bluuebunny/crossref_metadata_2025_split huggingface dataset:
In vitroimmunotoxicity of ±2′-deoxy-3′-thiacytidine, a new and-HIV agent
Authors: LISIGNOLI G , MONACO M C G , DEGRASSI A , TONEGUZZI S , RICCHI E , COSTIGLIOLA P , FACCHINI A 
Published: July 2010

SUMMARYThe present study compares the in vitro effect of (±)-2′-deoxy-3′-lhiacylidine (BCH 189) a new synthetic anti-HIV-l dideoxynucleosidc. with 3′-azido-3′-deoxythymidinc (AZT) on the immune function of lymphocytes from 10 normal and 12 HIV-1+ patients (CDC II and III). The effect of different doses of BCH 189 and AZT was analysed in vitro on: (i) T cell proliferation after stimulation with concanavalin A (Con A) or anti-CD3 MoAb: (ii) B cell proliferation and immunoglobulin production after stimulation with pokeweed mitogen (PWM); (iii) cytokine production (IL-2. IL-6. GM-CSF, tumour necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ)) from lymphocytes stimulated with anti-CD3 MoAb or phylohucmagglutinin (PHA). BCH 189 inhibited the proliferation of B and T lymphocytes from normal and HIV’ subjects less than AZT: even if lymphocytes from HIV+ (CDC HI) subjects produced higher levels of IL-6 and TNF-α, neither BCH 189 nor AZT molecule interfered with cytokine release. Immunoglobulin production from B lymphocytes was inhibited only by a high concentration (50 μm) of BCH 189 or AZT. These results show that BCH 189 affects lymphocyte proliferation in vitro less then AZT, and support its use in clinical trials in HIV-infected patients.
Elevated levels of antibodies against sulphatide are present in all chronic chagasic and dilated cardiomyopathy sera
Authors: AVILA J L , ROJAS M , CARRASCO H 
Published: July 2010

SUMMARYA natural anti-sulphatide antibody was found to be present in the serum of every normal individual studied. The reactivity of the antibody was assessed by its interaction with galactosylceramide-P-sulphate. Antigen-antibody binding was strongly blocked by 1 mm heparin, dextran sulphate and chondroitin sulphate A, and by 5 mM chondroitin sulphate B. Antibodies avidly absorb to rabbit erythrocytes, but discretely to rat erythrocytes, suggesting that they are different from galactocere-broside antibodies. Elevated levels of sulphatide antibodies were present in all of 102 chronic Trypanosoma cruzi-infected patients studied, but not in other patients having cutaneous or visceral leishmaniasis, T. rangeli infection or several other protozoal, helminthic or mycotic infections. Interestingly, 100% of 40 dilated cardiomyopathy patients also have elevated levels of sulphatide antibodies. As T. cruzi is rich in galactocerebroside sulphate, it is proposed that in chagasic patients this glycolipid could act as an immunogen, inducing elevated titres of sulphatide antibodies, which could be important in the pathogenesis of cardiac or peripheral nerve symptoms.
Failure of FK 506 to suppress the T cell-mediated immunity of mice toListeria monocytogenes
Authors: WAGNER J A , KRETSCHMAR M , NICHTERLEIN T , HOF H , QUADE B 
Published: July 2010

SUMMARYListeria monocytogenes belongs to the group of intracellular bacteria, which means that they reside and multiply within host cells. The protective immunity against such an infection is mediated by cellular immune mechanisms. Whereas the CD8+ T cell population plays a major role therein, the CD4+ T cells are held to be of minor importance in this defence system. Consequently, one can understand that immune suppression with FK 506 which acts primarily on this latter T cell subset, docs not interfere with protective immunity of mice infected with L. monocytogenes. We have demonstrated that the drug blocks neither curing of primary infection, nor formation of granulomas, nor induction of cell populations capable of mediating adoptive transfer of immunity, nor expression of pre-existing immunity.
Early IL-2/sIL-2R surge following surgery leads to temporary immune refractoriness
Authors: LAHAT N , SHTILLER R , ZLOTNICK A Y , MERIN G 
Published: July 2010

SUMMARYHigh serum level of immunoreactive but not biologically active IL-2 was detected 1 day after surgery in patients undergoing major operation (abdominal, open-heart), in proportion to the tissue injury caused by surgical trauma. IL-2 values were highest in those patients who underwent open-heart surgery and received blood transfusions. In all patients they declined in the third and fourth postoperative days. Elevated serum levels of soluble IL-2 receptors (sIL-2R) were already present 1 day after operation, and peaked in the third and fifth post-opperative days after mitogen triggering. Blood lymphocytes derived from operated patients secreted reduced amounts of bolh IL-2 and sIL-2R compared with control lymphocyies. The extent and duration of this reduction were also proportional to the tissue trauma and were affected by blood transfusions. Based on these data we suggest that early post-operative systemic immunological activation (appearance of IL-2 in the serum) is followed by elevation of sIL-2R. which then interferes with IL-2-dependent immunity. Blood lymphocytes are probably not involved in the post-operative immunological activation. The trigger for and the site of IL-2 /s IL-2R synthesis are not yet clear.
Ultrastructural studies bearing on the mechanism of UVB-impaired induction of contact hypersensitivity to DNCB in man
Authors: MOMMAAS A M , MULDER A A , VERMEER M , BOOM B W , TSENG C , TAYLOR J R , STREILEIN J W 
Published: July 2010

SUMMARYIn both murine and human experimental systems, acute, low dose exposure of skin to ultraviolet B light (UVB) impairs the induction of allergic contact dermatitis (ACD) by haptens such as dinitrochlorobenzene (DNCB) in a significant proportion of individuals. By light microscopy, epidermal Langerhans cells (LC) have been reported to be depleted by UVB exposure as well as by epicutaneous hapten application, implying that LC may be the locus of action of the effeeis of both UVB and DNCB. However, light microscopy can not readily distinguish cell density changes secondary to LC necrosis from changes resulting from down-modulation of expression of LC surface molecules. Using a highly sensitive immunogold electron microscopic approach, we have evaluated the differential effects of UVB and/or DNCB on human epidermal LC. The results reveal that DNCB alone eaused significant up-regulation of cell surface HLA elass II expression on a very small number of LC. the major fraction of LC expressing normal levels of HLA class II. Furthermore, DNCB alone caused a modest reduction in the density of LC at the treated sites without evidence of cell necrosis. Treatment with UVB alone or UVB exposure followed by DNCB resulted in a reduction in the density of LC. with widespread evidence of LC necrosis. However, the few remaining intact LC were all intensely HLA class II-positive after UVB exposure followed by DNCB. whereas treatment with UVB alone did not result in changes in LC HLA class II expression. The findings that after DNCB painting only a small proportion of the LC were strongly HLA class II-positive. but after UVB exposure followed by DNCB all intact LC displayed significant up-regulation of cell surface HLA class II expression, imply that UVB exposure inhibits the migration of epidermal LC. This is consistent with the view that DNCB fails to induce ACD when hapten is painted on UVB-exposed skin because insufficient LC are available to initiate T cell activation in the draining lymph node.
Concomitant enhancement of the response to Mls-la antigens and the induction of post-thymectomy autoimmune gastritis in BALB/c mice
Authors: MURAKAMI K , HOSONO M , MARUYAMA H , MORI Y , NISHIO A , FUKUMOTO M , WATANABE Y , INABA M , KURIBAYASHI K , SAKA M , MASUDA T 
Published: July 2010

SUMMARYWe examined the role of Mis antigens in the induction of autoimmune gastritis (AIG) in BALB/c and DBA/2 mice subjected to thymeclomy. The prevalence of AIG in Mls-lb mice which underwent thymectomy on day 3 after birth (3d-Tx) was 78% (mean), while in Mis-1a DBA/2 mice it was &lt; 6%. Whereas AlG-negative 3d-Tx DBA/2 mice produced 2-mercaptoethanol (2-MF.)–sensitive anti-parietal cell autoantibody. AIG-positive BALB/c mice made 2–ME-resistant anti-parietal cell autoantibody. In addition, the prevalence of AIG in 3d-Tx BALB/c mice which were rendered tolerant to M Is-1a antigens by injection of bone marrow cells from (BALB/c ± DBA/2)F1 mice within 24 h after birth was decreased compared with the non-tolerant control mice: the prevalence being 80% in the controls and 30% in the tolerant animals. Thus, the activation of helper T cells, including T cells responding to Mls-1a antigens and including immunoglobulin class switch, appeared to be closely associated with the induction of AIG. Flowcytometric analysis confirmed that C'D4- Vβ6 T cells had increased in the regional lymph nodes of the stomach in AIG mice. However, an increase in the number of Vβll T cells, which are known to increase in 3d-Tx mice, occurred in the CD8, but not in the CD4 T cell population. Injection of MoAb to L3T4. but not Lyt2. Vβ6-or Vβ8–TCR, into 3d-Tx BALB/c and syngeneic nude mice which had received spleen cells of 3d-Tx BALB/c mice bearing AIG completely abrogated the development of AIG. despite there being remarkable decreases in T cells expressing relevant markers to the injected antibodies in all the mice. These findings suggest that the increase of V bT6+L3T4+ T cells in AIG mice was concomitant with the activation of A IG-inducing Vβ6- L3T4+ T cells.
An acute model for IgA-mediated glomerular inflammation in rats induced by monoclonal polymeric rat IgA antibodies
Authors: STAD R K , BRUIJN J A , van GIJLSWIJK-JANSSEN D J , van ES L A , DAHA M R 
Published: July 2010

SUMMARYAn acute model Tor IgA-mediated glomerular inflammation in rats was induced by the in situ deposition of IgA directly into the glomerular mesangium. F(ab')2 anti-Thyl MoAb was used to anchor an antigen. DNP (2,4-dinitrophenol), in the glomeruli of rats. Subsequent infusion of rat polymeric (p-) or monomeric (m-) IgA MoAb with specificity for DNP resulted in mesangial deposition of IgA in both groups of rats. However, acute proteinuria was observed only in p-IgA-treated rats and not in PBS- or m-IgA-treated rats. Immunofluorescence analysis revealed deposition of C3 in an identical pattern to that of IgA in the glomeruli of p-IgA-treated rats. No mesangial deposits of C4 or Clq were seen in these animals. Rats receiving m-IgA or PBS displayed no detectable C3, C4 or Clq deposition. The amount of proteinuria in p-IgA-treated rats was related to the amount of deposited C3. The presence of intraglomerular monocytes was only observed 2 days after p-IgA injection. By light microscopy, aneurysm formation, mesangial hypercellularity and matrix expansion were seen only in p-IgA-treated rats. However, by 37 days post-injection complete resolution of the lesions was observed. No histological renal changes were observed in PBS- or m-IgA-trcatcd rats. In conclusion, an acute form of IgA-mediated nephritis in rats was induced by p-lgA but not by m-IgA. This reproducible model provides a basis for further study into the mechanisms of IgA-mediated glomerular inflammation.
Comparison of potentiality to induce graft-versus-host reaction with small bowel, pancreas/spleen, and liver transplantation in the rat
Authors: KOBAYASHI E , KAMADA N , ENOSAWAJ S , TOYAMA N , DELRIVIERE L , GOTO S , KIM Y I L , MIYATA M 
Published: July 2010

SUMMARY
Although small bowel transplantation (SBT). or pancreas-spleen transplantation (PST) often lead to lethal graft-versus–host reaction (GVHR) in experimental animals, fatal GVHR is rare after clinical liver transplantation. This study describes a modified model of SBT and PST in the rat using cuff techniques applied to the renal artery and vein of the recipient. The ability of LEW (RTI1) or BN (RTln) lymphocytes accompanying intestinal, splenic, or hepatic grafts to induce lethal GVHR in (LEW BN) F1 hybrid recipients was compared. SBT and PST experiments showed that lethal GVHR always occurred in LEW-into-F1 combination, but was much less frequent in BN-into-F1 SBT. In mixed lymphocyte reaction (MLR), LEW mesenteric or splenic T cells showed significantly higher proliferative responses against BN stimulators than did BN mesenteric or splenic T cells against LEW. Adoptive cell transfer experiments using mesenleric or splenic cells also showed that LEW cells were higher responders than BN. In contrast with SBT and PST results, a lethal GVHR was not induced after liver or pancreas grafting alone in either parent-to-F1 combination. In MLR, hepatic T cells from either parent failed to elicit a proliferative response against allostimulators. These results indicate that the occurrence of lethal GVHR is dependent upon the reactivity of parental lymphocytes against allo-antigenicity of F1 hybrids and also upon the lymphoid tissue transplanted. The lack of alloreactivity of hepatic T cells accounts for the absence of lethal GVHR after liver grafting.
A soluble form of the human transferrin receptor is released by activated lymphocytesin vitro
Authors: WOITH W , NÜSSLEIN I , ANTONI C , DEJICA D I , WINKLER T H , HERRMANN M , PIRNER K , KALDEN J R , MANGER B 
Published: July 2010

SUMMARYSoluble transferrin receptors (sTfR) were detected in culture supernatants of activated human peripheral blood mononuclcar cells (PBMC) using a sandwich ELISA technique with two non-cross-reacting TfR MoAbs. Mitogenic stimulation of lymphoid cells induced both up-regulation of TfR surface density and release of sTf R to the medium. Peak levels of sTfR in culture supernatants occurred at day 4 after activation, 1 day later than maximum expression of TfR in the plasma membrane. Production of sTfR was independent of proliferation, as demonstrated by measuring sTfR release by PBMC, which had becn irradiated with a dose of 20 Gy before activation. In addition to these in vitro experiments, we tested the sera of 85 patients with systemic lupus erythematosus (SLE). an autoimmune disease accompanied by in vivo activation of lymphocytes, for their sTfR levels. No correlation of these data was detectable to serum concentrations of the soluble α-chain of the IL-2 receptor, an unequivocal marker of lymphocyte activation. However, they correlated negatively to the haemoglobin content of the patients’ erythrocytes. indicating that erythroid progenitors are the predominant source of sTf R in SLE patients’ sera.
Subsets of CD8+, CD57+ cells in normal, healthy individuals: correlations with human cytomegalovirus (HCMV) carrier status, phenotypic and functional analyses
Authors: WANG E C Y , TAYLOR-WIEDEMAN J , PERERA P , FISHER J , BORYSIEWICZ L K 
Published: July 2010

SUMMARYTwo different subsets of CD8+, CD57+ cells have been defined, one expressing high levels (CD8high+(CD57+)), the other expressing low levels of surface CD8 (CD8low+(CD57+)). Increased numbers of CD8high+(CD57+) cells correlated with previous HCMV infection. By three-colour fluorescence analysis, the CD8high+(CD57 +) population expressed T cell markers such as CD3 and CD5, and most were αβ T cell receptor (αβ TCR)-positive. A significant proportion also expressed CD71 (transferrin receptor) and MHC class II, although little if any CD25 (IL-2R-p55). Some (≥ 40%) co-expressed CD45RA and CD45RO. The CD8low+ (CD57+) population expressed classical natural killer (NK) cell markers—CD2, CD16 and CD56. The two subsets were also functionally distinct; CD8high+ (CD57+) cells suppressed pokeweed mitogen (PWM)-driven, but not phytohaem-agglutinin (PHA)-driven proliferation and immunoglobulin production; CD8low+ (CD57+) cells exhibited NK cytotoxic activity which was not increased by interferon-alpha (IFN-α). Supernatant from cultured CD8high+ (CD57+) cells suppressed PWM-driven immunoglobulin production, but not proliferation, and this effect was abrogated by physical separation with tissue culture inserts. Thus, a T cell subset expressing activation and memory T cell markers with direct non-specific suppressor activity was present in peripheral blood mononuclear cells (PBMC) of healthy subjects with asymptomatic HCMV infection.
IgM and IgG antibodies to hepatitis C virus in patients with mixed cryoglobulinaemia
Authors: L'ABBATE A , CUTRUPI S , ROGNETTA M , FABIANO C , CRAXI A 
Published: July 2010

SUMMARY
To assess the relationship between hepatitis C virus (HCV) infection and essential mixed cryoglobulinaemia (EMC), sera from 23 patients with EMC were tested for IgG and IgM antibodies to HCV antigens and for HCV RNA. Quantitative HCV antibody studies were performed on scrum and purified cryoglobulin fractions. HCV antibodies of both IgG and IgM class were found in 22 (96%) patients. Ten of these were also HCV-RNA positives. Higher litres of anti-HCV IgM were present in the 11 patients with evidence of liver damage. Anti-HCV IgG antibodies were shown to be concentrated in the IgG fraction of cryoglobulins in all eight patients studied. These results strongly suggest a role for HCV in the pathogenesis of EMC.
DistinctH-2complex control of mortality, and immune responses to tuberculosis infection in virgin and BCG-vaccinated mice
Authors: APT A S , AVDIENKO V G , NIKONENKO B V , KRAMNIK I B , MOROZ A M , SKAMENE E 
Published: July 2010

SUMMARYWe have studied the impact of distinct haplotypes and of difierent alleles at specific H-2 loci on: (i) the susceptibility to lethal form of experimental tuberculosis; (ii) the level of DTH to mycobacterial antigens: (iii) the efficacy of vaccination with bacille Calmette-Guerin (BCG); and (iv) the IgG production and T cell proliferative response to H37Rv antigens. On the basis of median survival lime (MST) following primary inoculation with lethal dose of Mycobacterium tuberculosis, susceptibility to infection associated with I-Ab and Db alleles. host resistance associated with I-Ak and Dd alleles. Mice bearing a disease-resistant phenotype also developed a vigorous DTH response. Vaccination with BCG before H37Rv infection significantly prolonged the survival time of both resistant and susceptible animals, except in B10.M (H-2f) mice. The latter exhibited intermediate resistance to infection before but slight decrease in the MST following a high-dose BCG vaccination. Distinct H-2 regulation of susceptibility to lethal infection and of BCG vaccination efficacy was confirmed in another relatively resistant H-2f-bearing strain A.CA, in which mortality occurred more rapidly in vaccinated compared with primarily infected animals. The expression of the H-2f haplotype was associated with a low DTH response to tuberculin following vaccination and subsequent lethal infection. The lack of BCG protection against Myco. tuberculosis challenge in B10.M mice associated with the high litre of specific IgG. In addition, these mice exhibited a unique ability to respond to 65-kD antigen by both IgG synthesis and T cell proliferation.
Anti-CD28 antibody- and IL-4-induced human T cell proliferation is sensitive to rapamycin
Authors: LUO H , CHEN H , DALOZE P , ST-LOUIS G , WU J 
Published: July 2010

SUMMARYRapamycin (RAPA) is a potent immunosuppressant. In this study we investigated the effect of RAPA on T cell proliferation triggered by various stimuli in an in vitro human model. The proliferation of T cells stimulated via an alternative pathway using phorbol myristate acetate (PMA) and anti-CD28 antibody (αCD28) in the absence of antigen-presenting cells (APC) was strongly inhibited by RAPA. T cell proliferation provoked via a combination of CD3/TCR and CD28 pathways using anti-CD3 antibody (αCD3) plus αCD28 was also inhibited by RAPA in the presence of APC. The mitogen (phytohaemagglutinin (PHA) or αCD3)-induccd up-regulation of expression of the IL-2 receptor a chain (IL-2Rα) and the IL-4 receptor (IL-4R) was sensitive to RAPA. This suggests that RAPA's interference with the IL-2 and IL-4 autocrine loops during T cell activation might contribute to RAPA's overall immunosuppressive effect. We have further demonstrated in a two-stage culture system that RAPA strongly inhibited IL-4-stimulated proliferation of T cells, the latter being either pretreated with αCD3 in the presence of APC, or with PMA plus αCD28 in the absence of APC. The result suggests that the Ca++ influx during the pretreatment is not obligatory for T cells to achieve IL-4 responsiveness. The results also indicate that RAPA's antiproliferative effect on IL-4-stimulated T cells is not contingent on the various mechanisms of cell priming. Therefore, RAPA's major target is probably at the second stage after the priming. Our study has extended current knowledge about the effect of RAPA on human T cells.
A high proportion of the Vδ1+ synovial fluid γδ T cells in juvenile rheumatoid arthritis patients express the very early activation marker CD69, but carry the high molecular weight isoform of the leucocyte common antigen (CD45RA)
Authors: KJELDSEN-KRAGH J , QUAYLE A J , VINJE O , NATVIG J B , FØRRE Ø 
Published: July 2010

SUMMARYWe have previously shown that γδ T cells in the synovial compartment of patients with juvenile rheumatoid arthritis (JRA) express activation antigens (CD69 and HLA-DR) and that they are predominantly of the Vδ1 subset. In this study we have analysed the expression of activation antigens (CD69 and HLA-DR) and different isoforms of the leucocyte common antigen (CD45RO and CD45RA) on the Vδ1 and the V52 subsets of γδ T cells in paired samples of synovial fluid and peripheral blood of nine patients with JRA, and in the peripheral blood of five children with idiopathie seoliosis. In the synovial fluid of children with JRA, there were significantly more Vδ1+CD69+ and Vδ2+CD69+ cells compared with the peripheral blood of the same patients. In contrast, however, in the synovial fluid the Vδ1 and the Vδ2 subsets differed with respect to the expression of the two isoforms of the leucocyte common antigen. The majority of the Vδ1+ cells expressed the high molecular weight isoform (CD45RA+) while most of the Vδ2+ cells carried the low molecular weight variant (CD45RO+) of this molecule.
Reduction of monocyte-macrophage activation markers upon anti-CD4 treatment. Decreased levels of IL-1, IL-6, neopterin and soluble CD14 in patients with rheumatoid arthritis
Authors: HORNEFF G , SACK U , KALDEN J R , EMMRICH F , BURMESTER G R 
Published: July 2010

SUMMARYAnti-CD4MoAbs have been successfully used in initial treatment trials of rheumatoid arthritis. One remarkable feature of this therapy was the early reduction of synovitis along with a decrease of the erythrocyte sedimentation rate (ESR) and the C-reactive protein (CRP). Since not only T helper celis. but also monocytes-maerophages bear the CD4 antigen, the question was raised whether the immediate elTects observed may have been in part due to an influence on the mononuclear phagocyte system. Inimediately after MoAb infusions, a significant reduction of the absolute peripheral blood monocyte count down to 30%(P &lt; 0·001) was noted within the firsl hour of injection. In contrast to strikingly elevated levels of soluble CD4 after treatment which was indicative of T cell lysis, soluble CD14 levels did not rise, but rather decreased from previously elevated levels. Before treatment, aetivation of the monocyte-macrophage system had been signified by elevated serum levels of IL-1, IL-6. CRP and neopterin as well as a marked in vitro production of IL-1. tumour necrosis faetor-alpha (TNF-α)and IL-6. Subsequent anti-CD4 treatment resulted in a rapid and significant reduction of monocyte-derived circulating cytokines and mediators concordant with a reduced capacity to produce IL-1. TNF-α, and IL-6 in those paiients who demonstrated clinical benefits. Therefore, studies of monocyte aetivation markers may be useful in identifying subsequent responders to anti-CD4 therapy.