bluuebunny/crossref_metadata_2025_split huggingface dataset:
The perinuclear factor, a rheumatoid arthritis-specific autoantigen, is not present in keratohyalin granules of cultured buccal mucosa cells
Authors: HOET R M , VOORSMIT R A C A , VAN VENROOIJ W J 
Published: July 2010

SUMMARY
Rheumatoid arthritis patients have antibodies in their serum directed against the perinuclear factor, a protein component present in keratohyalin granules in the cytoplasm of human buccal mucosa cells. The anti-perinuclcar factor (APF) can only be delected by an indirect immunofluorescence test performed on fresh buccal mucosa cells from 'selected donors'. To obtain a more reliable antigen source and to gain more insight into the origin and nature of the perinuclear factor we attempted to culture perinuclcar factor-containing buccal mucosa cells. Here we describe the successful culturing of such cells, which, however, did not contain keratohyalin granules nor the perinuclcar factor. By adding the phorbol ester 12-o-tetradecanoylphorbol-13-acctate (TPA) we were able to induce keratohyalin granules in both cultured primary buccal mucosa cells and a squamous carcinoma cell line of the cheek (SqCC/Y1). These induced keralohyalin granules do contain the protein profilaggrin, which in vivo, in fresh buccal mucosa cells, co-localizes with the perinuclear factor. However, we were not able to demonstrate the presence of the perinuclear factor, not even after induction of terminal differentiation of the cultured cells nor after Epstein-Barr virus infection. Our results suggest that the perinuclear factor, in contrast to profilaggrin. is not an integral component of buccal mucosa cells.
Nephrotoxic serum nephritis in nude rats: the roles of host immune reactions
Authors: SATO T , OITE T , NAGASE M , SHIMIZU F 
Published: July 2010

SUMMARYA description is made of renal lesions in rats induced by heterologous (rabbit) nephrotoxic serum with or without subsequent host immune reactions against it and the effects of immune reactions on the course of classical nephrotoxic serum (Masugi) nephritis are discussed. The disease was induced by injecting congenitally athymic ACI nude rats (rnu/rnu) and their normal heterozygous littermates (rnu/+) with rabbit anti-rat glomerular basement membrane (GBM) antiserum. In the autologous phase, rat IgG and immunoglobulins were localized in a linear pattern along capillary walls only in nephritic heterozygous rats. In the indirect plaque-forming cell (PFC) assay against rabbit immunoglobulins in the autologous phase, significantly more PFC could be detected in nephritic heterozygous rats than in nephritic nude rats. The nude and heterozygous rats were essentially the same with respect to the amount of urinary protein, histological change and clinical course. At least in classical nephrotoxic serum nephritis in rats, host immune reactions against GBM bound heterologous nephrotoxic serum were concluded to have no effect on the course of the disease.
Adhesion molecule expression in psoriatic skin lesions and the influence of cyclosporin A
Authors: HORROCKS C , DUNCAN J I , OLIVER M , THOMSON A W 
Published: July 2010

SUMMARYNormal skin of healthy individuals and both lesional and uninvolved skin from patients with psoriasis before and after receiving cyclosporin A (CsA; 25 or 5 mg/kg per day) was examined by immunocytochemistry for differences in expression of adhesion-relevant epitopes. Normal, lesional and uninvolved skin all showed staining of basal keratinocytes for CD29 (the common β chain of the βl-integrin family). No other adhesion molecule investigated was detected on structural components of normal skin. In uninvolved skin, weak expression of CD54 (intercellular adhesion molecule I, ICAM-1) was noted on vascular endothelium. Uninvolved keratinocytes were found to stain with anti-CD58 (leucocyte function-associated antigen3, LFA-3) and there was weak expression of CD1 Ib (α chain of complement C3bi receptor) and CD11c (αchain of p150, 95 molecule) but not CD1 la (leucocyte function-associated antigen1, LFA-I, α chain) on those cells. In lesional skin, in addition to expression of CD58, there was also enhanced expression of CD11c. Weak expression of CD54 on keratinocytes was also observed. Lesional blood vessels were found to stain strongly with anti-CD54, CD29 and CD58. CDlla was expressed only on infiltrating mononuclear cells. CsA treatment produced marked clinical improvement, accompanied by the loss of CD54 expression on keratinocytes. However, despite the loss of T cells from lesional skin with CsA treatment, CD54 persisted on blood vessels. CsA was found to have no effect on keratinocyte expression of CD29. CD58 or CD11bande. The persistence of CD54 on vascular endothelium and of adhesion molecule expression on keratinocytes, despite resolution of the skin lesions, may explain the universal and rapid recurrence of psoriasis on cessation of CsA administration.
Expression of MHC class I and II molecules by cadaver retinal pigment epithelium cells: optimization of post-mortem HLA typing
Authors: ZAVAZAVA N , HALENE M , WESTPHAL E , NÖLLE B , DUNCKER G , ECKSTEIN E , HARPPRECHT J , MÜLLER-RUCHHOLTZ W 
Published: July 2010

SUMMARYThe objective of this study was to investigate the expression of MHC antigens by retinal pigment epithelium cells (RPE) after stimulation with interferon-gamma (IFN-γ) and to improve the currently practised technique of cadaver HLA typing. A concentration of 100 U/ml IFN-γ induced expression of class I molecules up to &gt; 90% 3 days after stimulation, whereas 50 U/ml were required for the expression of HLA-DR to &gt; 90%. A concentration of 750 U/ml induced 35–45% expression of HLA-DP and &lt;25% HLA-DQ after 3 days. Cells were serologically typed using the standard lymphocytotoxicity assay 3 days after stimulation with 250 U/ml IFN-γ. Typing of class I specificities was complemented by one-dimensional isoelectric focusing (1D-IEF). We observed high concordance between the results of the RPE typing and the lymphocytotoxicity test on the same donors. Our results show complete typing of class I and II antigens post-mortem, which, in particular, enables graft matching and improvement of graft survival in recipients of organs removed many hours after death such as the cornea.
Internalization of MHC class I molecules is a prerequisite for endocytosis of endorphin by lymphocytes0
Authors: MOMMAAS A M , WIJSMAN M C , VERDUIJN W , VERMEER B J , CLAAS F M J 
Published: July 2010

SUMMARYThe nature of the inleraction between γ-type endorphins and the HLA class I molecules was studied by immunoelectronmicroscopy. The HLA molecules were not involved in the actual binding of endorphin to the cell. In contrast, for the endocytosis of γ-endorphin, co-internalization of the HLA class I molecules is essential. The internalization process starts with clustering of γ-endorphin and HLA class I molecules in coated pits. Cells that do not carry HLA class I molecules (Daudi) or do not internalize HLA class I molecules (EBV-transformed B cells) bind but do not internalize γ-endorphin. On the basis of these observations, we suggest that the MHC class I molecules may function as transport molecules. Whether it is a general phenomenon that non-immunological ligands use the HLA class I molecules to get into the cell and immunological ligands (viral proteins) to reach the cell surface, remains to be established.
Poor antibody response after tetanus and pneumococcal vaccination in immunocompromised, HIV-infected patients
Authors: OPRAVIL M , FIERZ W , MATTER L , BLASER J , LÜTHY R 
Published: July 2010

SUMMARYTen patients with symptomatic HIV infection (six with ARC, four with AIDS) received tetanus and 23-valent pneumococcal vaccination. Anti-tetanus IgG and IgM, and anti-pneumococcal IgG against all 23 capsular types of the vaccine were measured on days 0, 11, 17, 30, and 90. Anti-pneumococcal IgG were simultaneously determined in two plasma pools of 100 healthy unimmunized blood donors and of 112 healthy adults who had previously received a 14-valent pneumococcal vaccination. Peak IgG responses to both vaccines were observed on day 17; thereafer, the antibody levels gradually fell again. Anti-tetanus IgG rose from 0.6 U/ml (geometic mean) to 2.0 U/ml on day 17. Anti-tetanus IgM remained unchanged, Anti-paeumococcal IgG increased only by 1.14-fold compared with pre-vaccination levels (geometric mean of IgG rises against all 23 polysaccharides in 10 patients), and exceeded the upper 95% limit of unvaccinated blood donors in only 30 out of 230 specimens. Pre-vacination levels for pneumococcal type-specific IgG were significantly higher in HIV-infected patients compared with the pool of unimmunized healthy controls, possibly indicating a higher rate of previous pneumococcal infections in HIV-seropositive subjects. However, post-pneumococcal vaccination levels were significantly tower in HIV-infected patients than in the pool of healthy controls. The increase in anti-tetanus IgG significantly correlated with the level of CD4 lymphocytes and with in vitro lymphocyte proliferation by pokeweed mitogen (5 μg/ml) and phytohaemagglutinin (2.5 μg/ml), confirming a particularly low vaccination response in patients who were severely immunocompromied.
CD8+ T cells are the major lymphocyte subpopulatlon involved in the protective immune response toToxoplasma gondiiin mice
Authors: PARKER S J , ROBERTS C W , ALEXANDER J 
Published: July 2010

SUMMARYThe ability of the major T cell subsets to adoptively transfer resistance to T. gondii infection was studied. Spleen cells harvested from mice with a 3-month T. gondii infection and cells from uninfected mice were enriched for T cells by nylon/wool purification. Adoptive transfer of these cells from both groups of donor mice led to a significant increase in the survival of syngeneic recipient mice infected intraperitoneally with 20 T. gondii cysts. Increased survival was mediated particularly by CD4-depleted but also, to a lesser extent, CD8-deplcted subpopulations. These results were confirmed in T cell reconstituted athymic nude mice. Unfractionaled T cells from chronically infected donors produced a significant inhibition of cyst formation in the brains of recipient mice measured 10 weeks after infection compared with control mice. The inhibition of cyst formation was ablated by pretreating T cells with anti-CD8 antibody and complement, but not anti-CD4 antibody and complement. Mice receiving cells from infected donors produced an early increase in their IgG1 and IgG2a antibody titres compared with mice given cells from uninfected animals. The depletion of either CD8+ or CD4+ immune cells appeared to have little effect on the antibody responses in recipient mice and there was no correlation between antibody levels and immunity. The results indicate that CDS+ T lymphocytes from convalescent T. gondii-infected BALB/c mice are the principal mediators of resistance to T. gondii, although CD4+ Tcells appear to be involved during the acute phase of infection.
Immune responsiveness and parasite-specific antibody levels in human hepatobiliary disease associated withOpisthorchis viverriniinfection
Authors: HASWELL-ELKINS M R , SITHITHAWORN P , MAIRIANG E , ELKINS D B , WONGRATANACHEEWIN S , KAEWKES S , MAIRIANG P 
Published: July 2010

SUMMARYOpisthorchis viverrini infection is associated with human hepatobiliary disease and cholangiocarcinoma, but the role of the immune response in the pathogenesis of infection is unclear. Here ultrasonography was used to examine the biliary tracts of residents from an endemic community. Delayed-type hypersensitivity responses to unrelated antigens, and fluke-specific IgG and IgA levels in serum of this group were also examined. Relationships between immunological parameters, intensity of infection and radiologically measured variables are reported. Immune responsiveness to unrelated antigens did not vary with intensity of parasite infection or disease status. Of all the variables, IgG levels were most markedly elevated in disease cases compared with normal subjects and were closely associated with gall bladder size and dysfunction. This is consistent with the hypothesis that an immunopathologic mechanism is involved in opisthorchiasis and suggests that antibody levels may be useful in screening populations for fluke-associated hepatobiliary disease.
Characteristics of an anti-eosinophil monoclonal antibody that recognizes granulocytes from patients with blood eosinophilia but not from subjects without eosinophilia
Authors: OCHIAI K , IWAMOTO I , TAKAHASHI H , YOSHIDA S , NAKAGAWA N , TOMIOKA H , YOSHIDA S 
Published: July 2010

SUMMARYTo investigate cell surface antigens of activated human cosinophils using monoclonal antibodies, we established a murine anti-human eosinophil monoclonal antibody AE500 by immunizing with blood cosinophils from patients with idiopathic hypereosinophilic syndrome (HES) and characterized the reactivity to a variety of human leucocytes by a fluorescence-activated cell sorter. AE500 reacted with blood cosinophils and neutrophils in nine out of 11 patients with marked eosinophilia (≥ 2500/μI) (seven with idiopathic eosinophilia including HES and two with asthma), but not with those in asthmatic patients with mild eosinophilia (n = 10) or in healthy subjects (n= 8). AE500 did not react with blood lymphoyctcs. monocytes or platelets. AESOO did not react with human myeloid or lymphoid cell lines, including eosinophilic leukemia cell lines EOL-I and EOL-3. The reactivity of AE500 to blood eosinophils and neutrophils in patients with marked eosinophilia changed in relation to blood eosinophil counts and prednisolone therapy. In addition, the reactivity of AE500 to blood eosinophils was increased in three out of four AE500-positive eosinophils by the incubation of the cells with granulocyte-macrophagc colony-stimulating factor (GM-CSF) at 37 C for 30 min. but not with interleukin 3 or interlcukin-5. These results suggest that the anti-eosinophil antibody AE500 detects a cell surface antigen expressed on blood granulocytes in a hypercosinophilic state. This antieosinophil antibody would be useful for analysing the mechanism of eosinophilia.
Binding of human C-reactive protein to monocytes: analysis by flow cytometry
Authors: BALLOU S P , CLEVELAND R P 
Published: July 2010

SUMMARYAn opsonic role has been proposed as a major function of C-reactive protein (CRP) in humans. In support of this hypothesis, recent radiolabcltcd ligand binding studies have provided evidence for the presence of specific receptors for soluble human CRP on human phagocytic cells, including ncutrophits and monocytes. In order to confirm specific binding of CRP to monocytes and to quantify the percentage of such cells capable of expressing binding sites, we employed a sensitive biotin-avidin fluorescence assay to study the CRP-monocyte interaction. It was observed that 67% of monocytes bound biotinylated CRP in a dose-dependent manner, that the binding was calcium dependent, and that it could be inhibited by 60% in the presence of a greater than 20-fold excess of competing native CRP. In other experiments, neither IgG nor heat-aggregated IgG inhibited the binding of CRP to monocytes; and no significant binding to lymphocyte populations could be detected. These studies confirm the ability of human CRP to bind to a majority of human monocytes in a calcium-dependent and specific manner, and provide further support for a biologically important interaction of this acute-phase protein with phagocytic cells.
Glomerular subendothelial and subepithelial immune complexes, containing the same antigen, are removed at different rates
Authors: MANNIK M , STAPLETON S A , BURNS M W , ALPERS C E , GAUTHIER V J 
Published: July 2010

SUMMARY
To examine the persistence of immune deposits in the subendothelial and subepithelial areas of the glomerular basement membrane in rats, immune deposits were formed by injection of radiolabelled, cationized human serum albumin (HSA) as antigen, followed by rabbit antibodies to HSA. The disappearance of the radiolabelled antigen from immune deposits in glomeruli was described by a curve consisting of two exponential components. By electron microscopy, subendothelial and subepithelial immune deposits were initially present in glomeruli. At later time-points, only subepithelial immune deposits were present. The fast component of disappearance, attributed to subendothelial deposits, had a half-life of 3.89±0.32 h. The slow component of disappearance from glomeruli, attributed to subepithelial deposits, had a half-life of 85.5±3.1 h. Since some of the injected, radiolabelled antigen was sequestered in other compartments of the body, the possibility was raised that antigen from these sites might be released and contribute to the persistence of deposits in glomeruli. This possibility, however, was excluded when transplantation of kidneys with immune deposits to untreated recipients revealed no difference in the amount of antigen persisting in nontransplanted and transplanted kidneys.
Decreased immunoreactive beta-endorphin in mononuclear leucocytes from patients with rheumatic diseases
Authors: WIEDERMANN C J , SACERDOTE P , MUR E , KINIGADNER U , WICKER T , PANERAI A E , BRAUNSTEINER H 
Published: July 2010

SUMMARYThe neuroendocrine potypeptide hormone beta-endorphin (β-END), which is released from various tissues including the anterior pituitary gland and cells of the immune system, has recently been implicated as having an immunoregulalory role. We used a radioimmunoassay to measure β-END levels in circulating mononuclear leucocytes from normal subjects and patients with various rheumatic diseases. Levels of β-END in leucocytes from patients were lower than in leucocytes from healthy subjects (P&lt;0.001). Whereas levels of β-END in leucocytes from patients with the various rheumatic disorders were not significantly different, an inverse correlation was found between β-END levels in leucocytes and expression of rheumatoid factor (P&lt;0.025) and erythrocyte sedimentation rate (P&lt;0.025). This study demonstrates decreased content of β-END in cells of the immune system related to parameters of inflammatory activity in rheumatic diseases.
In situhybridization of IL-6 in rheumatoid arthritis
Authors: WOOD N C , SYMONS J A , DICKENS E , DUFF G W 
Published: July 2010

SUMMARYIL-6, an important mediator of the acute phase response, has been implicated in the pathogenesis of rheumatoid arthritis (RA). Many cell types including macrophages, T cells, B cells, endothelial cells and fibroblasts can produce this cytokine and production is largely regulated at the level of gene transcription or mRN A stabilization. In this paper we have first measured the levels of IL-6 activity in synovial fluid (SF) and serum from patients with RA and then localized IL-6-producing cells in the synovium by in situ hybridization combined with immunophenotyping. Patients with RA had raised levels of IL-6 in both SF and serum compared with patients with osteoarthritis and age-matched healthy controls. In individual RA patients tested serially after admission to hospital, serum IL-6 was initially raised and, unexpectedly, increased with clinical improvement, In situ hybridization of IL-6 mRNA showed positive cells both in the lymphocyte-rich aggregates and adjacent to small blood vessels. With immunophenotyping it was found that cells containing IL-6 mRNA were often in contact with CD14+ tissue macrophages and double immunophenotyping revealed that immunoreactive IL-6 was often associated with synovial T cells.
Mucosal cell-mediated immunity to mycobacterial, enterobacterial and other microbial antigens in inflammatory bowel disease
Authors: IBBOTSON J P , LOWES J R , CHAHAL H , GASTON J S H , LIFE P , KUMARARATNE D S , SHARIF H , ALEXANDER-WILLIAMS J , ALLAN R N 
Published: July 2010

SUMMARY
Culture studies have suggested that Mycobacterium paratuherculosis may play a role in the aetiology of Crohn's disease. However, evidence of sensilizalion to mycobactcrial antigens amongst patients with Crohn's disease has not yet been adequately demonstrated. Previous studies of cell-mediated immunity (CMI) in Crohn's disease were restricted to responses of peripheral blood mononuclcar cells (PBMC) to mycobacterial antigens. In this study we have investigated the proliferativc responses of both PBMC and mesenteric lymph node mononuclcar cells (MLNMC) to a range of mycobacterial and non-mycobactcrial antigens. There was no evidence of specific sensitization in the responses of MLNMC and PBMC from patients with inflammatory bowel disease (IBD) to the mycobacterial antigens. However, anergy to M. paratuherculosis could not be excluded. IBD MLNMC responses to most antigens were generally greater than those of PBMC. which were often undetectable. When compared with controls, there was evidence of increased CM 1 to a range of non-mycobactcrial antigens, especially Yersinia enterocolitica. amongst both MLNMC and PBMC from patients with Crohn's disease and ulcerative colitis (UC). These results do not provide support to the proposed role of mycobacteria in the pathogcnesis of Crohn's disease, but indicate that further investigation may determine a role for bacterial-specific T cell-mediated responses in the palhogcncsis of IBD.
Subclass composition and J-chain expression of the‘compensatory’ gastrointestinal IgG cell population in selective IgA deficiency
Authors: NILSSEN D E , BRANDTZAEG P , FRØLAND S S , KAUSA O 
Published: July 2010

SUMMARYThe subclass disiribution of IgG-producing immunocytcs was examined by two-colour immunohistochemistry in gastrointestinal mucosa of 14 patients with selective serum IgA deficiency providing the following biopsy material: gastric (n=1); jejunal (n=12); colonic (n=1); and rectal (n=2). All except two patients suffered from various infections, and coeliac disease was observed in six of them. Control reference data were based on biopsies from immunologically intact subjects, including histologically normal jcjunal (n= 10) and large bowel (n=10) mucosa and stomach mucosa with slight chronic gastritis (n= 8). The total mucosal population of immunoglobulin-producing cells per 500 μm gut length unit was only slightly decreased in IgA deficiency because of an increased number of IgG (30%) and especially IgM (71%) immunocytes. The IgG I immunocytc proportion in the proximal gut (median 87%) was higher than that in the comparable controls (gastric 69%, jejunal 66%). A similar trend was seen in the distal gut (69%) compared with controls from the large bowel mucosa (55%). Conversely. lgG2 and lgG3 cell proportions were significantly decreased compared with the respective controls from the proximal gut. The same was true for IgG4. which also was significantly reduced in jejunal mucosa. Paired staining for cytoplasmic J chain and immunoglobulin isotype showed 71% positivity for jejunal IgG-producing cells in IgA deficiency, which was somewhat reduced compared with comparable controls (89%). J chain appeared to be preferentially expressed by IgGl cells (75%). but was also found in lgG2 (70%). lgG3 (32%) and IgG4 cells (33%). IgM-producing cells showed a J-chain positivity (99%) in IgA deficiency similar to normal (100%). Our results suggested that the block in mucosal B cell differentiation to IgA expression in the proximal gut is mainly located immediately upstream to the CHαl gene, giving excessive terminal maturation of J-chain-positivc IgGl immunocytes.