bluuebunny/crossref_metadata_2025_split huggingface dataset:
Quantitative studies of monoclonal antibody 5-1-6-induced proteinuric state in rats
Authors: KAWACHI H , MATSUI K , ORIKASA M , MORIOKA T , OITE T , SHIMIZU F 
Published: July 2010

SUMMARYMurine monoclonal antibody (MoAb) 5-1-6 was already reported to bind to epithelial cell fool processes and to cause proteinuria in rats. In vivo kinetics of the injected MoAb 5-1-6, relationship between the quantity of kidney-binding antibody and proteinuria. and changes in the amount of antigenic molecule recognized by this MoAb in the proteinuric state were studied. The amount of total kidney-binding antibody (TK Ab) as determined I h after a 2 mg administration was 50.8 ± 10.4 μg/2 kidneys, and TKAb declined to 1.9 ± 0.4 at day 15. The minimum dose of MoAb required to induce proteinuria was 125 μg as the injected dose. This dose corresponded to 12-8 μg of TKAb at I h and 0.34 μg of TKAb at day 5. The amount of MoAb 5-1 -6 binding to isolated normal glomeruli was also shown to exceed 147-7 μg/76000 glomeruli, indicating proteinuria to be induced provided more than 8.7% (= 12.8/147.7) of the critical epitopes is specifically occupied by MoAb. The total amount of MoAb 5-1-6 bound to glomeruli in vivo and in vitro was assayed with [125I]-labelled anti-mouse IgG. The amount of [125I] anti-mouse IgG bound to glomeruli was 6.93 ± 0.45 μg/10 000 glomeruli from rat 5 days after this MoAb injection and 26.58 ± 0.66 μg/10000 control glomeruli, indicating the decrease in the number of MoAb 5-1-6-rccognizcd antigen molecules in glomeruli isolated from the rat in proteinuric state induced by this MoAb. Thus, the MoAb 5-1-6-recognized molecule itself may principally function to regulate the permeability of the glomerular capillary wall and the decrease of the molecule may lead to proteinuria.
Levels of soluble IL-2 receptor in plasma from asthmatics. Correlations with blood eosinophilia, lung function, and corticosteroid therapy
Authors: LASSALLE P , SERGANT M , DELNESTE Y , COSSET P , WALLAERT B , ZANDECKI M , CAPRON A , JOSEPH M , TONNEL A B 
Published: July 2010

SUMMARY
Evidence now suggests that cosinophils and T lymphocytes infiltrating bronchial tissues may play a key role in the pathophysiology of asthma. Circulating cosinophils, lung function, and plasma soluble IL-2 receptor (sIL-2R) were measured in 42 asthmatic patients referred for symptomatic asthma. The patients were divided into two groups based on the presence or absence of atopy. The group of non-atopic asthmatics was further divided according to the patients’ requirement for long term oral corticosteroids. The mean sIL-2R ± s.d. was 36.3 ± 9.9 pM in the control group, 28.9 ± 9.2 pM in the atopic asthmatics, 43.3 ±18.07 pM in the non-atopic asthmatics without oral steroid therapy, but was increased in the steroid-treated group (62.2 ±19-3 pM, P&lt;0.01). A significant correlation was found between I-FEV1 and circulating cosinophils in atopic asthmatics and in non-atopic asthmatics without oral corticosteroid therapy, but not in the steroid-treated group. Furthermore, significant correlations were found between sIL-2R and FEV1 and between sIL-2R and blood eosinophils, in the group of non-atopic asthmatics not on oral steroid therapy. No such correlations were evidenced in the other groups of asthmatics. Similar results were obtained during the clinical course of three non-atopic patients followed for more than I year. These data suggest that T cell activation appears more prominent in non-atopic asthma than in atopic asthma. Moreover, it appears that T cell activation can occur in severe forms of asthma despite steroid treatment. Finally, the results suggest a possible link between T cell activation, eosinophils. and lung function, which may reflect a particular pathogenetic mechanism involved in non-atopic asthma.
Enhancement of the antigen-presenting function of monocytes by cholesterol: possible relevance to inflammatory mechanisms in extrinsic allergic alveolitis and atherosclerosis
Authors: HUGHES D A , TOWNSEND P J , HASLAM P L 
Published: July 2010

SUMMARYExtrinsic allergic alveolitis (EAA) (synonym: hypersensitivity pneumonitis) is a hypcrscnsitivity lung disease characterized by lymphocytic infiltrates in the pulmonary interstitial tissues. We have previously reported that the numbers of lymphocytes in bronchoalveolar lavage (BAL) samples in this disease correlate with levels of cholesterol and neutral lipid-laden “foamy” macrophages. We have also reported that the macrophages express an increased density of MHC class II antigens (in particular HLA-DQ) which are known to be essential for antigen recognition by T lymphocytes. The aim of the present study was to explore whether cholesterol is capable of enhancing the antigen-presenting function of mononuclear phagocytes by modulating the expression of HLA-D region products. Incubation of purified monocytes from healthy volunteers with cholesterol in scrum-free medium induced a significant increase in both the percentages of monocytes expressing HLA-DQ (P&lt;0.02) and in the intensity of expression of the three HLA-D sub-region products. HLA-DQ. -DP and -DR (P&lt;0.02, &lt;0.01, &lt;005. respectively). The cholesterol pre-incubated monocytes also exhibited enhanced antigen-presenting function (P&lt;0.05), compared with controls pre-incubatcd without cholesterol. These findings indicate that increases in cholesterol in the extracellular milieu may augment antigen presentation by modulating the expression of HLA-D region products on antigen-presenting cells. Apart from EAA. this observation may also have relevance to inflammatory mechanisms in atherosclerosis, where‘foamy’ macrophages also occur in association with hypercholestcrolaemia.
Anti-P30 IgA antibodies as prenatal markers of congenital toxoplasma infection
Authors: DECOSTER A , DARCY F , CARON A , VINATIER D , DE L'AULNOIT D HOUZE , VITTU G , NIEL G , HEYER F , LECOLIER B , DELCROIX M , MONNIER J C , DUHAMEL M , CAPRON A 
Published: July 2010

SUMMARYThis study extends a previous study and confirms that the detection of anti-P30 IgA antibodies is very helpful in the diagnosis of acute acquired or congenital toxoplasmosis. Moreover, we demonstrate that an anti-P30 IgA response can be mounted in the fetuses infected by Toxoplasma gondii during their inira-utcrine life as early as week 23 of gestation. A double-sandwich ELISA described in our previous work was used to detect anti-P30 IgA antibodies in 1378 human serum samples collected from 551 patients, including 162 fetuses whose mothers had been infected by T. gondii during pregnancy, 46 congenitally infected and 90 uninfected newborns and 253 women suspected of having been infected during pregnancy, including the mothers of fetuses and newborns previously described. Anti-P30 IgA antibodies were detected in all cases of acute toxoplasmosis but in no case of chronic toxoplasmosis: in the majority of cases, the IgA antibody litre fell below cut-off in 3–9 months. Among the 46 congenitally infected newborns, anti-P30 IgA antibodies were detected in sera of 41 infected newborns (38 at birth, two in the first months of life, one in the seventh month of life), while anti-P30 IgM antibodies were detected in only 30 cases at birth and in one case during the first month of life. Among 162 fetuses, anti-P30 IgA response was observed in five infected fetuses, but was not detected in either 152 uninfected fetuses or in five fetuses considered as infected. The absence or presence of anti-P30 IgA antibodies in the fetus is discussed in relation to the date of maternal infection and collection of the fetal blood. It clearly appears from our study that the combined testing of both IgM and IgA in the fetus and the newborn is essential for a more efficient diagnosis of infection.
Involvement of HLA class II molecules in acquisition of staphylococcal enterotoxin A-binding activity and accessory cell activity in activation of human T cells by related toxins in vascular endothelial cells
Authors: UCHIYAMA T , ARAAKE M , YAN X J , MIYANAGA Y , IGARASHI H 
Published: July 2010

SUMMARYHuman umbilical vascular endothelial cells (HUVEC) express HLA class II molecules upon stimulation with recombinant human interferon-gamma (IFN-γ). Staphylococcal enterotoxin (SE) A (SEA)-binding assay using [125I]-SEA showed the presence of specific SEA binding in HUVEC stimulated with IFN-γ but not in unstimulated HUVEC. Levels of HLA class II expression and SEA-binding increased as the IFN-γ concentration and the period of stimulation were increased. Binding of [1254I]-SEA to the IFN-γ-stimulated HUVEC was reduced markedly by an anti-DR/DP MoAb. T cells produced IL-2 upon stimulation with a group of SEs (SEA, SEB, SEC, SED and SEE) in the presence HUVEC stimulated with IFN-γ but not in the presence of control HUVEC. The level of accessory cell activity in the IFN-γ-stimulated HUVEC was related to the level of HLA class II expression and SEA-binding activity. Antibodies to HLA class II molecules almost completely inhibited the response. These results indicate that HLA class II molecules are directly involved in the acquisition of these activities in HUVEC.
Induction and expression of protective T cells duringMycobacterium aviuminfections in mice
Authors: APPELBERG R , PEDROSA J 
Published: July 2010

SUMMARYMycobacterium avium is an opportunistic pathogen that infects individuals suffering from chronic lung disease or immunocompromised patients such as AIDS patients. Here we show that a highly virulent isolate of M. avium proliferated as extensively in T cell deficient as in immunocompetent mice. T cell deficient mice allowed a progressive growth of a less virulent AIDS-derived isolate of M. avium while immunocompetent mice arrested the growth of this isolate. Adoptive transfer of T cell enriched spleen cells between congenic strains of mice differing at the Bcg/Ity/Lsh locus showed that only naturally resistant BALB/c. Bcgr (C.D2) mice infected with the highly virulent strain of M. avium or the naturally susceptible BALB/c mice infected with the lower virulence isolate developed protective T cells and that these cells only mediated protection when transferred to naturally susceptible, but not to naturally resistant, mice. Both strains of M. avium proliferated in bone marrow-derived macrophages cultured in vitro and they were both susceptible to the bacteriostatic effects induced in the macrophages by crude lymphokines produced by concanavalin A-stimulated spleen cells.
Immune complex glomerulonephritis in experimental kala-azar II: Detection and characterization of parasite antigens and antibodies eluted from kidneys ofLeishmania donovani-infectedhamsters
Authors: SARTORI A , ROQUE-BARREIRA M C , COE J , CAMPOS-NETO A 
Published: July 2010

SUMMARYIn a previous report analysing kidney sections by immunofluorescence we showed that hamsters infected with L. donovani develop a glomerulonephritis (GN) associated with deposition of hamster immunoglobulins and parasite antigens in the glomeruli. In this study we characterize these immune components eluted from the kidneys. The eluted immunoglobulins showed specificity for L. donovani antigens and hamster immunoglobulins (rheumatoid factor-like activity). The four isotypes IgG1, IgG2, IgA and IgM were detected. Several L. donovani antigens were detected in the renal eluates by Western blot and immunoprecipitation using 125 I-labelled eluates. Proteins with mol. wt of 134, 82, 52, 31, and 26 kD were detected by Western blot and proteins with 134, 110, 93, 89 and 48 kD were detected by immunoprecipitation. With the exception of the 134 kD protein which was recognized by both rabbit anti-promastigote and rabbit anti-amastigote sera all the others were recognized only by the anti-amastigote serum. The 134 kD protein was the only one isolated from the kidneys of infected hamster immunocomplexed with IgG and was the only one detected in a promastigote lysate using IgG from L. donovani- infected hamsters.
Specific inhibition of mRNA accumulation for lymphokines in human T cell line Jurkat by mycobacterial lipoarabinomannan antigen
Authors: CHUJOR C S N , KUHN B , SCHWERER B , BERNHEIMER H , LEVIS W R , BEVEC D 
Published: July 2010

SUMMARYThe immunomodulatory effect of Mycobucterium tuberculosis-derived lipoarabinomannan (LAM) on mitogen/antigen-induced expression of mRNAs for a number of cytokines in human monocytic cell line Mono-Mac-6 and in T cell line Jurkat was investigated. Interestingly, LAM exhibited a down-regulatory effect on the accumulation of mRNAs for IL-2, IL-3, granulocyle-macrophage colony-stimulating factor (GM-CSF), and IL-2 receptor alpha (IL-2Rα) in T cells co-stimulated with phytohaemagglutinin-P (PHA) and 4β-phorbol-12-myristyl-13-acetate (PMA). In human Mono-Mac-6 cells, LAM has a weak inhibitory effect on the lipopolysaccharide (LPS)-induced mRNA accumulation for IL-1β, a slight stimulatory effect on mRNAs accumulation for IL-8 and tumour necrosis factor-alpha (TNF-α). but clearly no effect on mRNA accumulation for intercellular adhesion molecule-1 (ICAM-I). These findings imply that LAM may contribute to the immunologic defects associated with a number of mycobacterial infections by modulating these mediators.
Combined total deficiency of C7 and C4B with systemic lupus erythematosus (SLE)
Authors: SEGURADO O G , ARNAIZ-VILLENA A , IGLESIAS-CASARRUBIOS P , MARTINEZ-LASO J , VICARIO J L , FONTAN G , LOPEZ-TRASCASA M 
Published: July 2010

SUMMARY
The first inherited combined total deficiency of C7 and C4B complement components associated with SLE is described in a young female. Functional C7 assays showed a homozygous C7 deficiency in the propositus and her sister, and an heterozygous one in their parents. C4 molecular analyses showed that both the propositus and her mother had two HLA haplotypes carrying only C4A-spccific DNA sequences and a normal C4 gene number. Thus, only C4A proteins could be expressed, with resultant normal C4 serum levels. The coexistence of a combined complete C7 and C4B deficiency may therefore abrogate essential functions of the complement cascade presumably related to immune complex handling and solubilization despite an excess of circulating C4A. These findings challenge the putative pathophysiological roles of C4A and C4B and stress the need to perform both functional assays and C4 allotyping in patients with autoimmune pathology and low haemolytic activity without low serum levels of a classical pathway complement component.
Decreases in αβ T cell receptor negative T cells and CD8 cells, and an increase in CD4 +CD8+ cells in active Hashimoto's disease and subacute thyroiditis
Authors: IWATANI Y , AMINO N , HIDAKA Y , KANEDA T , ICHIHARA K , TAMAKI H , MATSUZUKA F , FUKATA S , KUMA K , MIYAI K 
Published: July 2010

SUMMARYWe examined peripheral lymphocyte subsets in patients with autoimmune thyroid disease, or subacute thyroiditis, in the active stage when possible. During destructive thyrotoxicosis arising from aggravation of Hashimoto's thyroiditis, both the numbers and proportions of αβ T cell receptor (TCR) negative T (WT31−CD3+) cells and CD8 (CD4−CD8+) cells decreased and those of CD4+CD8+ cells increased slightly, resulting in proportional increases in CD4 (CD4+CD8−) cells. non-T, non-B (CD5−CD19−) cells, and the CD4/CD8 cell ratio. Changes were similar in active subacute thyroiditis. During stimulative thyrotoxicosis in active Graves' disease, the numbers of such T lymphocyte subsets were not changed, but only the number of CD5+ B (CD5+CD19+) cells increased markedly, resulting in proportional decreases in total T (CD3+) cells, αβ+ TCR T (WT31+CD3+) cells, CD8 cells, and non-T, non-B cells. A serial study of some of the patients showed opposite changes in αβ TCR− T cells, the CD4/CD8 cell ratio, and CD5+ B cells between the active stages of Graves' and Hashimoto's diseases. αβ TCR− T cells were mostly γδ TCR+ T (IIF2+CD3+) cells in these patients. These data suggest that αβ TCR T (γδTCR+ T), CD8, and CD4+CD8+ cells are important in thyroid destruction in Hashimoto's disease and subacute thyroiditis, and that CD5+ B cells are important in thyroid stimulation in Graves' disease.
Analysis of different protein kinase C-dependent events in T cells from allogeneic bone marrow transplantation recipients
Authors: BALBOA M A , IZQUIERDO M , SÁNCHEZ-MADRID F , FERNÁNDEZ-RAÑADA J M , LÓPEZ-BOTET M 
Published: July 2010

SUMMARYIn order to understand the mechanisms underlying the T lymphocyte dysfunction associated to allogeneic bone marrow transplantation (BMT), we assessed two different protein kinase C (PKC) dependent events in T cells from BMT recipients: the PKC-dependent membrane expression and function of the CD69 early activation antigen; and the rapid phorbol ester-induced phosphorylation of PKC protein substrates in lysates from T cells permeabilized with digitonin, in the presence of (γ-32P)ATP. Most BMT recipient T cells detectably expressed the CD69 surface antigen after 24 h of stimulation with either phorbol 12-myristate 13-acetate (PMA) or anti-CD3 MoAb and PMA, thus indicating that PKC activity is sufficient to induce de novo gene expression. Nevertheless, it is noteworthy that the fluorescent staining intensity with anti-CD69 MoAbs was significantly lower in BMT recipient T cells than in normal T lymphocytes, although no clear-cut correlation was found between the expression of CD69 and the proliferative capacity. However, the pattern of PMA-induced phosphoproteins analysed as early as 1 min after PKC activation in T cells from BMT recipients displaying a low response to mitogenic stimuli, was undistinguishable from that detected in T cells from healthy subjects. In all cases a major 110-kD phosphoprotein was observed, which was inducible with PMA. phorbol 12,13-dibutyrate (PDBu). 1-oleoyl-2-acetylglycerol (OAG) and a phorbol-ester-related activator of PKC (mezerein); moreover, its phosphorylation was blocked by pretreating cells with the PKC inhibitor H-7. Altogether our results suggest that the depressed mitogenic responses, which were also observed in the present study when T cells were stimulated via CD69, cannot be simply attributed to a defective PKC activity.
Vasoactive intestinal peptide stimulates immunoglobulin production and growth of human B cells
Authors: ISHIOKA C , YOSHIDA A , KIMATA H , MIKAWA H 
Published: July 2010

SUMMARYThe effect of vasoactive intestinal peptide (VIP) on human lymphoblastoid B cell lines and tonsil B cells was studied. VIP increased immunoglobulin production and proliferation by lymphoblastoid B cell line. GM-1056, in a dose-dependent manner. As little as 10-12 M of VIP was effective, and higher concentrations of VIP induced an approximately five-fold increase in IgA production. Moreover, this enhancement was blocked by VIP antagonist. Similarly, VIP enhanced IgM and IgG production by other lymphoblastoid B cell lines, CBL and IM-9, respectively. In contrast to VIP, another neuropeptide substance P (SP) or somatostatin failed to enhance immunoglobulin production and thymidine uptake. VIP also enhanced IgA production and thymidine uptake by purified tonsil B cells. However, in contrast to B cell lines, VIP failed to enhance IgM and IgG production by tonsil B cells. SP or somatostatin failed to enhance immunoglobulin production or thymidine uptake by tonsil B cells. These results indicate that VIP acts as B cell stimulatory factor and that VIP may also have preferential effect on IgA production on tonsil B cells.
Characterization of neutrophil-mediated degradation of human C-reactive protein and identification of the protease
Authors: SHEPHARD E G , KELLY S L , ANDERSON R , FRIDKIN M 
Published: July 2010

SUMMARYHuman C-reactive protein (CRP) is shown to mediate a release of enzymatic activity from neutrophils which promotes its own degradation in the extracellular medium. This egress of proteolytic activity, which was upregulated by phorbol 12-myristate 13-acetate (PMA), was found to occur from both the cytoskeleton and membrane fractions of neutrophils and was dependent on the time of incubation of CRP with the cells and the concentration of CRP. Neutrophil kinases activated by PM A are found to be involved in upregulating the activity of the CRP-degrading protease. The apparent molecular weight of the CRP-degrading protease associated with the conditioned medium from PMA-stimulated neutrophils and neutrophil membrane and cytoskeleton preparations, was found by size exclusion chromatography to be 600 kD and migrated on 3–13% SDS-PAGE as four discrete bands to positions corresponding to apparent molecular weights of 209 kD, 316 kD, 398 kD and 501 kD.
Human trophoblast cells express CD4 and are permissive for productive infection with HIV-1
Authors: DAVID F J E , AUTRAN B , TRAN H C , MENU E , RAPHAEL M , DEBRE P , HSI B L , WEGMAN T G , BARRE-SINOUSSI F , CHAOUAT G 
Published: July 2010

SUMMARYThe European collaborative study of HIV-infected pregnant women in Europe now indicates a 13% risk of fetal HIV infection (originally thought to be about 30%, and possibly higher in some countries). Several reports suggest trans-placental passage. However, the detailed mechanisms associated with such vertical transmission have not yet been clarified. We have examined the possibility that HIV enters placental tissue from maternal blood via binding to CD4 and Fc receptors (FcR) at the trophoblast level, allowing intraplaccntal infection. Here we report the detection of several FcR with distinct localization in the placental villus as well as CD4 surface expression on human trophoblast cells. In addition, we show that trophoblastic cells interact specifically with the gp120/gp160 viral envelope protein. By their tissue localization, these receptors could be responsible for the entry of HIV into the fetal placental cells. Furthermore, purified placental cells can be directly infected by HIV in vitro, and the infection is inhibited by soluble CD4. This suggests a crucial role of the CD4 receptor but an additional way of entry cannot be excluded. Such an in vitro model may be suitable for further studies concerning placental HIV transmission and its prevention.
CD4 lymphocyte subset abnormalities associated with impaired delayed cutaneous hypersensitivity reactions in patients with X-linked agammaglobulinaemia
Authors: CROCKARD A D , BOYD N A M , McNEILL T A , McCLUSKEY D R 
Published: July 2010

SUMMARYCirculating CD4 lymphocyte subset (CD45RA; CD45RO; CD29; Leu8) levels were determined in nine patients with -inked agammaglobulinaemia (XLA), nine patients with common variable immunodeficiency (CVI) and in 18 age– and se-atched controls. CD4CD45RO and CD4CD29 cells were significantly lower (P&lt;001) in the XLA patient group (CD45RO, 15.7·10.2%; CD4CD29, 32.1 ±14.6%) compared with CVI patients (61.8·2504%; 6001 ±11.2%) and normal controls (43.7·22.3%, 54.5·22.0%). The levels of CD4CD45RA and CD4Leu8 cells were not abnormal in the XLA patient group. No selective reduction in CD4 subsets was observed in the CVI patient group. Delayed cutaneous hypersensitivity testing of five XLA and five CVI patients revealed a significantly reduced response to recall antigens in patients with XLA. This may relate to the deficiency of circulating memory T cells observed in these patients.