bluuebunny/crossref_metadata_2025_split huggingface dataset:
Antiretroviral treatment reverses HIV-induced reduction in the expression of surface antigens on alveolar macrophages in AIDS patients
Authors: BRAY D H , SQUIRE S B , KAWANA A , JOHNSON M A , POULTER L W 
Published: July 2010

SUMMARYMoAbs and immunoperoxidasc methods were used to identify antige-resenting and phagocytic cells and to assess expression of HL-R molecules on cells obtained by bronchoalvcolar lavagc (BAL) from 33 AIDS patients and nine normal volunteers. In 17 patients, not receiving antiretroviral therapy, the expression of HL-R molecules (MoAb RFDR1) as well as the percentages of cells expressing RFD1 marker for antige-resenting cells and RFD7 marker for mature phagocytes were significantly reduced. However, in BAL obtained after commencing treatment with zidovudine (AZT) in 21 patients or with 2′,3′–dideoxyinosine(DD1)in five patients, the expression of the markers studied was found to have returned to levels of expression seen in normal lavages. The changes observed were clearly associated with antiretroviral treatment and did not correlate with applications of other drugs, blood CD4 counts or presence of infectious organisms in BAL fluid. As the alterations in the expression of HLA-DR molecules and RFD1 marker on macrophages have been shown to be associated with functional capacities of these cells, the reversal of impaired expression of phenotypic markers on alveolar macrophages in AIDS patients by AZT and DDI signifies an important ability of these drugs to modify immune reactivity and emphasizes the need to monitor such functions in HIV disease.
Defective expression of CD23 and autocrine growth-stimulation in Epstein-Barr virus (EBV)-transformed B cells from patients with Wiskott-Aldrich syndrome (WAS)
Authors: SIMON H-U , HIGGINS E A , DEMETRIOU M , DATTI A , SIMINOVITCH K A , DENNIS J W 
Published: July 2010

SUMMARYWAS is an X-linked, recessive, immune deficiency syndrome, characteristically associated with lymphocyte and platelet dysfunction. Peripheral B lymphocytes from WAS patients are non-responsive to polysaccharidc antigens and show reduced numbers of cells expressing the integral membrane glycoprotein, CD23. The release of CD23 proteolytic fragments, so-called soluble CD23 (sCD23). by B lymphoblasts and EBV-transformed B cell lines has previously been described, and these fragments have been shown to stimulate autocrine growth of these cells. We have found that the surface expression of CD23 is reduced on WAS compared with control EBV-B cells. Surface CD23 levels were reduced two-fold in four WAS cell lines (group I) and nine-fold in four other lines (group II). Group II WAS cell lines also showed reduced growth rates in serum-free medium when compared with group I cell lines and EBV-B cell lines from eight normal subjects. In contrast to the group II WAS lines, group I and EBV-B cells from normal individuals produced an autocrine-growth factor activity which could be absorbed by anti-CD23 antibodies. Immunoprecipitation of sCD23 from culture supernatants confirmed that group I WAS cell lines produced less sCD23, particularly the 37K fragment which was prevalent in control EBV-B cells. Northern analysis showed that CD23 mRNA levels were increased three-fold in group I and unchanged in group II WAS compared with normal EBV-B cell lines, suggesting that decreased surface expression in WAS EBV-B cells reflects post-transcriptional events. Together these results suggest that reduced cell surface expression and aberrant proteolysis of CD23 occurs in WAS patients'B lymphocytes and may contribute to impaired immune function in these patients.
Delineation of pulmonary alveolar macrophage subpopulations by flow cytometry in normal subjects and in patients with lung cancer
Authors: MCDONALD C F , HUTCHINSON P , ATKINS R C 
Published: July 2010

SUMMARYWe have previously described alterations in pulmonary alveolar macrophage (PAM) function in patients with lung cancer when compared with control subjects. This study examined PAM from five patients with lung cancer, seven normal volunteers and nine control patients, to assess whether any differences in surface phenotypic markers were present in lung cancer versus non-cancer subjects, and what changes might be induced with interferon-gamma (IFN-γ) stimulation. After 3 days'culture with or without IFN-γ no differences were seen in the percentages of cells staining positively in each group for HLA class I. class II and ICAM-1 (CD54) antigens. However, in 13 out of 14 control subjects, and only one out of the five cancer subjects, dual PAM populations were identified. The second PAM population (PAM-2) was larger and demonstrated a higher expression of class I and ICAM-1 antigens. Unlike the unfractionated PAM population, PAM-2 consistently responded to IFN-γ stimulation with an increase in both class I (90 ± 25%) and ICAM-1 (45 ± 10%) antigens, while there was no change in class II antigen expression. In three subjects PAM-2 was found to induce a significantly greater mitogen response than the rest of the PAM population. If confirmed in a larger group of patients, the absence of PAM-2 in the majority of patients with lung cancer may underlie the functional PAM defects observed in these patients.
Nephrotoxic serum nephritis in nude rats: the roles of host immune reactions in the accelerated type
Authors: SATO T , KAWACHI H , MORIOKA T , TAKASHIMA N , SAEKI T , OITE T , SATO N L , TAKEUCHI M , SHIMIZU F 
Published: July 2010

SUMMARY
By immunization with rabbit immunoglobulins and the injection of a subnephritogenic dose of rabbit nephrotoxic serum (NTS), accelerated-type nephrotoxic serum nephritis (NTN) was induced in heterozygous (rnu/+) rats but not in athymic nude (rnu/rnu) rats. By transferring rat antibody against rabbit immunoglobulins, marked proteinuria was induced also in nude rats (202.0 ± 98.4 mg/ day on day 3) as in rnu/+ rats (122.6 ± 35.3 mg/day on day 3). No marked differences in histological findings could be found between both groups. The most marked increase in the number of intraglomerular infiltrating cells was observed in heterozygous rats indicating that the presence of thymus-derived cells leads to the accumulation of more cells in glomeruli. We conclude that humoral immunity alone is enough to accelerate the pathogenic mechanism which induces glomerular injury with heavy proteinuria in this model.
Interferon-gamma activates the oxidative killing ofCandida albicansby human granulocytes
Authors: STEVENHAGEN A , van FURTH R 
Published: July 2010

SUMMARYAlthough granulocytes are essential for the resistance against infections with Candida albicans, these cells do not kill the ingested yeast optimally. Various cytokines can enhance functional activities of granulocytes. but until now only interferon-gamma (IFN-γ) has been applied more widely, namely in patients with chronic granulomatous disease. Since it is not certain whether IFN-γ is able to enhance the candidacidal activity of granulocytes the present study was undertaken. Human granulocytes incubated with various concentrations of recombinant human IFN-γ (rIFN-γ) were studied for the phagocytosis and intracellular killing of C. albicans and their oxygen metabolism after stimulation with opsonized Candida. Results showed a small increase in the rate of phagocytosis and a dose-dependent increase of the intracellular killing of C. albicans and the production of H2O2. The increased candidacidal activity and H2O2 production by rIFN-γ-stimulated granulocytes were inhibited by diphenylenc iodonium (DPI). From these results it is concluded that the increased candidacidal activity of granulocytes activated by rIFN-γ is caused by the increased production of reactive oxygen radicals.
Association of C4B deficiency (C4B*Q0) with erythema nodosum in leprosy
Authors: de MESSIAS I J T , SANTAMARIA J , BRENDEN M , REIS A , MAUFF G 
Published: July 2010

SUMMARYA considerable number of studies have postulated significant associations between susceptibility to the different clinical manifestations of leprosy and the MHC, In this investigation, the association between the MHC class III complement proieins C2, BF, C4A and C4B and leprosy in a patient population of Southern Brazil was studied. A total of 109 non-related leprosy patients was investigated; 73 presented wilh lepromatous leprosy (LL), 46 of Ihem had the immunopathological reaction of erythema nodosum (ENL), the remaining 36 were tuberculoid, borderline and indeterminate leprosy (TIBL) patients. The control group included 172 healthy individuals matched with the patients according lo their ethnic and geographical origin, C2, BF, C4A and C4B allotypes were determined by slandard technologies including Western blots for C2 and C4 variant alleles wilh monoclonal and polyclonal antibodies. Non-expressed (‘silent’) C4 alleles in hemizygously deficient individuals were estimated semiquantitatively on the basis of the C4A and C4B isolype ratio and by the M ASC (‘minimal chi-square’) method. The results showed a significantly elevated presence of the non-expressed C4B allele (C4B*Q0) in the LL and ENL patient groups in comparison with the controls. The most signifieant difference was observed in the ENL group when compared with the controls. In addition, all patients who were homozygously C4B-deficient had ENL, and most of them had the BF*F1 allele. The comparison between LL patients with and without ENL also showed a statistically significant difference in the presence of C4B*Q0, indieating thai C4B deficiency itself is associated with ENL. The relative risk of LL patients with the C4B*Q0 allele suffering from ENL was 53 compared with LL palients without C4B*Q0, Since immune complexes (IC) are considered to be the palhogenic cause of ENL, our findings indicate thai C4B deficieney may play an important role in the abnormal immune response against Myeobaeterium leprae and in the lack of IC clearance, leading to ENL reactions. Individuals wilh this allele seem to be at a higher risk of developing pathologieal immune reactivity in lepromatous leprosy.
Lymphoid cells in afferent and efferent intestinal lymph: lymphocyte subpopulations and cell migration
Authors: ROTHKÖTTER H J , HUBER T , BARMAN N N , PABST R 
Published: July 2010

SUMMARYGut wall emigrating cells have been characterized in the intestinal lymph. The intestinal lymph duct was cannulated in 6-month-old minipigs. Under non-restraining conditions the efferent lymph from the mesenteric lymph nodes was collected in seven normal animals. Lymph coming directly from the guv (afferent lymph) was also collected in 18 pigs after resection of the mesenteric lymph node chains 3 months previously. The intestinal lymph How was similar in both groups (around 18 ml/h). The lymphoid cell yield was 1·2±1·0 ± 106/h in control animals, while in mesenteric lymph node resected pigs it was around 20 times higher (26·2±17·6 × 106/h). In the gut-derived lymph 76·5±8·8% T lymphocytes were observed (CD4+, 48·1±15·5%; CD8+, 53·6±12·7%). The percentage of immunoglobulin-positive cells was lower (IgM+, 10·1±4·5; IgA+, 1·7±1·1). In 14 mesenteric lymph node resected pigs a mean of 5·6±3·1 × 108 lymphocytes from the gut lymph were labelled in vitro with a fluorescent dye and retransfused. The labelling index of fluorescent cells in the intestinal lymph increased rapidly and remained at a high level until 44 h after cell transfusion. A four-to-ten times lower labelling index was found in the spleen, various lymph nodes and Peyer's patches. Most of the recovered lymphocytes were T cells. This model provides access to the cell pool leaving the gut wall, thus allowing an examination of its role in the gastrointestinal tract and other mucosal-lined organs.
Expression of various MHC class II molecules and of intracellular adhesion molecule-1 (ICAM-1) on focal clusters of dendritic cells in iodine deficiency goitres
Authors: DIMAL P , WILDERS-TRUSCHNIG M , MOOIJ P , LEB G , EBER O , LANGSTEGER W , HEBENSTREIT J , BEHAM A , STIEGLER C , DOHR G , DREXHAGE H A 
Published: July 2010

SUMMARY
Thyroid sections from 18 consecutive euthyroid patients undergoing surgery for iodine deficiency goitre were investigated by means of immunohistochemistry and immunotluorescence. evaluating the expression of MHC class II antigens (HLA-DR, -DP, -DQ, and RFDI) and intercellular adhesion molecule-1 on the formerly described clusters of dendritic cells, as well as on thyrocyles. Eleven of 18 iodine deficiency goitres contained clusters of dendritic cells. These clusters appeared to express only HLA-DR in two cases: in nine of 12 cases they showed a differential expression of class II molecules in the following frequency: HLA-DR &gt; DQ and/or -DP &gt; RFDI. These dendritic cells also were ICAM-1+. In four of 18 iodine deficiency goitres, thyroid epithelial cells showed MHC class II expression in several combinations, but were ICAM-1-. In normal thyroids and in nodular goitres from inhabitants of the endemic area not having an actual iodine deficiency, only sparse clusters of dendritic cells were found; these cells were only HLA-DR+. Follicle lining cells were negative for the MHC class II molecules. In normal thyroids from an area with sufficient iodine supply, no clusters of dendritic cells were seen. The few dendritic cells observed were lying isolated in the interstitium and only positive for H LA-DR and ICAM-1; epithelial cells were negative for the studied markers. These data show clusters of dendritic cells in thyroids of inhabitants of an endemic area. When goitre is accompanied by iodine deficiency at the moment of operation, there appears to be activation of these dendritic cells and of thyroid epithelial cells.
Detection of a circulating form of vascular cell adhesion molecule-1: raised levels in rheumatoid arthritis and systemic lupus erythematosus
Authors: WELLICOME S M , KAPAHI P , MASON J C , LEBRANCHU Y , YARWOOD H , HASKARD D O 
Published: July 2010

SUMMARYWe have developed a panel of MoAbs against four separate but overlapping epitopes on endothclial cell (EC) vascular cell adhesion molecule-1 (VCAM-1). Two of the MoAbs(1G11 and IE5) inhibited T cell adhesion to tumour necrosis factor (TNF)-activated EC, whilst two MoAbs (1.4C3 and 6D9) did not. Using these MoAbs we have identified a circulating form of VCAM-1 (cVCAM-l) which has identical epitope distribution to the EC form, and which is able to support the adhesion of the human lymphoblastoid cell line Jurkat J6 by a VLA-4- and VCAM-1-dependent mechanism when immobilized from plasma. cVCAM-l isolated by immunoaffinity and size-exclusion chromatographies was shown by SDS-PAGE to have an apparent mol. wt of 85 90 kD. Levels of cVCAM-l were significantly raised (P &lt; 0.001) in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) compared with normal individuals. It is possible that cVCAM-l may be a useful plasma marker for the diagnosis and management of patients with inflammatory diseases. Furthermore, detection of elevated cVCAM-l levels may act as a guide to the importance of VCAM-1-dependent cell adhesion in different pathological settings.
Divalency of the monoclonal antibody 5-1-6 is required for induction of proteinuria in rats
Authors: NARISAWA M , KAWACHI H , OITE T , SHIMIZU F 
Published: July 2010

SUMMARYA single i.v. injection of 3 mg of the F(ab')2 fragment of MoAb 5-1-6 into rats induced immediate proteinuria (128.1 ± 80.7 mg/24 h on day 1) which lasted 1–2 days. In contrast, rats administered 10 mg of the corresponding Fab fragment did not develop abnormal proteinuria even though an equivalent dose of the intact MoAb 5-1-6 far exceeded the nephritogenic dose. The total kidney binding of 125I-Fab fragment was 209.5 ± 34.3 μg/2 kidneys. This exceeded that obtained by injection of 3 mg MoAb 5-1-6 IgG1 (58.9 ± 12.5 μg/2 kidneys at 1 h)and was similar to that obtained following injection of 3 mg F(ab')2 fragment (235.3 ± 16.9 μg/2 kidneys). Immunofluorescence (IF) showed a linear pattern along the glomerular capillary wall at I h after the administration of MoAb 5-1-6 IgG1. F(ab')2 or Fab fragment. On day 5, fine to coarse granules were observed scattered in F(ab')2 injected rat glomeruli. whereas granules were densely localized in Fab-injected rat glomeruli. Complement-depleted rats injected with 3 mg of MoAb 5-1-6 IgG 1 developed proteinuria with the same time course as non-depleted rats. This observation, together with the ability of F(ab')2 to induce proteinuria. indicates that proteinuria induced by MoAb 5-1-6 is complement-independent. This study suggests that MoAb 5-1-6-induced proteinuria is initiated by cross-linking of the epitopes by divalent MoAb 5-1-6 and is independent of complement activity.
The influence of genetic factors on the immune response as judged by pneumococcal vaccination of mono- and dizygotic Caucasian twins
Authors: KONRADSEN H B , HENRICHSEN J , WACHMANN H , HOLM N 
Published: July 2010

SUMMARYEighty-four mono- and dizygotic Caucasian twins randomly chosen, except for age and sex distribution, were vaccinated with a 23-valent pneumococcal vaccine. Blood samples were drawn before and after vaccination and the concentration of IgG. IgG1 and IgG2 pneumococcal antibodies was meaured using an ELISA technique which only detects type-specific capsular antibodies, since C-polysaccharide antibodies in serum were removed. A significantly closer correlation was found regarding mean IgG and IgG2 antibody concentrations after vaccination in mono- compared with dizygotic twins, and this correlation was seemingly type-specific. Since environmental factors in our study population should not contribute more to the immune response in one type of twins compared with the other, we conclude that genetic factors influence the IgG and IgG2 antibody response to pneumococcal vaccination, and that this influence seems to be type-dependent.
The suppressive effect of gelatin-conjugated superoxide dismutase on disease development and severity of collagen-induced arthritis in mice
Authors: KAKIMOTO K , KOJIMA Y , ISHII K , ONOUE K , MAEDA H 
Published: July 2010

SUMMARYWe studied the effect of superoxide dismutase (SOD) on murine collagen-induced arthritis (CIA), an animal model of human rheumatoid arthritis (RA). Among SOD derivatives studied, only gelatin-SOD conjugate which has prolonged half life in vivo was effective to suppress the development of CIA. while native SOD or gelatin carrier alone was ineffective. Interestingly, pyran polymer-conjugated SOD which also has a long half life showed no suppressive effect on the disease. No significant effect on immune response against type II collagen (CII) was found in any of the experimental groups. In addition, induction of suppressor cells was not detected in spleen or lymph node cells of the gelatin-SOD-treated group. Therefore, these results suggest that oxygen radicals may have an important role in the effector phase of the immune response to manifest this chronic autoimmune polyarthritis. Thus, the use of appropriate antioxidants for the treatment of human RA may be rationalized.
Effect of pregnancy on proteoglycan-induced progressive polyarthritis in BALB/c mice: remission of disease activity
Authors: BUZÁS E I , HOLLÓ K , RUBLICZKY L , GARZÓ M , NYIRKOS P , GLANT T T 
Published: July 2010

SUMMARY
Proteoglycan-induced arthritis is a murine autoimmune model displaying many similarities to human rheumatoid arthritis and ankylosing spondylitis, as has been documented by clinical, immunological and histopathological studies. Since the onset of arthritis correlates with the serum antibody level to mouse cartilage proteoglycan (PG), it is believed that these autoreactivc antibodies may play crucial roles in the pathological mechanisms of PG-induced arthritis. We have found that fertility in these PG-induced arthritic mice had been reduced but, unlike collagen-induced arthritis, had not been completely lost. Moreover, pregnancy had a beneficial effect upon the clinical symptoms with very little or no influence on scrum antibody levels. Although fertility was retained and arthritic mothers delivered healthy offspring, the birth frequency was significantly less than in non-arthritic age-matched controls. Furthermore, the presence of anti-PG autoantibodies (predominantly IgG1 subclass) transmitted from arthritic mothers to infants transplacentally and by milk during the lactation period did not render these offspring either resistant or more sensitive to subsequent induction of arthritis. Subsequent immunization of infants with ‘arthritogenic’ PG revealed an unaltered susceptibility to arthritis induction.
Complete functional C1q deficiency associated with systemic lupus erythematosus (SLE)
Authors: KIRSCHFINK M , PETRY F , KHIRWADKAR K , WIGAND R , KALTWASSER J P , LOOS M 
Published: July 2010

SUMMARYA complete functional deficiency of Clq is described in a patient suffering from SLE. From reduced plasma C1 activity of the parents a hereditary trait was assumed. The defective C1q molecule was haemolytically inactive, did not bind to immune complexes, and was not recognized by the monocyte C1q receptor. C1 activity in the patient's serum could be restored by the addition of purified C1q. Analysis by gelfiltration and ultracentrifugation experiments revealed an immunoreactive molecule of about 150 kD mol. wt, corresponding to one structural subunit of the C1q macromolccule, containing two A chain-B chain dimers and a C-C chain dimer. Applying Southern blot analysis with cDNA clones encoding for the three individual chains of the C1q molecule, no restriction fragment length polymorphism was detected, ruling out possible major alterations of the genetic information.
Factors influencing the occurrence of active cytomegalovirus (CMV) infections after organ transplantation
Authors: BOLAND G J , HENE R J , VERVERS C , De HAAN M A M , De GAST G C 
Published: July 2010

SUMMARYIn this study, several factors influencing the occurrence of active CMV infection after organ transplantation (Tx) arc analysed. For this purpose, 105 heart, kidney and lung transplant recipients who were CMV-positive or had a CMV-positive donor, were closely monitored for active CMV infection by antigenaemia, cultures. CMV serology and lymphocyte proliferation (LP) to CMV. Univariate and multivariate regression analysis were performed. As pretransplant risk factors the HLA-type and numbers of HLA mismatches between recipients and their donors, and the CMV serology of the recipient and donor were analysed. A new finding was that recipients of donors positive for HLA-B7 were especially at risk for developing active CMV infection (P = 0.03) and CMV disease (P= 0.03). This was not due to increased rejection treatment in these patients. Post-transplant risk factors for development of active CMV infection were absence of detectable cellular immunity to CMV (lymphocyte proliferation) after Tx (P&lt;0.01) and rejection treatment with OKT3 or ATG (P = 0.05). High levels of IgG anti-CMV did not prevent occurrence of active CMV infection or CMV disease in the CMV+ recipients.
Neutrophil activation in ivermectin-treated onchocerciasis patients
Authors: NJOO F L , HACK C E , OOSTING J , STILMA J S , KIJLSTRA A 
Published: July 2010

SUMMARYInvermectin is a safe and effective drug for onchocerciasis treatment. In certain individuals, however, therapy is accompanied by adverse reactions. The mechanisms underlying these reactions are not yet known. The aim of the present study was to investigate whether neutrophils are involved in the development of these adverse reactions. Elastase and lactoferrin, two markers for the release of neutrophil azurophilic and specific granule contents respectively, were measured by radioimmunoassays in plasma of onchocerciasis patients with varying degrees of side effects, as well as in control subjects before and 1 and 2 days after ivermectin treatment. A considerable increase of elastase levels after treatment was observed, whereas lactoferrin levels did not change. The percentage of patients with elevated elastase levels was significantly correlated with the degree of side effects. These findings suggest that neutrophil activation may be involved in the development of adverse reactions in these patients.