bluuebunny/crossref_metadata_2025_split huggingface dataset:
Influence of the G2m(n) allotype and age on IgG subclass distribution in antibodies to dietary proteins in children with coeliac disease
Authors: RAUTONEN N , RAUTONEN J , SAVILAHTI E 
Published: July 2010

SUMMARYIn 47 children with coeliac disease, IgG 1 was the dominant IgG subclass (mean 61 %) in antibodies to gliadin, a protein component of wheat; IgG2 (22%) and IgG3 (15%) were also found. Very little IgG4 (3%) was detected. Both G2m(n)allotype and the age of the patient had an independent effect on the subclass distribution. The effects of these two factors seem similar to those described earlier on responses to polysaccharides; both G2m(n) and age increase the expression of IgG2 antibodies and concomitantly the share of IgGl is decreased. The average increase in the share of IgG2 brought about by n/n-genotype was 25-3% (95% confidence limits 12.2–38.4%; P&lt;0.001) and that brought about by each additional year of age of the patient 11% (0.3–1.9%;P=0.006). IgG antibodies to /Mactoglobulin and ovalbumin consisted mainly of IgGl and IgG4. The titres of the IgG subclasses were low and in many cases below detection level. No association with G2m(n) genotype and share of IgGl or IgG4 could be demonstrated. Age was inversely correlated with the shares of IgGl in antibodies to β-Mactoglobulin and ovalbumin.
Enhanced expression of the tumour necrosis factor/cachectin gene in peripheral blood mononuclear cells from patients with systemic vasculitis
Authors: DEGUCHI Y , SHIBATA N , KISHIMOTO S 
Published: July 2010

SUMMARY
The expression of tumour necrosis factor-alpha (TNF-α) gene in peripheral blood mononuclear cells from patients with systemic vasculitis. periarteritis nodosa and Wegener's granulomatosis, has been studied by RNA dot blot and Northern blot assays. We further examined the transcriptional level of TNF-α gene in peripheral blood mononuclear cells from these patients by performing nuclear run on transcription assay. We demonstrate enhanced TNF-α gene expression in mononuclear cells from these patients compared with healthy subjects and patients with bronchial asthma. These findings suggest that the enhanced transcription of TNF-α gene in peripheral blood mononuclear cells from patients with systemic vasculitis may be involved in the pathophysiology/pathogenesis of these diseases by cylokine dysregulation.
Stimulation of neutrophil elastase and myeloperoxidase release by IgG fragments
Authors: ECKLE I , KOLB G , HEISER C , HAVEMANN K 
Published: July 2010

SUMMARYHuman leucocyte elastase (HLE) cleaves IgG into Fab and Fc fragments. The Fc fragment bears an elastase-specific antigen and has previously been reported to be found in synovial fluid during rheumatoid arthritis, In addition, biological activity of clastasc-specific Fc fragments has been described in modulating granulocyte oxidative metabolism. To investigate further regulatory effects of the elastase-induced IgG cleavage products, we tested the elaslase and myeloperoxidase release of granulocytes. IgG fragments induce no enzyme release of unstimulated neutrophils. But elastase and myeloperoxidase release of cytochalasin b/FMLP-treated neutrophils is stimulated in a dose-dependent manner by the Fab fragments. The extent of stimulation depends on stimulus concentration and is at its maximum for low (e.g. 2.5 × 10−8m) FMLPconcentration. Ten nanomoles Fab/4 × 106 PMN augment elastase release to 206% and myeloperoxidasc release to 155% after prestimulation with 2.5 × 10−8 m FMLP. Fc fragments stimulate elaslasc release to 162% but no MPO release. Untreated IgGl and analog Fab and Fc fragments produced by papain cleavage react similarly. Elastase-generated IgG fragments may therefore up-regulate their concentration by stimulating elastase release. The concomitantly stimulated release of myeloperoxidase may influence bactericidal activity and termination of oxidative burst.
A complex component modulating immune-deficient cells in leprosy patients leading to loss of viability ofMycobacterium leprae—a possible vaccine
Authors: MAROLIA J , ROBINSON P , MAHADEVAN P R 
Published: July 2010

SUMMARYMacrophages from peripheral blood of leprosy patients, both multi-bacillary and paucibacillary are unable to kill phagocytosed Mycobacterium leprae due to their inability to produce superoxide (O2−) and hydroxyl radicals (OH ·). The macrophages from healthy individuals are able to kill M. leprae along with release of O2− and OH · radicals. The deficiency in the macrophages of both types of leprosy patients is removed by activation of these cells when exposed to a culture supernatant obtained after stimulation of peripheral blood mononuclear cells from the same patients with delipidified cell components of M. leprae which are most likely cell wall proteins. The activation of macrophages also leads to recognition of whole live M. leprae as an antigen by cells from lepromatous patients. This activation of the phagocytes by delipidified cell components is blocked by cyclosporin A, indicating the possible role of several steps involved in immune activation of cells. The observations thus indicate the significant ability of delipidified cell components to eliminate the deficiencies in the macrophages from leprosy patients and restore them to behave like the cells from healthy individuals. Considering all these, it is suggested that delipidified cell components could be potential modulators, and are probably capable of functioning as a vaccine for leprosy.
Anti-myeloperoxidase antibodies in systemic vasculitis
Authors: LEE S S , ADU D , THOMPSON R A 
Published: July 2010

SUMMARY
Anti-neutrophil cytoplasmic antibodies (ANCA) are important diagnostic markers in vasculitic disorders. In a study of 164 patients with various clinical syndromes associated with vasculitis, 60 were found to have the antibody, as detected by indirect immunofluorescence; 23 had the so-called perinuclear antibody pattern, and of these, 15 had antibodies to neutrophil myeloperoxidase in an ELISA. These patients had multi-system involvement, and 14 of the 15 had histological evidence of small-vessel arteritis in the kidneys. In preliminary experiments, the isolated IgG from one patient was shown to inhibit luminol-dependent chemiluminescence of fluid phase myeloperoxidase.
Liver membrane antibodies (LMA) recognize a 26-kD protein onthe hepatocellular surface
Authors: HOPF U , JAHN H-U , MÖLLER B , STEMEROWICZ R , WITTENBRINK C , KLEIN R , BERG P A 
Published: July 2010

SUMMARY
Sera from 82 patients with chronic inflammatory liver diseases and from patients with systemic lupuserythemalosus (SLE). rheumatoid arthritis (RA) and Hashimoto's thyroiditis were studied byimmunoblotting against purified liver plasma membranes (LPM) and soluble liver protein (SLP)fractions from different species after previous separation by SDS-PAGE. Eighteen of 19 sera withLMA of IgG type in immunofluorescencc assay and six LMA-negatiuve sera (three sera from patientswith RA) showed antibodies of the IgG or IgM classes against a protein with a molecular weight of 26kD which was present in LPM and SLP fractions from rats, rabbits, pigs and humans. The reactionwith 26-kD liver protein did not correlate with other known autoantibody-antigen systems. All serawere negative in the 26-kD region with liver mitochondria, liver microsomes and soluble proteins ofkidney (with one exception), heart and gut from the rat. The 26-kD protein was purified by affinitychromatography on immobilized anti-26-kD protein antibodies from patients, eluted from the 26-kDband of immunoblots. Studies with purified 26-kD liver protein and with SLP as antigens afterseparation in two-dimensional electrophoresis confirmed that patient serum and experimental rabbitantiserum react with the same protein. Eluted patient antibodies and rabbit antisera showed a linearfluorescence pattern on isolated hepatocytes from rat and rabbit. The data indicate that one of thetarget antigens of LMA is a species-nonspecific 26-kD protein located on the hepalocellular surface.
Tumour necrosis factor production and cell-mediated immunityin anorexia nervosa
Authors: SCHATTNER A , STEINBOCK M , TEPPER R , SCHONFELD A , VAISMAN N , HAHN T 
Published: July 2010

SUMMARYFourteen patients with anorexia nervosa (AN) were studied for the production of tumour necrosisfactor (TNF), the activation of the interferon (IFN) system and cell-mediated cytotoxicity (CMC)and the results were compared with 16 age-matched healthy women. AN patients had significantlyincreased spontaneous TNF production by peripheral blood mononuclear cells (PBMC) in vitro(16 ± 5 U/ml versus 4 ± 3 U/ml in the control group; P &lt; 005), although no TNF was detectable in theplasma from either group. TNF production in vitro, following stimulation of PBMC byphytohaemagglutinin (PHA) or tumour cells, was similar in AN patients and controls; however, lipopolysaccharide (LPS) induced TNF production was found to be lower in AN (P &lt;0.1). CMC wassignificantly lower in AN patients (4 ± 2 versus 10 ± 3 in controls, expressed as lytic units/106 cells;P&lt;0.05), but no difference could be found between AN and controls in IFN activity as reflected bythe level of the IFN-induced enzyme 2′-5′oligoadenylate synthetase (2-5A) in PBMC. Beta-endorphins in the plasma were higher in the AN group (P &lt; 0.05) but these levels could not becorrelated to those of lFN, CMC or TNF. Defective CMC and increased TNF production by PBMCin patients with anorexia nervosa may possibly result from the nutritional deficiencies andneuroendocrine abnormalities associated with the disease, and may contribute to the pathophysiology of AN.
Pathogenesis of experimental lupus nephritis: a role foranti-basement membrane and anti-tubular brush border antibodiesin murine chronic graft-versus-hostdisease
Authors: BRUIJN J A , HOGENDOORN P C W , CORVER W E , VAN DEN BROEK L J C M , HOEDEMAEKER P J , FLEUREN G J 
Published: July 2010

SUMMARYThe pathogenesis of renal involvement was studied in murine chronic graft-versus-host disease(GVHD), which is a model for human systemic lupus erythematosus. GVHD was induced by Tour i.v.injections of lymphocytes from DBA/2 donor mice into (C57BL/10 x DBA/2)Fi hybrids at 3-4-dayintervals. Two weeks after the first injection, antibodies were found to have been deposited in themesangium and along the glomerular basement membrane (GBM) in a linear arrangement, whichchanged to a granular pattern after 6–8 weeks. In this stage, large electron-dense complexes werepresent both subepithelially and subendothelially along the GBM. Proteinuria increased up to11 300 ± 2140 μg/ 18 h. Indirect immunofluorescence studies and ELISA showed that sera and kidneyeluates contained autoanlibodies directed against nuclear antigens and GBM component laminin aswell as against renal tubular epithelial antigens (RTE). The specificity of the anti-RTE antibodies wasfurther characterized by the use of absorption techniques as well as immunoblotting. The early linearimmunofluorescence pattern seems to be associated with glomerular binding of anti-GBMantibodies, while electron-dense complex formation in later stages may be induced by thesuperimposed deposition of anti-RTE antibodies. Similar phenomena were recently described inHeymann's nephritis in the rat, a model for human membranous nephropathy.
Hashimoto's thyroiditis manifesting monoclonal lymphocytic infiltration
Authors: MATSUBAYASHI S , TAMAI H , MORITA T , FUKATA S , MATSUZUKA F , SUZUKI T , KUMA K , NAGATAKI S , VOLPÉ R 
Published: July 2010

SUMMARY
Hashimoto's thyroiditis (HT) and lymphoma arc sometimes difficult to distinguish between. Moreover, lymphoma sometimes develops in a thyroid gland from pre-existing HT. Open- or large-needle biopsy usually distinguishes between them; the specimen may be examined histologically and subjected to immunohistochemistry. Another possible method of examination is fine-needle aspiration biopsy (FNAB). The cells obtained may be evaluated cytologically, and subjected to flow cytometry, using various antibodies. In this study, anti-kappa and anti-lambda antibodies are especially important, as a gross predominance of kappa or lambda B lymphocytes infiltrating the thyroid is evidence for a B cell monoclone. In this study, 15 patients were selected because of their rapidly growing goitres. They all underwent FNAB. Five had cytology typical of HT, and no evidence of monoclonality on flow cytometry. They were diagnosed as HT without further histopathology. The remaining 10 patients had cytology suspected of lymphoma, or evidence of monoclonality on flow cytometry, or both. These patients underwent open- or large-needle biopsy. Only three of them were diagnosed histopathologically as lymphoma; the other seven were diagnosed histopathologically as HT, making 12 cases of HT in all. Five of these 12 cases, and one of the three cases of lymphoma showed flow cytometrical evidence of monoclonality; thus evidence of monoclonality from FNAB, while interesting, does not necessarily serve to differentiate between HT and lymphoma. Furthermore, the immunohistochemical assessment of monoclonalily did not correlate with the flow cytometrical assessment. Follow-up evidence will be required to discover whether those patients with a B cell monoclone in their HT are the ones who develop a lymphoma.
The effect of cyclosporin A on the interstitial mononuclear cell infiltration and the induction of Heymann's nephritis
Authors: GRÖNHAGEN-RISKA C , VON WILLEBRAND E , TIKKANEN T , HONKANEN E , MIETTINEN A , HOLTHÖFER H , TÖRNROTH T 
Published: July 2010

SUMMARY
Heymann's nephritis was induced with brush-border (BB) antigen. Interstitial mononuclear cell infiltration was studied with cytological examinations of fine-needle aspiration biopsies (FNAB), and with immunoperoxidase stains of frozen sections with monoclonal antisera. The effect of cyclosporin A (CyA), 20 mg/kg when administered intraperitoneally for 8 days in association with both initial immunization, and with the booster 4 weeks later, on the interstitial leukocyte infiltration and on the development of membranous glomerulonephritis (MGN) and proteinuria were investigated. Another group of rats was immunized, but not given CyA. Experimental animals were killed in groups 3, 6 and 20 weeks after initial immunization. CyA inhibited significantly the initial interstitial lymphocyte and blast cell response at 3 weeks (FNAB), but did not inhibit the secondary response after the booster. The anti-BB titre reacted in a similar fashion. Immunoperoxidase stains indicated a clearly suppressed T suppressor/cytolytic (T s/c) cell response. Glomerular basement membrane (GBM) deposits of IgG developed more slowly and were more scarce in the CyA-treated rats, when compared with the untreated group. Only one out of 15 CyA treated rats developed C3 deposits in the GBM during the course of the study, and none developed proteinuria, when most untreated rats (10/ 17) had C3 deposits and were nephrotic at 20 weeks. Thus, CyA depressed the initial interstitial cellular response after immunization with BB antigen, and also inhibited the development of antibody response, C3 deposits and proteinuria of Heymann nephritis. These effects of CyA may be contributed to an inhibited amplification of the autoimmune response associated with interstitial damage and continuous release of autoantigen.
Role of antigen-presenting cells in variation in immunogenicity of mycobacteria
Authors: SHROFF K E , SAINIS K B , SENGUPTA S R , KAMAT R S 
Published: July 2010

SUMMARYThe route of immunization was observed to play a significant role in deciding the outcome of immunization with killed mycobacterial vaccines. Whereas the slow growers were immunogenic by both intraperitoneal and intradermal routes, the rapid growers were immunogenic only by intradermal route. The non-responder state of mice to Mycobacterium vaccae by i.p. route of immunization could be corrected by prior treatment with poly I:poly C, an interferon inducer, or indomethacin, a prostaglandin inhibitor. Antigen-presenting efficiency of peritoneal and spleen cells were compared employing M. vaccae and M. tuberculosis H37Rv primed T cells and corresponding sonicates as antigens in an in vitro lymphocyte transformation test. Irradiated spleen cells presented both the antigens efficiently. However, with peritoneal cells as antigen-presenting cells, proliferative response against only M. tuberculosis was observed; proliferation of M. vaccae primed T cells was very poor. Peritoneal cells of poly I:poly C treated mice showed distinct improvement in their efficiency of presentation; even paraformaldehyde-fixed peritoneal cells gave an efficient stimulation with M. vaccae. The percentage of la-positive fraction in peritoneal cells was very low (5.95%) in comparison with spleen cells (38.37%). Poly I: poly C treatment resulted in increase in the la-positive cell fraction of the peritoneal cells to 24.5%.
Requirement of the T cell receptor for antigen presentation by T lymphocytes. Effect of envelope glycoproteins of HIV-1 on antigen presentation by T cells
Authors: CHIRMULE N , KALYANARAMAN V S , SLADE H , OYAIZU N , PAHWA S 
Published: July 2010

SUMMARYWe have developed CD4+, tetanus antigen-specific T cell clones that proliferate in the presence of tetanus antigen and autologous irradiated peripheral blood leucocytes (PBL) as antigen-presenting cells (APC). There have been several reports that T cells can present antigen themselves. We have used tetanus antigen-specific T cell clones to examine the effects of envelope glycoproteins of HIV-1 on processing and presentation of antigen to T cells. Cloned T cells were pre-incubated with soluble crude preparation of tetanus antigen for 4 h at 37°C, irradiated, and used as APC (T-APC). These cells could present antigen, as assessed by the ability of the autologous cloned T cells to proliferate. Resting T cells and phytohaemagglutinin-activated T cell blasts from autologous PBL could not present tetanus antigen to the responder cloned T cells. Antigen presentation by T-APC was abrogated by treating cells with anti-HLA-DR but not by anti-HLA-DQ monoclonal antibodies; treatment of tetanus antigen-pulsed T-APC with anti-tetanus antibody also blocked the ability of these cells to induce proliferation in responder T cells. Antigen presentation by cloned T cells was by a chloroquine-resistant pathway. Pretreatment of T-APC with envelope glycoprotein of HIV-1, gp120. did not affect the proliferative responses of the responder T cells. These data suggest that gp 120 does not inhibit the antigen-presenting function while suppressing antigen-specific responses.
Degradation of aggregates of activated C3 (C3b) by monocytes of patients with rheumatoid arthritis is related to vasculitis
Authors: HEURKENS A H M , BREEDVELD F C , KEUR C VD , BRAND R , DAHA M R 
Published: July 2010

SUMMARY
We investigated whether a decreased complement receptor expression or function of monocytes isolated from peripheral blood of 52 patients with rheumatoid arthritis (RA) and rheumatoid vasculitis (RV) could account for the previously observed diminished degradation of immune complexes by monocytes of patients with RA and RV. On average, monocytes from all patients expressed significantly less CR1, and degraded significantly less AC3b when compared with monocytes of healthy controls. In addition, monocytes from RV patients degraded significantly less AC3b when compared with monocytes from patients with RA. The expression of both CR1 and CR3 on monocytes of RV patients was lower compared with RA patients but this difference was only significant for CR3. No differences were found between AC3b degradation and the expression of CR1 and CR3 between patients with active and inactive RA. Using linear discriminant analysis on the variables AC3b, CR1 and CR3, 94% of the patients could be classified correctly as healthy controls, RA or RV, suggesting a true multi-variate relationship between these parameters and patients groups. Our results suggest that the diminished capacity of monocytes from RA patients to degrade AC3b is due partly to a decreased expression of CR1 and CR3.
Immunological study of histologically non-involved jejunum during Crohn's disease: evidence for reduced in vivo secretion of secretory IgA
Authors: MARTEAU P , COLOMBEL J F , NEMETH J , VAERMAN J P , DIVE J C , RAMBAUD J C 
Published: July 2010

SUMMARY
We studied the local humoral immunity of histologically non-involved jejunum in patients with Crohn's disease. Normal subjects and patients with ulcerative colitis served as controls. Jejunal fluid samples were collected during segmental jejunal perfusion, under an occluding balloon and the in vivo jejunal secretion of the following proteins was determined: albumin, orosomucoid, transferrin, α2-macroglobulin, secretory component, monomeric and polymeric IgA, IgG, and IgM. The densities and number of IgA-, IgG-, and IgM-containing cells in the lamina propria of the jejunum were measured on perendoscopic biopsies. Jejunal secretion of polymeric IgA and the density of IgA-containing plasma cells in the lamina propria were significantly lower in patients with Crohn's disease than in both control groups. This abnormal intestinal immune response, which was not correlated to the activity of the disease, might be involved in its pathogenesis.
The specificity of the antibody response to internal antigens ofAscaris: heterogeneity in infected humans, and MHC (H-2) control of the repertoire in mice
Authors: KENNEDY M W , TOMLINSON L A , FRASER E M , CHRISTIE J F 
Published: July 2010

SUMMARYChildren from an area of Africa endemic for the large round worm of humans, Ascaris lumbricoides, were found to vary considerably in the specificity of their serum IgG response to the internal antigens of the parasite. This was particularly noticeable for responses to a 14-kD protein (ABA-I) of the parasite that has previously been shown to be the subject of a strong IgE antibody response in infected animals. The possibility that this heterogeneity in immune repertoire has a genetic basis was explored in inbred mice infected with Ascaris suum. This showed that no strain responded to all the potential antigens, that the recognition profiles of strains bearing independent haplotypes were unique, and only H-2-indentical strains had responses of similar specificities. Major histocompatability complex (MHC) restriction was confirmed using H-2-congenic animals on BALB and BIO backgrounds, which responded according to their H-2 haplotype. It is likely, therefore, that it is the MHC which controls the repertoire to Ascaris antigens in infected people. If this is so, then there will be implications for immunopathology associated with ascariasis. and possibly also for resistance and susceptibility to infection.
Tetrandrine, a plant alkaloid, inhibits the production of tumour necrosis factor-alpha (cachectin) hy human monocytes
Authors: FERRANTE A , SEOW W K , ROWAN-KELLY B , THONG Y H 
Published: July 2010

SUMMARYHuman mononuclcar leucocytes (MNL) or the adherent fraction (monocytes) produced tumour necrosis factor-alpha (TNF-α) (by EL1SA) in culture when stimulated with killed Staphylococcus aureus. The bisbenzylisoquinoline alkaloid, tetrandrine inhibited the capacity of MNL and monocytes to produce TNF-α at a concentration range of 0·1 to 5 μg/ml. Tetrandrine may be potentially useful in the treatment of inflammatory diseases in which TNF-α plays a major role.