigens and T lymphocytes. First, we found that a subpopulation of CD56+ cells freshly isolated from human peripheral blood expressed class II MHC molecules. The amount of HLA-DR expression varied between individuals, ranging from 9.3% to 37.7%. CD56+ (NK) cells were purified from the peripheral blood by cell sorting and were tested for their ability to support SEB-mediated T cell activation as assessed by surface expression of IL-2 receptor α-chain (CD25) on CD3+ lymphocytes. We observed that when enriched T cells were incubated with SEB in the presence of NK cells, there was a significant up-regulation of CD25 expression on the T cells. When HLA-DR+ cells were removed from sorted CD56+ populations, the remaining HLA-DR− NK cells were unable to support SEB-mediated T cell activation. Also, SEB up-regulated the expression of HLA-DR on CD56+ cells in peripheral blood mononuclear cell (PBMC) populations after 24 h of incubation, implying that the ability of NK cells to function as superantigen-presenting cells is up-regulated by superantigens themselves. Together, these data demonstrate for the first time that human CD56+HLA-DR+ NK cells can function as superantigen-presenting cells, and imply that NK cells may be involved in the activation of non-specific T cell reactivity during early host defences against superantigen-elaborating microorganisms in vivo. Furthermore, the physical linkage of NK cells and T cells by the interaction of superantigen with HLA class II molecules and T cell receptors, respectively, may lead to NK cell activation and augmented lytic potential, helping to clear the body of superantigen-elaborating microorganisms.
Circulating IgA, IgG, and IgM class antibody against Haemophilus parainfluenzae antigens in patients with IgA nephropathy
Authors: Suzuki S , Nakatomi Y , Odani S , Sato H , Gejyo F , Arakawa M 
Published: November 2003

SUMMARY
We previously demonstrated a close relationship between the outer membranes of Haemophilus parainfluenzae (HP) antigens (OMHP) and IgA nephrophathy (IgAN). Our objective was to clarify the relationship among IgA, IgG, and IgM class antibody against OMHP in the sera of 44 patients with IgAN and 62 patients with other glomerular diseases (OGD) by ELISA. Patients with IgAN showed a significantly higher level of IgA antibodies (P &lt; 0.0005) and IgG antibodies (P &lt; 0.001) against OMHP, than did patients with OGD. Positive correlations were observed between IgA and IgG antibodies, between IgA and IgM antibodies, and between IgG and IgM antibodies against OMHP in the sera of patients with IgAN. Immunoblotting showed that IgA, IgG, or IgM antibodies against OHMP in the sera of all patients with IgAN bound to the components of OMHP. Amino acid sequences of three components of OMHP recognized by the sera from patients with IgAN revealed homology with those reported for outer membrane protein (OMP) P6 precursor, OMP P5, and P2 porin protein of H. influenzae. Results suggest that patients with IgAN have glomerular deposits of OMP P6 precursor, OMP P5, or P2 porin protein of HP, and a specific increase in the production of IgA antibodies against OMHP via polyclonal activation against these, with switching of production from one isotype to another, e.g. from IgM to IgA.
Beneficial effect of Salmonella typhimurium infection and of immunoglobulins from S. typhimurium-infected mice on the autoimmune disease of (NZB×NZW)F1 mice
Authors: Matsiota-Bernard P , Hentati B , Pié S , Legakis N , Nauciel C , Avrameas S 
Published: November 2003

SUMMARY
Various infections can precede or aggravate autoimmune diseases. Yet a beneficial effect of infection has also been described and various mechanisms have been postulated to explain this effect. The aim of this study was to examine the hypothesis that infection can have an immunoregulatory effect on the autoimmune process via the increased production of natural polyreactive antibodies. The effect of Salmonella typhimurium infection on the lupus-like disease of (NZB×NZW)F1 (B/W) mice was therefore studied. The effect of IgM and IgG preparations isolated from the serum of S. typhimurium-infected C57Bl/6 and CBA mice on the autoimmune disease of B/W mice was also tested. C57Bl/6 and CBA mice were chosen because they are respectively genetically susceptible and resistant to S. typhimurium infection and they differ in their antibody response during the early phase of infection. CBA mice can mount a specific anti-bacterium antibody response, whereas C57Bl/6 mice present increased production of polyreactive antibodies. The infection effect was evaluated on several disease parameters, i.e. survival, incidence of high grade proteinuria and serum IgM and IgG antibody activity directed against a panel of autoantigens. Our main findings were: (i) infection of B/W mice with an attenuated strain of S. typhimurium delayed the course of the autoimmune disease when performed before the appearance of autoimmune symptoms; and (ii) IgM and IgG preparations from S. typhimurium-infected C57Bl/6 mice had a similar effect, whereas the IgM and IgG preparations from infected CBA mice, as well as from normal C57Bl/6 and CBA mice, were ineffective. These results suggest that S. typhimurium infection can beneficially influence the development of the autoimmune disease of B/W mice. The immunoregulatory effect of the infection seems to be related, at least partially, to the increase of a particular population of antibodies, the polyreactive antibodies.
Structural differences between the human and mouse 52-kD Ro autoantigens associated with poorly conserved autoantibody activity across species
Authors: Keech C L , Gordon T P , McCluskey J 
Published: November 2003

SUMMARY
Anti-nuclear autoantibodies found in human autoimmune diseases frequently cross-react with homologous autoantigens in distant species, supporting the notion that autoantibodies target conserved functional domains. However, the 52-kD Ro(SS-A) protein is an exception, in that human autoantibodies are not known to recognize any equivalent antigen in the cells of rodents and other non-primate species. To understand this lack of cross-reactivity we have isolated cDNAs encoding the mouse 52-kD Ro molecule. The cDNA encoding mouse 52-kD Ro revealed an open reading frame of 470 amino acids, with 70% sequence identity to the human 52-kD Ro antigen. The putative leucine-zipper and zinc-finger motifs present in human Ro52 were conserved in the mouse protein. Recombinant mouse 52-kD Ro protein reacted with human autoantibodies by ELISA and immunoblot, but with approximately 10-fold lower reactivity than recombinant human 52-kD Ro protein under the same conditions. Detection of both human and mouse 52-kD Ro by immunoblot was dependent on antigen concentration which was limiting in the cell equivalents generally used in immunoblot assays. Differential chaotropic disruption of antibody binding suggested a lower avidity of human autoantibody binding to the mouse 52-kD Ro protein compared with the human antigen. Thus the poor reactivity of native mouse 52-kD Ro with human autoantibodies is associated with species divergence diffusely distributed throughout the primary structure of the 52-kD Ro molecule.
Affinity-purified cardiolipin-binding antibodies show heterogeneity in their binding to oxidized low-density lipoprotein
Authors: Vaarala O , Puurunen M , Lukka M , Alfthan G , Leirisalo-Repo M , Aho K , Palosuo T 
Published: November 2003

SUMMARY
Antiphospholipid antibodies in autoimmune sera have been shown to react with a complex of phospholipids (cardiolipin) and a plasma phospholipid-binding protein, β2-glycoprotein I (apolipoprotein H). The binding of these antibodies was inhibited by oxidized low-density lipoprotein (LDL) in sera from patients with systemic lupus erythematosus (SLE), suggesting cross-reactivity between antiphospholipid antibodies and antibodies binding to oxidized LDL. We purified antiphospholipid antibodies by cardiolipin-polyacrylamide column from seven SLE sera and studied the reactivity of eluted fractions with cardiolipin–β2-glycoprotein I complex and oxidized LDL (malondialdehyde-conjugated LDL) in solid-phase enzyme immunoassay. In four sera the binding of IgG antibodies to cardiolipin–β2-glycoprotein I complex and to oxidized LDL appeared in the same fractions, whereas in three sera reactivities against cardiolipin and oxidized LDL were observed, at least in part, in separate fractions. The binding to solid-phase cardiolipin was dependent on the presence of exogenous β2-glycoprotein I in all fractions. Our findings show that antiphospholipid antibodies are heterogeneous in their binding to oxidized LDL, indicating that these two antibodies may have different subspecificities. Some eluted fractions reacted only with oxidized LDL, and did not show binding to cardiolipin–β2-glycoprotein I complex, suggesting that the lipid part in the antigenic complex might be responsible for the cross-reactivity of these antibodies. Accordingly, the biological functions of antibodies against phospholipid–β2-glycoprotein I complex and antibodies against oxidized LDL may also be different.
The allergenic properties of fresh and preserved Hevea brasiliensis latex protein preparations
Authors: Kekwick R , Bhambri S , Chabane M H , Autegarden J-E , Levy D A , Leynadier F 
Published: November 2003

SUMMARY
The allergenic properties of the proteins of two lyophilized fractions of fresh natural rubber latex obtained by ultracentrifugation, the C serum and the sedimented bottom or lutoid fraction, have been compared with those of the serum proteins of two samples of high ammonia latex (HAL), [A]HALS obtained from HAL stored for more than 1 year, and [M]HALS derived from HAL stored for 6 weeks before ultracentrifugation and lyophilization. The most potent source of allergenic polypeptides both for skin prick testing of latex-sensitive patients and for immunoblots of their blood serum was the lutoid fraction of fresh latex. Skin prick tests and immunoblots of patients' sera showed that the allergenicity of the ammoniated latex decreased during storage. Skin prick tests using fractions of [A]HALS, C serum and lutoid proteins obtained after passage through a Sephacryl S300 column showed that the components of all three preparations which eluted in the largest volumes were almost equally effective in provoking the largest number of responses. Immunoblots of the sera of 43 latex-sensitive individuals showed that the majority (66%) of sera of the adult allergic patients reacted with a polypeptide of 19 kD. No characteristic pattern of binding latex polypeptides could be recognized in the sera from patients who were also asthmatic or from those who had had an anaphylactic response to latex proteins.
Idiotype-induced T cell stimulation requires antigen presentation in association with HLA-DR molecules
Authors: Yi Q , Holm G , Lefvert A K 
Published: November 2003

SUMMARY
An important and yet unresolved question concerns the mode of T cell recognition of idiotypic epitopes on immunoglobulin molecules in humans. Results from murine and human studies show that some idiotype-specific T cells recognize conformational epitopes on immunoglobulin, and such T cells are not MHC-restricted. In the present study T cell stimulation induced by idiotypic determinants on the autologous monoclonal IgG (M-components) from patients with monoclonal gammopathies was studied. In parallel, T cell stimulation in response to a conventional antigen, purified protein derivative, was also examined. It is shown that, as with conventional antigen, idiotype-induced T cell stimulation requires the presence of antigen-presenting cells (APC; monocytes and/or B cells), and is MHC class II (DR)-restricted. B cells, but not monocytes, can present idiotypic determinants to T cells at very low antigen concentrations, while monocytes do so only when antigen is present at high concentrations. Antigen processing and presentation is abrogated by treatment of APC with chloroquine. In conclusion, our study demonstrates that human idiotype-specific T cells recognize processed idiotypic determinants presented by MHC class II (HLA-DR) molecules on APC, and that B cells require about 1000-fold less antigen than monocytes.
Effect of intrajejunal elemental diet perfusion on local secretion of soluble CD4 and CD8
Authors: Desreumaux P , Levy A , Vaerman J P , Capron M , Cortot A , Colombel J F 
Published: November 2003

SUMMARY
The effects of nutrients on the mucosal immune system are poorly understood. The aim of this work was to study the cellular mucosal immune response to intrajejunal perfusion of an elemental diet (ED) or a control (C) electrolyte solution by measuring jejunal secretion of soluble CD4 (sCD4) and sCD8. sCD4 and sCD8 are markers of helper/inducer and suppressor/cytotoxic regulatory functions of T cells, respectively. A four lumen tube with a proximal occluding balloon at the angle of Treitz was used for jejunal perfusion in seven healthy volunteers (mean age 23 years). The length of the test segment was 40 cm. The jejunum was successively perfused with C for 80 min and then with ED containing 21.3g/l of free amino acids and 104.2g/l of oligosaccharides for 100 min. Jejunal fluid and serum concentrations of sCD4 and sCD8 were measured and their jejunal outputs calculated. When compared with C perfusion, jejunal perfusion with the ED resulted in a significant increase of sCD8 but not sCD4 jejunal secretion rates. sCD8 jejunal values increased early after ED perfusion and stayed at roughly the same level during the perfusion. Serum concentrations of sCD4 and sCD8 were not modified during ED perfusion. These data support the hypothesis that ED suppresses the immunologic tone of the gut, which could explain its beneficial effect in the management of intestinal inflammatory disease.
Dose- and time-dependent activation of rat alveolar macrophages by glucocorticoids
Authors: Broug-Holub E , Kraal G 
Published: November 2003

SUMMARY
Effects of glucocorticoids on immune functions are generally thought to be suppressive and anti-inflammatory. However, most reports dealing with this issue describe effects of long-term treatment with high doses of glucocorticoids on immune functions. In the present study we have investigated both dose and timing effects of exposure of alveolar macrophages with dexamethasone on lipopolysaccharide (LPS)-induced IL-1β and nitric oxide secretion. For this purpose, alveolar macrophages were preincubated with various doses of dexamethasone during varying intervals, followed by stimulation of the cells with endotoxin, either in the absence or presence of dexamethasone. Subsequently, the effects of this treatment on IL-1β and nitric oxide secretion were measured. It was shown that both short-term incubation of alveolar macrophages with high doses of dexamethasone and long-term incubation with low doses of dexamethasone lead to enhanced nitric oxide and enhanced IL-1β secretion upon subsequent stimulation of the cells with LPS. In contrast, long-term incubation of alveolar macrophages with high-dose dexamethasone leads to decreased IL-1β and nitric oxide secretion upon subsequent stimulation. Thus, it is concluded that the effects of dexamethasone on rat alveolar macrophages are both time- and dose-dependent. It is therefore argued that effects of glucocorticoids on immune functions are not a priori suppressive, but that both dose and timing effects should be taken into account.
T cell receptor (TCR) repertoire and function of human epidermal T cells: restricted TCR Vα-Vβ genes are utilized by T cells residing in the lesional epidermis in fixed drug eruption
Authors: Komatsu T , Moriya N , Shiohara T 
Published: November 2003

SUMMARY
Human epidermis contains a phenotypically heterogeneous population of T cells. No information, however, is available regarding the TCR repertoire of these T cells and their relevant physiologic and pathologic functions in vivo. To this end, T cells were prepared from the lesional epidermis in two patients with fixed drug eruption (FDE) and their phenotype, function and TCR repertoire were examined in parallel. Both epidermal T cells, termed FDE-1 and -2 cells, respectively, expressed αβ TCR, but displayed some phenotypic heterogeneity. These T cells were induced to display cytolytic activity by ligation of the CD3/TCR-αβ complex. Comparative analyses of TCR Vα and Vβ expression in the epidermal T cells and the paired peripheral blood lymphocytes (PBL) by quantitative polymerase chain reaction (PCR) demonstrated that the epidermal T cells, but not the paired PBL, utilized a very limited range of Vα and Vβ genes. These results indicate that some expansion or preferential migration of epidermal T cells that recognize a restricted set of antigens expressed within the epidermis could occur in situ following ingestion of the causative drug. The persistence of these epidermal T cells in FDE lesions suggests their pathologic role in a drug-induced flare.