bluuebunny/crossref_metadata_2025_split huggingface dataset:
Accelerated onset of collagen-induced arthritis by remote inflammation
Authors: JOOSTEN L A B , HELSEN M M A , VAN DEN BERG W B 
Published: July 2010

SUMMARYCollagen-induced arthritis (CIA) in DBA-1 lac/J mice often has a low incidence, with gradual disease expression occurring over a broad time span (between days 35 and 70). The exact mechanisms underlying spontaneous expression are still poorly understood, although it is evident that some inflammatory cytokines like IL-1, tumour necrosis factor-alpha (TNF-α) and transforming growth factor-beta (TGF-β) are potent accelerators. We have investigated whether we could trigger collagen type II-driven inflammation by: (i) enhancing anti-collagen type II (CII) antibodies, or (ii) a non-related inflammatory process. Male DBA-1 lac/J mice were immunized with 100 μ bovine type II collagen in Freund's complete adjuvant (FCA), resulting in a low disease expression at day 28, Addition of anti-CH antibodies slightly enhanced the expression of CIA. Zymosan (3mg), given intraperitoneally, induced consistent expression of CIA after I week, whereas a retarded onset was noted with higher dosages. Local injection of a low dose of Zymosan (60μ) in the knee joint, clearly potentiated the expression of CTA at that particular site. Higher concentrations not only elicited prolonged CIA expression at the injection site, but also induced marked CIA in the draining ankle joint. In contrast, intra-articular injection of Zymosan in non-immunized DBAs or methylated bovine serum albumin (mBSA)/FCA-immunized controls only induced transient joint inflammation. The nature of the highly erosive CIA was confirmed histologically, and could easily be discriminated from the reversible changes induced with Zymosan. Our data indicate that latent autoimmune reactions may come to expression at the moment of non-specific inflammation, even at a remote site.
Immunohistological assessment of cutaneous drug hypersensitivity in patients with HIV infection
Authors: CARR A , VASAK E , MUNRO V , PENNY R , COOPER D A 
Published: July 2010

SUMMARY
The pathogenesis of drug hypersensitivity in patients with HIV infection is unknown. To study further the nature of hypersensitivity. The histopathological features of morbilliform drug hypersensitivity reactions were examined in a group of HIV-infected patients. Skin sections from 23 HIV-infected subjects with morbilliform drug hypersensitivity reactions were examined by light microscopy, direct immunofluorescence and immunohistochemistry, to determine the nature of the inflammatory infiltrate and the role of immunoglobulin. complement and cytokines. The principal light microscopic findings were spongiosis, hydropic generation of the basal layer, civatte bodies, an epidermal Iymphocytic infiltrate (48%). and a perivascular dermal infiltrate of lymphocytes (87%) and macrophages (52%). Two patients had findings consistent with toxic epidermal necrolysis. Immunohistochemistry demonstrated that the lymphocytic infiltrate consisted of CDS+. HLA-DR+ T lymphocytes (some of which also stained for CD38), a marked depletion of epidermal Langerhans cells (90%), and strong cytoplasmic staining of keratinocytes for IL-6 (60%), IL-1β(50%). tumour necrosis factor-alpha (TNF-α) (45%) and to a lesser degree, interferon-gamma (IFN-7) (35%). Immunofluorescence did not demonstrate any significant deposition of immunoglobulin or complement. The histological findings were independent of there responsible drug, the duration of either therapy or the rash, and of peripheral blood CD4+ and CD8+ cell counts. These findings suggest that activated CD8+ lymphocytes and perhaps epidermal production of cytokines are involved in the pathogenesis of cutaneous drug hypersensitivity in HIV-infected patients. The common histological features, regardless of the causative drug, suggest a common pathogenesis.
The role of natural killer cells in resistance to coccidiosis: investigations in a murine model
Authors: SMITH A L , ROSE M E , WAKELIN D 
Published: July 2010

SUMMARYNatural killer (NK) activity, detected by the lysis of Yac-1 target cells, was examined in splenic and mesenteric lymph node (MLN) cells throughout the course of infection with Eimeria vermiformis in BALB/c and C57BI/6 (B6) mice. These strains are, respectively, relatively resistant and susceptible to primary infections, which render them equally, and completely, resistant to challenge. Resting levels of NK activity were higher in B6 than in BALB/c, and B6 responded earlier in the course of infection than BALB/c, but splenic peak values were higher in BALB/c; the pattern of response in MLN cells was similar in both strains, but the peak was higher in BALB/c. At the lime (7 days p.i.) of peak NK response in BALB/c mice there was, depending upon the choice of NK-resistant/lymphokine-activated killer (LAK)-sensitive target cells, either little (P388D1), or no (P815) splenic LAK activity. Challenge of immunized BALB/c mice did not evoke a detectable NK response. Although the higher NK activity in BALB/c mice correlated with greater control of primary infection, depletion of NK activity (demonstrated in splenic cells) in vivo by treatment with anti-asialo GM1 antibodies did not greatly affect the course of infection. Furthermore, this treatment did not augment the exacerbation of infection produced by treatment with antiinterferon-gamma (IFN-γ) MoAb, indicating that, at least in this system, NK cells are not a fundamentally important source of this controlling cytokine of eimerian infections. The results suggest that NK cells may not greatly influence the outcome of coccidial infections.
Reduced NK activity correlates with active disease in HIV- patients with multidrug-resistant pulmonary tuberculosis
Authors: RATCLIFFE L T , LUKEY P T , MACKENZIE C R , RESS S R 
Published: July 2010

SUMMARYThere has been a global increase in the incidence of multidrug-resistant pulmonary tuberculosis (TB). As there are no previous reports of immune function in HIV- patients with multidrug-resistant pulmonary TB, a comprehensive assessment of cellular immunity in this setting was undertaken. This involved a prospective, case-controlled study which included five patients with active multidrug-resistant pulmonary TB and five matched controls with active non-resistant infection, and documented the changes in immune parameters which occurred upon clinical resolution. Patients with multidrug-resistant TB had significantly lower fresh natural killer (NK) cell activity than matched controls with non-resistant pulmonary TB (P &lt; 0.05). This was a specific abnormality, as there were no significant differences in antigen-specific cytotoxicity or lymphocyte proliferation in the case-controlled study. Follow-up assessment of the patients with multidrug-resistant infections indicated that clinical improvement correlated with a moderate increase in NK cell activity. Impaired NK cell function may be involved in the pathogenesis of multidrug-resistant TB.
Effects of decomplementation with cobra venom factor on experimental vasculitis
Authors: MATHIESON P W , QASIM F J , THIRU S , OLDROYD R G , OLIVEIRA D B G 
Published: July 2010

SUMMARY
Mercuric chloride (HgCl2) induces autoimmunity in susceptible rat strains, with hyper-IgE, appearance of a number of autoantibodies and wide spread tissue injury, including necrotizing vasculitis in the gut. In the early phase of tissue injury there is granulocyte infiltration; later there is immunoglobulin deposition along basement membranes in vessels. We have analysed the role of complement in this model using cobra venom factor (CVF). which causes decomplementation lasting around 5 days. The characteristic time course when HgCl2 is given over 10 days is that tissue injury and autoantibody levels reach a peak at around day 15 (start of HgCl2= day 0). We therefore gave CVF either early (day 0). intermediate (day 5) or late (day 10); a fourth group (controls) received HgCl2 but no CVF. At each time point, CVF caused complete decomplementation which lasted for al least 5 days, Serum IgE and autoantibody levels were similar in all four experimental groups. Tissue injury in the “early” CVF group and in the ‘Jale’ CVF group was not significantly different from control, but in the intermediate group tissue injury was significantly more severe than in controls. These data indicate that the complement system does not play a major rote in the induction of autoantibodies by HgCl2, nor in the effector phase of tissue injury. We speculate that the exacerbation of tissue injury by CVF in the group given this agent al an intermediate stage of the model is explained by the presence of products of C3 activation which have proinflammatory effects during the phase of active granulocyte-mediated tissue injury.
Possible association of CD3 and CD4 polymorphisms with insulin-dependent diabetes mellitus (IDDM)
Authors: GHABANBASANI M ZAMANI , BUYSE I , LEGIUS E , DECORTE R , MARYNEN P , BOUILLON R , CASSIMAN J-J 
Published: July 2010

SUMMARY
Population and family studies show that predisposition to type I diabetes (IDDM) is multi-factorial, and that polymorphisms in the MHC region contribute substantially to the susceptibility to IDDM. In the present study the association of polymorphisms in the CD4 and the 6 subunit of CD3 with IDDM were examined in a Belgian population. We observed that the frequency of the CD4*A4/A4 genotype and of the CD3*91 allele were significantly increased (P= 0·0077) and decreased (P = 3·8 × 10−5), respectively, in IDDM compared with controls. These results therefore suggest that CD4, CD3 or neighbouring genes might contribute to IDDM susceptibility. These results are, however, preliminary and cannot be considered as established until re-tested in a new population.
Expression and functional role of 1F7 (CD26) antigen on peripheral blood and synovial fluid T cells in rheumatoid arthritis patients
Authors: MUSCAT C , BERTOTTO A , AGEA E , BISTONI O , ERCOLANI R , TOGNELLINI R , SPINOZZI F , CESAROTTI M , GERLI R 
Published: July 2010

SUMMARYThe expression and the functional role of the CD26 (1F7) T cell surface molecule, an ectoenzyme which seems to represent a functional collagen receptor of T lymphocytes and to have a role in T cell activation, were analysed in both peripheral blood (PB) and synovial fluid (SF) T cell samples from patients with active and inactive rheumatoid arthritis (RA). Although patients with active disease displayed higher percentages of PB CD26+ CD4+ T cells than inactive RA and control subjects, CD26 antigen expression on RA SF T lymphocytes was low. The anti-1F7 binding to the T cell surface, that led to CD26 antigen modulation and enhancement of both IL-2 synthesis by, and 3H-TdR incorporation of, anti-CD3- or anti-CD2-triggered PB T cells in RA and control subjects, was unable to affect significantly both expression and functional activity of RA SF T lymphocytes. Since the 1F7 antigen spontaneously reappeared on the surface of unstimulated SFT cells after 2-5 days of culturing, the low IF7 antigen expression of anti-lF7 in the SF T cell compartment may be the result of in vivo molecule modulation exerted by the natural ligand in the joint, with important implications for T cell activation and lymphokine synthesis.
The influence of anti-fibronectin antibodies on interactions involving extracellular matrix components and cells: a possible pathogenic mechanism
Authors: ATTA M S , POWELL R J , TODD I 
Published: July 2010

SUMMARY
Antibodies, directed to the 30-kD collagen binding domain (CBD) of fibronectin (Fn), have been previously demonstrated in sera from patients with systemic lupus erythematosus (SLE), and we now investigate the possible pathogenic effects of these antibodies on collagen-Fn and cell-Fn interactions. The binding of type 1 collagen to Fn was demonstrated by ELISA, and could be specifically inhibited by the preincubation of solid-phase immobilized Fn with anti-Fn antibodies from SLE sera. By using indirect immunofluorescent staining, anti-Fn antibody containing SLE sera but not normal human serum (NHS) reduced the deposition of newly synthesized collagen and Fn on living human skin fibroblasts. We also found that sera from SLE patients containing anti-Fn antibodies significantly reduced thyroid cell attachment to Fn immobilized on plastic compared with NHS. These effects were shown to be due to the presence of anti-Fn antibodies in these sera, as SLE sera depleted of anti-Fn antibodies did not reduce the deposition of collagen or Fn on cultured fibroblasts, nor did they inhibit cell attachment.
Elevation of serum soluble intercellular adhesion molecule-1 (sICAM-1) and sE-selectin levels in bronchial asthma
Authors: KOBAYASHI T , HASHIMOTO S , IMAI K , AMEMIYA E , YAMAGUCHI M , YACHI A , HORIE T 
Published: July 2010

SUMMARYAdhesion molecules such as ICAM-1 and E-selection have been shown to play important roles in the production of allergic inflammation. In the present study, we measured serum soluble ICAM-1 (sICAM-1)and soluble E-selection (sE-selectin) levels by ELISA in 42 patients with bronchial asthma (22 atopic and 20 non-atopic) during asthma attacks and in stable conditions in order to assess the state of ICAM-1 and E-selectin in allergic inflammation. Both serum sICAM-1 levels and serum sE-sclectin levels in sera obtained during bronchial asthma attacks were higher than those in sera obtained in stable conditions. These findings were observed regardless of atopic status. To examine the regulatory mechanism in the elevation of serum sICAM-1 and sE-selectin levels, serum tumour necrosis factor-alpha (TNF-α) levels were measured by ELISA. TNF-α levels in sera obtained during bronchial asthma attacks were higher than those in sera obtained in stable conditions. There was a correlation between the nature of change in serum TNF-α levels and the nature of change in serum slCAM-1 levels or serum sE-selectin levels, though serum TNF-α levels did not correlate with serum sICAM-1 levels or serum sE-selectin levels. These results suggest that higher levels of sICAM-l and sE-selectin during asthma attacks may reflect the up-regulation of ICAM-1 and E-selectin expression in allergic inflammation, and that the soluble form of these adhesion molecules may be useful markers for the presence of allergic inflammation. TNF-α is shown to enhance the expression and release of ICAM-1 and E-selectin in vitro, however; the regulatory mechanism in the elevation of serum sICAM-1 and sE-selectin levels remains to be clarified.
Detection of antibodies to ovarian antigens in women with premature ovarian failure
Authors: WHEATCROFT N J , TOOGOOD A A , LI T C , COOKE I D , WEETMAN A P 
Published: July 2010

SUMMARY
Premature ovarian failure is a common condition of uncertain aetiology in most cases, although autoimmunity is thought to play a role in a proportion of eases. The frequency of ovarian antibodies, which may be markers for an autoimmune aetiology in this condition, remains unclear. To define this further, we have examined the sera of 45 women with premature ovarian failure (five with iatrogenic ovarian failure, nine with an associated autoimmune disease, and 27 with idiopathic ovarian failure), as well as four women with infertility due to Turner's syndrome and 41 pre- and post-menopausal controls. Using two human ovarian antigen preparations, 24% and 60% of the ovarian failure patients reacted in an ELISA (P &lt; 0·05 and P &lt; 0·001 compared with controls), but frequent cross-reactivity was found with fallopian tube antigens. The apparent aetiology of ovarian failure did not correlate with the presence of ovarian antibodies. Using bovine ovary as an antigen, there was a significant overall increase in binding by the ovarian failure patients, but this was almost identical to binding in an ELISA with bovine fallopian tube. In contrast to a previous report, there was no significant increase of binding to soluble or Triton-extracted membrane fractions of bovine corpora lutea containing the LH/hCG receptor by the patients with ovarian failure. These results suggest that ovarian antibodies are common in premature ovarian failure, but their specificity and pathogenic role are questionable.
Characterization of EN4 monoclonal antibody: a reagent with CD31 specificity
Authors: BURGIO V L , ZUPO S , RONCELLA S , ZOCCHI M , RUCO L P , BARONI C D 
Published: July 2010

SUMMARYEN4 MoAb was originally described as a MoAb that reacts specifically with human endothelial cells, and the reagent was not assigned to any of the presently known CD. Here, we provide evidence indicating that EN4 reacts with the CD31 antigen. Thus, EN4 stains strongly murine fibrobtasts transfected with the human CD31 gene. Furthermore, SDS-PAGE analysis of immunoprecipitates of cell lysates from surface-iodinated Jurkart T cells demonstrated that EN4 and reference CD31 MoAb recognized the same antigen, of 130 kD mol. wt. Finally, both EN4 and CD31 gave the same pattern of reactivity when tested on tonsillar or peripheral blood lymphoid cells by FACS analysis or by immunohistochemistry on sections of a variety of human tissues. EN4, however, proved consistently more efficient than the reference anli-CD3l MoAb as judged by both the intensity of fluorescence or of tissue staining. This property has thus allowed a better characterization of the tissue and cellular distribution of CD31.
Anti-idiotypic activity against anti-myeloperoxidase antibodies in pooled human immunoglobulin
Authors: PALL A A , VARAGUNAM M , ADU D , SMITH N , RICHARDS N T , TAYLOR C M , MICHAEL J 
Published: July 2010

SUMMARYWe investigated the ability of six different pooled human immunoglobulin (PHIG) preparations to inhibit the binding of anti-myeloperoxidase (MPO) antibodies to MPO. All six PHIG preparations inhibited the binding of anti-MPO antibodies from six sera to MPO in a concentration-dependent manner in the concentration range 0·016 10 mg/ml. There was considerable variation in the ability of each PHIG preparation to inhibit the binding of anti-MPO antibody in a given serum. Further differences were seen in the ability of a given PHIG to inhibit anti-MPO binding in different sera. F(ab′)2: fragments from two PHIG preparations also inhibited in a concentration-dependent manner anti-MPO binding to MPO in all six sera in the concentration range 0·002 2·65 mg/ml, with a maximum inhibition of 42%. Little inhibition was seen with F(ab′)2 of normal human IgG from individual donors (1·8–12·2% al the maximum concentration of 2 mg/ml). F(ab′)2 fragments from three anti-MPO containing sera and two affinity-purified anti-MPO antibodies were eluted by affinity chromatography from Sepharose-bound PHIG F(ab′)2 and showed anti-MPO antibody activity. We have shown that PHIG and F(ab′)2 fragments of PHIG inhibit anti-MPO binding to MPO, and further that F(ab′)2 fragments of PHIG bind to F(ab′)2 fragments of anti-MPO antibodies. These observations indicate binding between the variable regions of PHIG and the antigen binding site of anti-MPO antibodies, and are consistent with an anti-idiotypic reaction. The variability seen in the inhibitory effect of the different PHIG preparations in anti-MPO-positive sera implies differences in their anti-idiotype content, while the variability of the inhibitory effect of a particular PHIG preparation between different sera suggests heterogeneity in the idiotypic repertoire of anti-MPO antibodies. Such variations in the inhibitory effect of different PHIG preparations on antibody binding may be an important determinant of their therapeutic effect.
The significance of blood levels of IgM, IgA, IgG and IgG subclasses in Sudanese visceral leishmaniasis patients
Authors: ELASSAD A M S , YOUNIS S A , SIDDIG M , GRAYSON J , PETERSEN E , GHALIB H W 
Published: July 2010

SUMMARYWe developed an ELISA test using leishmania antigenic extracts to detect antigen-specific antibody responses, including subclass and isotype analysis, in visceral leishmaniasis (VL) patients from the Sudan. A total of 92 parasitologically proven patients were compared with cutaneous leishmaniasis, schistosomiasis, malaria, onchocerciasis and tuberculosis patients, as well as with healthy endemic and non-endemic controls. Some VL patients were examined before and after chemotherapy. VL patients showed significantly higher IgG responses compared with all other groups (93·4% sensitivity, 93·7% specificity), and higher (but not significantly) IgM responses. All groups showed low IgA levels. All groups showed low IgA levels. All IgG subclasses, IgG1, 2, 3, and 4, showed higher levels in patients than all other groups, with IgG1 and IgG3 levels being significantly reduced following treatment. The rank order for specificity and sensitivity for IgG subclasses was IgG3 &gt; IgG I&gt; IgG2&gt; IgG4.
High levels of circulating IL-10 in human malaria
Authors: PEYRON F , BURDIN N , RINGWALD P , VUILLEZ J P , ROUSSET F , BANCHEREAU J 
Published: July 2010

SUMMARYIL-10 is a monocyte/lymphocyte derived cytokine which has been shown to inhibit certain cellular immune responses such as delayed hypersensitivity. In particular, the production of tumour necrosis factor (TNF), IL-I and IL-6, which are involved in malaria pathology, are strongly inhibited by IL-10. Accordingly, we examined whether IL-10 could be involved in a human acute parasitic infection such as Plasmodium falciparum malaria. Human IL-10 levels in plasma were determined by two-site ELISA method, taking care to avoid non-specific reactions due to autoantibodies. Fourteen cerebral, 11 severe, and 20 mild malaria cases had mean IL-10 levels of 2812, 2882 and 913 pg/ml, respectively, while 98% of healthy individuals had undetectable (less than 100 pg/ml) circulating IL-10. Thirteen of the 25 cerebral/severe cases had &gt;2000 pg/ml. In 11 hospitalized patients, circulating IL-10 levels were found to return to virtually normal levels 7 days after antimalarial chemotherapy when biological and clinical malaria features had disappeared (mean levels fell from 3880 to 333 pg/ml). Further studies are required to determine whether these elevated levels of IL-10 play a beneficial role by reducing the parasite-induced inflammatory response, or a detrimental one by decreasing the cellular immune responses.
C6 haplotypes: associations of a Dde I site polymorphism to complement deficiency genes and the Msp I restriction fragment length polymorphism (RFLP)
Authors: FFRNIE B A , HOBART M J , DELBRIDGE G , POTTER P C , ORREN A , LACHMANN P J 
Published: July 2010

SUMMARY
Complement C6 has a common charge polymorphism designated A and B with gene frequencies of 0·65 and 0·35. The probable molecular basis for this is a Glu (C6A) for Ala (C6B) substitution at amino acid position 98, and is detected by digestion with the restriction enzyme Dde I of a polymerase chain reaction (PCR)-amplified fragment of genomic DNA. C6A was found to be Dde I-positive and C6B corresponds to Dde I-negative. We have applied out Dde I A/B polymorphism genotyping method to the investigation of C6-delicient individuals with complete (C6Q0) and sub-total deficiency (C6SD) protein phenotypes, including members of four families. We have also investigated the RFLP detected by digestion of genomic DNA with the enzyme Msp I, which is due to a polymorphic site located in the 5′ section of the gene, the variable sequence of which has yet to be determined. Sixteen out of seventeen unrelated C6Q0 subjects were found to be genotypically Dde I B/Msp I-negative: the remaining subject was heterozygous at both the loci under investigation. The C6SD phenotype was found to be associated with the Dde I A/Msp I-positive genotype in two families with combined C6/C7 subtotal deficiency and two with C6SD. It can be concluded that the two forms of C6 deficiency, C6Q0 and C6SD, arose independently on two different C6 allelic backgrounds. These associations have allowed the genotyping of the rare families that contain both types of deficiency. We have also defined a number of normal C6 Dde I/Msp I haptotypes in Caucasians and Cape Coloured populations.