bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sera from patients with rheumatic diseases recognize different epitope regions on the 52-kD Ro/SS-A protein
Authors: BOŽIČ B , PRUIJN G J M , ROZMAN B , VAN VENROOIJ W J 
Published: July 2010

SUMMARYPatients suffering from systemic lupus erythematosus (SLE) or Sjögren's syndrome (SS) often contain autoantibodies directed to the Ro(SS-A) complex. In this study the antigcnic determinants on two of the components of the Ro complex, i.e. the Ro60 and the Ro52 polypeptides, were investigated. Anti-Ro+ sera were selected by counter-immunoelectrophoresis. Depending on the detection method. 59–68% of the SLE patients produced anti-Ro but not anti-La antibody, while 72–81 % of the SS patients produced both anti-Ro and anti-La antibody. Immunoprecipitation of recombinant Ro-proteins showed that 61 sera (87%) were reactive with both Ro proteins, seven sera with Ro60 only, one serum with Ro52 only, and one serum did not precipitate the proteins at all. The anti-Ro60 reactivity of human sera is strongly associated with the native form of Ro60. suggesting that conformational autoepitopes are an important feature of Ro60. In the case of Ro52, frequently the residues located between amino acids 216 and 292 were essential for reactivity with the antibodies. With 70% of the lupus sera tested this appeared to be the only region important for reactivity. The antibodies of SS patients generally recognized multiple B cell epitopes located between amino acids 55 and 292. The results of this study indicate that the antigenic determinants on Ro52 are different for autoantibodies produced by lupus patients compared with those of SS patients.
CD21-CD23 ligand pair expression in children with allergic asthma
Authors: RABATIĆ S , GAGRO A , MEDAR-LASIĆ M 
Published: July 2010

SUMMARYThe CD23 antigen, a low affinity receptor for IgE, was recently shown to interact with another ligand, CD21, and the pairing of these molecules is important in T cell-B cell interaction and control of IgE production. Here, we analysed the expression of CD21 and CD23 on CD4+ and CD20+ lymphocytes in 25 allergic children and 12 age-matched non-allergic controls. Both the percentage (P&lt;0.01) and the absolute number (P&lt;0.00l) of CD23+ cells were increased in allergic children. There was no difference of CD21+ cells. Double positive CD4+CD23+ cells (2.5%) were only detected in one patient, in others all CD23 being expressed on B cells. The CD21 antigen was expressed only on B cells. Furthermore, allergic children had an increased mean fluorescence intensity of both the CD21 (P&lt;0.00l) and the CD23 (P&lt;0.001) receptor. To analyse the possible difference in B cell subsets expressing CD21 and CD23 antigens, three-colour fluorescence analysis was performed. In allergic children the subset of CD20+CD21− cells expressed more CD23 than in controls (P&lt;0.001). These results may mean an impaired expression and possibly regulation of CD21-CD23 interaction in allergic conditions.
Antigen-presenting capacity of macrophages and dendritic cells in the peritoneal cavity of patients treated with peritoneal dialysis
Authors: BETJES M G H , TUK C W , STRUIJK D G , KREDIET R T , ARISZ L , BEELEN R H J 
Published: July 2010

SUMMARYIn this study the antigen-presenting capacity of human peritoneal cells and the influence of continuous ambulant peritoneal dialysis (CAPD) were studied. On average 6% of the peritoneal cells were dendritic cells (DC), with no difference between CAPD and control peritoneal cells. DC were enriched by selecting for non-adherent, Fc receptor-negative, low density cells. A typical spot-like CD68 positivity was seen in DC, in contrast to the pancytoplasmic staining pattern in macrophages. Peritoneal DC morphologically and functionally showed features of cells belonging to the DC lineage. Peritoneal DC were superior antigen-presenting cells for both allo-antigen, and Candida albicans antigen or purified protein derivative. CAPD peritoneal macrophages were two- to threefold better stimulator cells for allogeneic T cells compared with control macrophages. The level of integrins/adhesins or MHC class I or II, as measured semi-quantitatively on the FACS, could not account for this phenomenon. In addition, a double chamber system showed that dialysate-activated macrophages produced soluble factors that could enhance DC-induced allogeneic T cell proliferation. In conclusion, human peritoneal cells contain a relatively high percentage of classical DC. CAPD treatment does not impair the antigen-presenting capacity of peritoneal cells, but instead up-regulates the allo-antigcn-presenting capacity of peritoneal macrophages.
Macrophage depletion decreases IgG anti-DNA in cultures from (NZB · NZW)F1 spleen cells by eliminating the main source of IL-6
Authors: ALARCÓN-RIQUELME M E , MÖLLER G , FERNÁNDEZ C 
Published: July 2010

SUMMARYWe have studied ihe rote of macrophages in the produclion of IgG anli-DNA autoanlibodies by (NZB × NZW)F1 tnice(B/W). One of the main features of the syslemic lupus cryibematosus(SLE)-like disease that aftects these mice, h ihe presence of circuialing IgG autoantibodies and immune complexes, which lead lo renal failure and death by the age of 8–9 months. IgG autoantibodies are produced without in vitro siimulallon by lolal spleen eells from these miee when they reach tbe age of 6 monlhs. We have demonstrated ihat IL-6 increases ihe production of IgG autoantibodies in cultures of splenic purified B cells from the old B/W miee. The aim of this study was to show the involvement of macrophages in the production of IL-6 and consequently in the produclion of IgG anti-DNA antibodies in ritro. We show thai elimination of the macrophages by different treatments led to reduction of the content of IL-6 in ihe supernalants as well as of IgG anti-DNA autoantibodies. Addition of fresh, splenic or peritoneal macrophages restored the produclion of autoantibodies in macrophage-depleted cultures from old B/W miee. There were no ditferences in the capacity of IL-6 produelion between macrophages from old or young B/W miee. but an imporiani difference was observed between peritoneal and splenic maerophages, where the former produced mueh higher levels ol IL-6, and eonsequently were more potent inducers of IgG autoantibodies. The present results reinforee Ihe role of macrophages and lL-6 in Ihe production of IgG anti-DNA autoantibodies in B/W mice. The implieations of these results in the pathogenesis of the disease are discussed.
Prognostic value of serum immunoglobulin A antibodies to pol gene products during HIV-1 infection
Authors: QUESNEL A , POZZETTO B , MOJA P , GRATTARD F , LUCHT F R , TOURAINE J L , GAUDIN O G , GENIN C 
Published: July 2010

SUMMARY
Serum specimens from 66 HIV-t-infected subjects were tested by ELISA for the presence of IgA antibodies to HIV-t:44 samples were found positive and 37 were confirmed by immunoblot. In these subjects, the presence of anti-HIV IgA antibodies was studied in relation to the total count of circulating CD4+ lymphocytes and to the level of serum IgA. A significative correlation (P &lt; 0·03) was found between the absence of IgA to the subunit p68 of the reverse transcriptase and a count of CD4+ cell &lt; 400/mm3 or total IgA level over 4–25 g/l. The same pattern was observed for the IgA antibodies to the p52 subunit but the association was just not significant (P &lt; 0·07). No significant decrease was noted for the IgA directed towards the other proteins of HIV-1, especially the products of the gag gene.
Differential requirements for HIV-1 replication in naive and memory CD4 T cells from asymptomatic HIV-1 seropositive carriers and AIDS patients
Authors: CAYOTA A , VUILLIER F , SCOTT-ALGARA D , FEUILLIE V , DIGHIERO G 
Published: July 2010

SUMMARYOne of the major routes for modulating HIV-1 expression by infected T cells is through the control of transcription initiation from the HIV-1 long terminal repeat (LTR), which is regulated either by ils own viral gene products or by several cellular DNA-binding proteins induced during T cell activation. Previous work reported preferential HIV-1 infection and replication of memory CD4 T eells from infected individuals, which was explained either by a higher viral burden of this subset or by differences between naive and memory cells in the activation of the general transcription machinery involved in HIV-1 replication. In this work, we have studied HIV-1 replication by highly purified naive and memory CD4 T eells from asymptomatic seropositive carriers (ASC) and AIDS patients following different activation signals. Our results demonstrate that viral replication in memory cells from ASC was observed after mitogenic (phytohaemagglutinin (PHA) and/or phorbol myristate acetate (PMA)) recombinant tumour necrosis factor-alpha (rTNF-α) and CD3-mediated activation. In contrast, in naive subsets, early viral replication was almost exclusively observed upon CD3-mediated activation. AIDS patients are characterized by similar levels of viral replication in both subsets after PHA and soluble or immobilized anti-CD3 MoAb activation. However, naive subsets from AIDS patienis still displayed differential requirements since they failed to replicate HIV-1 after treatmenl with PMA and rTNF-a. Taken together, these results provide evidence thai HIV-1 replication in CD4+ T cells from infected individuals is a function of the differentiation stage of the eells, the disease stage of the patient and the aetivation signal employed.
Detection of glomerular-binding immune elements in murine lupus using a tissue-based ELISA
Authors: BERNSTEIN K , BOLSHOUN D , GILKESON G , MUNNS T , LEFKOWITH J B 
Published: July 2010

SUMMARYThe glomerulonephritis in systemic lupus erythemalosus (SLE) is presumably triggered by ihe binding of circulating immune elements (autoantibodies and immune complexes) to the glomerulus; however, the nature of these elements is unclear. In order to detect and characterize such elements, we developed an ELISA using whole intact glomeruli as the substrate. With this assay, glomerular binding activity (GBA) was detected in the serum of MRLlpr, NZB × W, and B × SB mice, but not in non-autoimmune BALB/c mice. Less activity was present in the serum of C3H lpr, C57B1/6J Ipr and AKR lpr animals which develop signs of autoimmunity but only modest renal disease. The GBA in MRLlpr mice contained IgG (subclasses 1, 2a and 2b), but not IgG3. IgM. igA, orC3. GBA was not significantly decreased by preadsorption of MRL lpr serum by DNA-agarose (although anti-DNA antibodies were). Binding activity in serum, however, was diminished by DNAase treatment. Fractionation of MRL lpr serum over a molecular sizing column showed that GBA eluled in a broad peak. GBA bound to the glomerulus ex vivo in a tissue-specific fashion and was enriched in renal eluates relative to serum in vivo. In sum, the binding activity detected by this assay appeared to be a heterogeneous entity (possibly in part immune complexes containing DNA) which bound specifically to the glomerulus and which appeared to parallel the presence of renal disease. This novel assay system may help elucidate the pathogenesis of SLE nephritis and have utility as a disease marker.
Spontaneousin vitroproduction of rheumatoid factor during infectious exacerbations of cystic fibrosis: correlation with circulating immune complex levels
Authors: KEOGAN M T , CALLAGHAN M , YANNI G , MULHERIN D , FEIGHERY C , BROWN D L , FITZGERALD M X , BRESNIHAN B 
Published: July 2010

SUMMARYRheumatoid factor (RF) production has been demonstrated during infections, including infectious exacerbations of cystic fibrosis (CF). The aim of this study was to evaluate the relationship of RF production to infection, and examine the mechanisms involved. Serial peripheral blood mononuclear cell (PBMC) cultures with measurement of spontaneous production of IgM RF, IgA RF, total IgM and IgA, and measurement of serum levels of immune complexes were carried out during exacerbations of CF. The percentage of B cells expressing CDS was examined in a second cohort of acutely infected CF patients, and related to IgM RF production. IgM RF production was significantly elevated during acute infection compared with convalescence (P&lt;0·05), stable CF subjects (P&lt;0·005) and normal controls (P&lt;0·05). IgM RF production did not correlate with total IgM production in the majority of patients, but was closely related to circulating immune complex levels in 8/10 subjects. IgA RF production did not increase significantly during infection, and did not correlate with total IgA or IgM RF production, or with circulating immune complex levels. CDS+ B cells were not increased in the CF group, and the percentage of CD5+ B cells did not correlate with IgM RF synthesis. These observations suggest that RF production during infection is specifically induced, possibly by immune complex autoimmunization, and is not simply the result of polyclonal B cell activation. Different patterns of IgM RF and IgA RF synthesis suggest different mechanisms of induction.
Determination of the cytokine profile in American cutaneous leishmaniasis using the polymerase chain reaction
Authors: CACERES-DITTMAR G , TAPIA F J , SÉNCHEZ M A , YAMAMURA M , UYEMURA K , MODLIN R L , BLOOM B R , CONVIT J 
Published: July 2010

SUMMARYThe lymphokine profiles were determined in the skin lesions of the three distinct clinical forms of American cutaneous leishmaniasis (ACL), using a reverse transcriptase polymerase chain reaction (RT-PCR) and primers for various lymphokines. The message for interferon-gamma (IFN-y). tumour necrosis factor-beta (TNF–β) and IL-8 was expressed in the three clinical forms of ACL. IL-lβ in RNA was expressed in most localized (LCL) and mucoeutaneous (MCL) leishmaniasis. but in only few of the diffuse cutaneous leishmaniasis (DCL). IL-2 mRNA was detected in about half of the lesions, with more prominent values for MCL. IL-4 mRNA was present in most lesions from the three clinical forms, but markedly increased in DCL. IL-5 and IL-10 mRNAs were expressed in all MCL and in half of the DCL lesions and weakly expressed in LCL lesions. IL-10 mRNA was more abundant in MCL lesions. In contrast. IL-6 and TNF-s mRNAs were expressed in a Iarge number of LCL. In MCL, IL-6 mRNA was expressed in most cases and TNF–α mRNA in all the cases. In DCL. 11,–6 mRNA was absent and TNF–α mRNA was weakly expressed. These results suggest that most T cells present in the MCL and DCL lesions secrete a mixture of type 1 and type 2 cytokine patterns, but in DCL granulomas type 2 cytokines predominate. In LCL the cytokine patterns show a mixture of type l and type o with a preponderance of IFN–γ over IL-4, and low levels of IL-5 and IL-10. The Iack of IL-6 and TNF–α mRNAs, and the low expression of IL-lβ in DCL lesions suggest a defect in the anligcn-processing cells that may account for the state of unrcsponsiveness in these patients.
Interferon-gamma stimulates the secretion of IL-1, but not of IL-6, by glomerular mesangial cells
Authors: KAKIZAKI Y , KRAFT N , ATKINS R C 
Published: July 2010

SUMMARYIL-1 activity in culture supernatant and cell lysate from rat mesangial cells stimulated with interferon-gamma (IFN-γ) was measured by a thymocytc proliferation assay. While IFN-γ alone had no effect on the secretion or the intracellular pool of IL-1, the enhancement by IFN-γ of IL-1 secretion in response to lipopolysaccharide (LPS) was observed. The stimulatory effect of culture supernatant on thymocyte proliferation was abrogated by preincubation with the anti-IL-l antibody. At least 4–h incubation with IFN-γ and LPS was required to detect enhancing effect of I FN-γ. The addition of as little as 1 U/ml IFN-γ significantly increased IL-1 secretion in the presence of 10 μg/ml LPS. The IL-6 activity in culture supernatants was determined by measurement of thymidine uptake in mouse IL-6-dependent cell line (MH60.BSF2). Mesangial cells secreted IL-6 in culture supernatant without additional stimuli and LPS distinctly increased it as described previously. However, in contrast to IL-1 production, no effect of IFN-γ on IL-6 secretion was observed in the presence or absence of LPS. Moreover, we determined whether enhanced IL-1 release is associated with la expression on mesangial cells. IFN-γ alone and the combination with LPS induced marked expression of la antigen, whereas LPS alone did not. We conclude that IFN-γ stimulates the production of IL-1, but not IL-6, by mesangial cells and suggest an important role of IFN-γ in the pathogenesis of glomerulonephritis by regulating the mesangial production of IL-1 and the accessory cell function of mesangial cells.
Tumour necrosis factor soluble receptors behave as acute phase reactants following surgery in patients with rheumatoid arthritis, chronic osteomyelitis and osteoarthritis
Authors: CHIKANZA I C , ROUX-LOMBARD P , DAYER J-M , PANAYI G S 
Published: July 2010

SUMMARYTumour necrosis factor-alpha (TNF-α) is involved in diverse biological processes including immune and inflammatory reactions and the response to surgical stress. Two soluble TNF receptor protein fragments. TNF-sR55 (from the p55 kD TNF receptor) and TNF-sR75 (from the p75 kD TNF receptor), are released by cells during inflammation and may modulate the effects of TNF-α. We have studied the kinetics of secretion of TNF-α, TNF-sR55 and TNF-sR75 in the sera of patients with rheumatoid arthritis (RA) and control subjects with osteoarthritis (OA) or chronic osteomyelitis (OM) before and after major surgery. Significantly higher pre-operative levels of TNF-sR55 and TNF-sR75 were found in RA and OM as compared with OA (P&lt;0·02). Following surgery, TNF-sR55 increased within 24 h in RA, OM and OA (P&lt;0·05), whereas TNF-sR75 increased significantly only in OM and OA patients (P&lt;0·05). By contrast, no TNF-α was detectable before and after surgery in any of the subjects, but this may have been due to impaired detection (by ELISA) of TNF-α when it is bound to TNF-sR. These findings suggest that TNF-sR55 and TNF-sR75 may be further markers of the host's reaction to inflammatory insults. They may also play a role in modulating the immune and inflammatory reactions by inhibiting the systemic effects of TNF-α.
Cytokines involved in the progression of multiple myeloma
Authors: MERICO F , BERGUI L , GREGORETTI M G , GHIA P , AIMO G , LINDLEY I J D , CALIGARIS-CAPPIO F 
Published: July 2010

SUMMARYWe have investigated which of the cytokines that are relevant in the in vitro growth of multiple myeloma (MM) malignant plasma cells are actually produced in vivo by MM patients. To this end, we have measured the levels of IL-1β, IL-3, IL-4, IL-6, IL-7, IL-8 and tumour necrosis factor-alpha (TNF-α) both in sera and in the supernatant of bone marrow (BM) stromal cell cultures from patients with MM and monoclonal gammopathy of undetermined significance (MGUS). The significance of our findings is three-fold. First, IL-6 and IL-8 are produced by MM BM stromal cells, while IL-1β, TNF-α, IL-4 and IL-7 are not. Second, IL-3 is the only cytokine consistently raised in serum samples; we have also detected low levels of serum IL-6 in a minority of cases, usually in advanced stage of the disease. Third, MM BM stromal cells are active IL-6 and IL-8 producers, while both normal and MGUS BM stromal cells are low producers, thus suggesting that in the BM of MM a number of environmental cells, that would normally be quiescent, are instead activated and that, in MM, activated BM stromal cells play an active role in supporting the progressive expansion of the B cell clone.
A novel specificity of anticytoplasmic autoantibodies directed against eosinophil peroxidase
Authors: DOLMAN K M , DAMSMA I , TOOL A T J , SONNENBERG A , von dem BORNE A E G Kr , GOLDSCHMEDING R 
Published: July 2010

SUMMARYVasculitis associated anticytoplasmic autoantibodies (ANCA) are directed against enzymes in the granules of both neutrophils and monocytes. These autoantibodies can be detected by indirect immunofluorescence technique (IIFT) using ethanol-fixed cytospins. We here report the identification of a novel specificity of autoantibodies, present in the sera of eight patients, that reacted only with eosinophils in the IIFT. By immunoprecipitation and ELISA experiments it was shown that the autoantibodies in these sera were directed against eosinophil peroxidase (EPO). There was no apparent influence on initial substrate conversion rate, but reduced plateau levels suggested increased inactivation of the enzyme in the course of the peroxidase reaction. Flow cytometry studies demonstrated the presence of EPO on the surface of primed eosinophils. Anti-EPO sera and purified anti-EPO immunoglobulins significantly increased the release of reactive oxygen species from primed eosinophils. The patients with anti-EPO antibodies suffered from clinically diverse disorders, with more or less generalized manifestations involving the kidneys, blood vessels, lungs and/or joints.
Autoantibodies in malaria, tuberculosis and hepatitis B in a West African population
Authors: ADEBAJO A O , CHARLES P , MAINI R N , HAZLEMAN B L 
Published: July 2010

SUMMARY
Following reports of associations between autoantibodies and living in the tropics, we have studied the seroprevalence and nature of anti-nuclear antibodies, anti-cardiolipin antibodies, antibodies to extractable nuclear antigens and anti-neutrophilic cytoplasmic antibodies in 351 West Africans with malaria, tuberculosis or hepatitis B, or in good health. Amongst healthy West Africans we found a seroprevalence of 7% for anti-nuclear antibodies with several staining patterns, and of 30·3% for anti-cardiolipin antibodies. Among patients with tuberculosis and malaria there was twice that frequency of anti-nuclear antibodies (predominantly speckled in pattern), and anti-neutrophil cytoplasmic antibodies (predominantly IgM) were demonstrated in a few cases. A possible association beween IgG anti-cardiolipin antibodies and tuberculosis was observed (P&lt;0·05), but antibodies to double-stranded DNA were not elevated and no antibodies to extractable nuclear antigens were found in any of the patients or healthy individuals studied. Our findings suggest the need for caution in the interpretation of autoantibody tests in subjects from or living in the tropics, as well as in patients with tropical infections.
IL-4 and interferon-gamma production in children with atopic disease
Authors: TANG M , KEMP A , VARIGOS G 
Published: July 2010

SUMMARYIn vitro studies have implicated reciprocal roles for IL-4 and interferon-gamma (IFN-γ) in the regulation of IgE production. As elevated IgE is a major feature of atopic disease, an important question is whether an imbalance of IL-4 and IFN-γ is present in vivo. The production of IL-4 and IFN-γ in phytohaemagglutinin (PHA)-stimulated peripheral blood mononuclear cell cultures from atopic children was examined to determine if there is an increased production of IL-4 and/or a reduced production of IFN-γ. Highly atopic children with IgE &gt;600 U/ml produced significantly more IL-4 and less IFN-γin vitro than age-matched non-atopic controls. Production of IL-4 and IFN-γ in mildly atopic children was equivalent to controls. These findings indicate that highly atopic children have an imbalance of IL-4 and IFN-γ production and that the degree of imbalance relates to severity of the atopic state. The ratio of in vitro IL-4: IFN-γ production correlated positively with serum IgE, which suggests that the balance of these two cytokines is a factor in the regulation of IgE, in vivo. It remains to be determined whether this imbalance of IL-4 and IFN-γ in the highly atopic children is the cause or result of the disease process.