bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evidence for circulating activated cytotoxic T cells in HIV-infected subjects before the onset of opportunistic infections
Authors: VANHAM G , KESTENS L , GIGASE P , COLEBUNDERS R , VANDENBRUAENE M , BRIJ L , CEUPPENS J L 
Published: July 2010

SUMMARYThe activity of both cytotoxic T lymphocyte (CTL) and natural killer (NK) cells were measured cross-sectionally in 43 subjects seropositive for HIV, in 27 HIV- blood donors and in 24 HIV persons from the Outpatients Clinic for sexually transmitted diseases. CTL activity was evaluated using the HL-60 cells coated with OKT3 as the targets and freshly separated peripheral blood lymphocytes as the effectors. In 20 out of 43 HIV+ subjects, CTL activity was significantly enhanced in comparison to the HIV subjects. This lytic activity correlated positively with the percentages of CD3+ HLA-DR+, of CD8+ CR3- and of CD57+CD16- lymphocytes, and was greatly reduced after elimination of CD8+ of HLA-DR+ or of CD57+ cells. The median CTL activity seemed to increase from CDC group II to CDC group IV (Centers for Disease Control classification), but to return back to control levels in those patients with a history of opportunistic infections. NK function in HIV+ subjects was not significantly different from that in the blood donors. In seropositive patients, NK activity correlated positively with the percentages of both CD16+CD57+ and of CD8+ CR3+ cells and was strongly diminished after elimination of CD16 + or of CD57+ cells. There was no significant change in NK function according to the clinical stage. The data show that circulating CD8+HLA-DR+ CTJ57+ T cells in HIV+ subjects are activated cytotoxic T cells and point to progressive (over) activation of this T cell compartment until the onset of opportunistic infections.
In vitroproduction of interferon-gamma by peripheral blood from patients with Graves' disease, Hashimoto's thyroiditis and rheumatoid arthritis
Authors: MATSUBAYASHI S , AKASU F , KASUGA Y , SNOW K , KEYSTONE E , VOLPÉ R 
Published: July 2010

SUMMARYThe production of interferon-gamma (IFN-γ) by peripheral blood mononuclear cells (PBMC), CD4 cells, or CD8 cells in response to interleukin-2 (IL-2) stimulation has been studied; the samples were obtained from 12 healthy control subjects, 19 patients with Graves' disease (10 hyperthyroid and nine euthyroid), 13 patients with Hashimoto's thyroiditis (four hypothyroid and nine euthyroid), and 15 patients with rheumatoid arthritis (11 active and four inactive). A dose of IL-2 (25 U/ml) was utilized to induce IFN-γ by PBMC from all four groups. The incremental increase in IFN-γ values (with IL-2 stimulation minus without stimulation) was significantly less in PBMC from patients with Graves' disease, Hashimoto's thyroiditis, and rheumatoid arthritis than that in PBMC from control subjects. The values from PBMC in patients with Graves' disease in a euthyroid state were below normal but greater than those from patients with Graves' disease in a hyperthyroid state. The incremental increase in IFN-γ values from Graves' disease PBMC correlated with the serum TSH values (r=0.622, P &lt; 0.01), but not with thyroid autoantibodies (anti-thyroid microsomal antibodies, anti-thyroid microsomal antibodies, nor TSH-binding inhibitory immunoglobulin activities). The incremental increase in IFN-γ from PBMC from both control subjects and Graves* disease was correlated with that from CD4 cells (r=0.711, P &lt; 0.01), but not with that from CD8 cells. The production of IFN-γ in response to IL-2 from PBMC in Graves' disease correlated inversely with thyroid function, appearing to reflect the very effect of hyperthyroidism in this process. The precise explanation of these phenomena remains unclear. The decreased response of IFN-γ to IL-2 stimulation by PBMC from patients with Graves' disease, Hashimoto's thyroiditis, and rheumatoid arthritis seems to be a non-specific phenomenon occurring in both organ specific autoimmune disease and systemic autoimmune disease. It may be due to a down-regulation in autoimmune disease of CD4 cells in response to IL-2, a decreased level of IL-2 cellular receptors or a decreased receptor affinity, associated increased soluble IL-2 receptors, or a defect of the intra-CD4 cellular IL-2 signal to produce or release IFN-γ in the conditions studied.
Cord blood B cells are mature in their capacity to switch to IgE-producing cells in response to interleukin-4in vitro
Authors: PASTORELLI G , ROUSSET F , PENE J , PERONNE C , RONCAROLO M G , TOVO P A , DE VRIES J E 
Published: July 2010

SUMMARYNeonatal B cells have been considered immature because of their impaired capacity to produce immunoglobulins in response to polyclonal activators in vitro. Here we demonstrate that cord blood mononuclear cells (MNC) produce normal levels of IgE in vitro when cultured in the presence of interleukin-4 (IL-4), indicating that the B cells are mature in their capacity to switch to IgE-producing cells. However, in contrast to adult peripheral blood T cells, cord blood T cells failed to produce detectable levels of IL-4 upon activation by phytohaemagglutinin (PHA) concanavalin A (Con A) or combinations of PHA and the phorbol ester TPA. Interferon-gamma (IFN-γ) production by cord blood T cells following activation by Con A or PHA was also strongly reduced. However, high levels of IFN-γ, significantly higher than those produced by adult T cells, were synthesized in response to combinations of PHA and TPA, indicating that IFN-γ production by cord blood T cells is not intrinsically defective. In contrast, cord blood T cells produced levels of IL-2 that were significantly higher than those obtained by adult T cells tested in parallel. Collectively, our data indicate that the minimal levels of IgE production measured in cord blood (&lt; 1 U/ml) are not due to immaturity of the cord blood B cells, but may be associated with the failure of cord blood T cells to produce detectable levels of IL-4, which has been shown to be responsible for induction of IgE synthesis both in vitro and in vivo.
The capacity of interleukin-4 to inducein vitroIgE synthesis by B cells of patients with common variable immunodeficiency
Authors: PASTORELLI G , RONCAROLO M G , PERONNE C , TOVO P A , DE VRIES J E 
Published: July 2010

SUMMARYInterleukin-4 (IL-4) has been shown to induce IgE synthesis by peripheral blood mononuclear cells (PBMC) of normal donors in vitro. However, induction of PBMC of patients with common variable immunodeficiency (CVI) with IL-4 resulted in IgE production in only two out of eight cases tested. PBMC of the first patient that produced IgE in response to IL-4 also secreted normal levels of IL-4 upon activation. PBMC of the second patient secreted very low levels of IL-4 in vitro which may account for the very low serum IgE levels in this patient. Of the other six patients who had very low serum IgE levels and whose PBMC failed to produce IgE in response to IL-4 in vitro, five did not secrete IL-4 upon in vitro activation. The capacity of the T cells to produce IL-4 was intact in the sixth patient. Collectively our data indicate the PBMC of the majority of patients with CVI are defective since they failed to respond appropriately to IL-4 and they failed to produce IL-4, contributing to the view that CVI is a heterogeneous disorder in which a variety of T and B cell defects occur.
Chronic oral administration of dexamethasone to rats increases cytotoxicity, but not interleukin-1 elaboration, by alveolar macrophages
Authors: BECK J M , SUZARA V V , SHELLITO J 
Published: July 2010

SUMMARYChronic administration of corticosteroids has been used to induce pulmonary infection in animals, but the specific mechanisms by which corticosteroids modulate pulmonary host defence have not been clarified. Specifically, little is known about how corticosteroids influence the function of lung cells, such as alveolar macrophages. Cytotoxicity and interleukin-1 elaboration are two important mechanisms of macrophage defence against pathogens. To determine whether chronic administration of dexamethasone alters cytotoxicity and interleukin-1 elaboration by alveolar macrophages, we studied alveolar macrophages from rats treated with oral doses of dexamethasone for 2 weeks. We found that unstimulated alveolar macrophages from dexamethasone-treated rats exhibited increased cytotoxicity compared with alveolar macrophages from control rats. Moreover, alveolar macrophages from both groups of rats showed enhanced cylotoxicity after in vitro interferon-gamma and lipopolysaccharide treatment, in a dose-dependent manner. Although no spontaneous interleukin-1 elaboration was detected from alveolar macrophages from either group of rats, lipopolysaccharide increased interleukin-1 elaboration by alveolar macrophages from both groups of rats equivalently. These results indicate that chronic oral administration of dexamethasone to rats increases cytotoxicity, and does not alter the capacity of alveolar macrophages to elaborate interleukin-1. Therefore, chronic corticosteroid administration appears to produce selective alterations in these defence mechanisms of alveolar macrophages.
Effect of IgG for intravenous use on Fc receptor-mediated phagocytosis by human monocytes
Authors: JUNGI T W , BRCIC M , KUHNERT P , SPYCHER M O , LI F , NYDEGGER U E 
Published: July 2010

SUMMARYPolyspecific IgG given intravenously at high doses (IVIG) is used for immunomodulatory therapy in autoimmune diseases such as idiopathic thrombocytopenic purpura and myasthenia gravis. It is assumed that the clinical effect is brought about in part by a modulation of mononuclear phagocyte function, in particular by an inhibition of Fc receptor (FcR) mediated phagocytosis. In the present study, the effect of IVIG on FcR-mediated phagocytosis by monocytes was analysed in vitro. Since monocytes exposed to minute amounts of surface-bound IgG displayed impaired phagocytosis of IgG-coated erythrocytes (EA), the effect of IVIG was studied with mononuclear cells suspended in teflon bags in medium containing 10% autologous serum and IVIG 2–10 mg/ml). Monocytes pre-exposed to IVIG and then washed, displayed impaired ingestion of EA when compared with control cells cultured in 10% autologous serum only. The decrease in phagocytosis was observed with sheep erythrocytes treated with either rabbit IgG or bovine IgGl and with anti-D-treated human erythrocytes. This suggests that phagocytosis via both FcR type I (FcRI) and type II (FcRII) was decreased. The impairment of phagocytosis was dependent on the presence of intact IgG and was mediated by IVIG from nulliparous donors and from multigravidae to the same extent, suggesting that alloantibodies contained in IVIG have a minor role in modulating FcR-mediated phagocytosis by monocytes. A flow cytometric analysis using anti-FcRI, FcRII and FcRIII monoclonal antibodies showed that IVIG treatment upregulated FcRI expression but did not significantly alter the expression of FcRII and FcRIII.
CD8+/DR+ T gamma cells inhibit the autologous mixed lymphocyte reaction
Authors: HAYNES M K , MILLER J , FULLER L 
Published: July 2010

SUMMARYThe proliferative response of T cells during autologous mixed lymphocyte reactions (AMLR) was affected by depletion of IgG Fc receptor+ T lymphocytes (Tg). Removal of Tg cells resulted in enhanced proliferation, and EA-rosette isolated Tg cells, when added to AM LR cultures as irradiated third components, reduced the uptake of 3H-thymidine by 63–87% in a dose-dependent manner. Negative selection using an avidin-biotin affinity chromatography technique demonstrated that the suppression was mediated by DR+ Tg cells; the major proportion of which also expressed the CD8 antigen. By comparing AMLR supcrnatants collected from control (lacking Tg) and suppressed (containing Tg) cultures on days 2, 3, and 4, it was established that supernatants from suppressed cultures had significantly reduced levels of cytokine activity. These data indicate that the CD8 +/DR+ Tg cells function as suppressor cells during an AMLR and reduce the proliferative response by inhibiting AMLR responder T cells from producing the cytokines necessary for in vitro growth.
Characterization of two monoclonal antibodies (UCL4D12 and UCL3D3) that discriminate between human mantle zone and marginal zone B cells
Authors: SMITH-RAVIN J , SPENCER J , BEVERLEY P C L , ISAACSON P G 
Published: July 2010

SUMMARYTwo new monoclonal antibodies (MoAbs), UCL3D3 and UCL4D12 were obtained following immunization with follicular lymphoma (UCL3D3) or low-grade primary B cell gastric lymphoma cells (UCL4D12). In normal splenic white pulp, tonsil and small intestinal Peyer's patches, UCL4D12 recognizes marginal zone B cells and a subpopulation of follicle centre cells, whereas mantle zone B cells are UCL4D12 negative. In contrast, UCL3D3 recognizes mantle zone B cells and follicular dendritic cells, but not marginal zone B cells or follicle centre B cells. Double-immunofluorescence studies showed that in the splenic white pulp, these antibodies stain reciprocally. The majority of UCL3D3+ cells are slgM+ andsIgD+ whereas a higher proportion of UCL4D12+ cells express surface IgM (sIgM) but not surface IgD (slgD). Less than 10% of splenic B cells express both 3D3 and 4D12 antigens. None of the cell lines tested expressed either antigen. Functional studies showed that both antigens play a role in B cell activation as the MoAbs increase the mitogenic effect of Staphylococcus aureus Cowan I on tonsil B cells. This effect was maximal at 72 h in culture. TPA activation was reduced, and no effect was observed with anti-immunoglobulin (anti μ) or CDw40 (G28.5). UCL3D3 and UCL4D12 did not show any stimulatory effect on their own. Biochemical studies show that both MoAbs recognize proteins of 80–90 kD under reducing conditions. These two MoAbs appear to recognize new B cell surface antigens which may be useful for identifying subpopulations of B cells.
Cytostasis of different tumours by a murine PPD-reactive CD4+ T lymphocyte clone is mediated by interferon-gamma and tumour necrosis factor alone or synergistically
Authors: WING M G , MONTGOMERY A M P , HARLEY C , LACHMANN P J 
Published: July 2010

SUMMARYWe have shown that a murine CD4+ PPD-reactive T lymphocyte clone was weakly cytotoxic towards the syngeneic tumour B16 melanoma and MC6A fibrosarcoma which had been coated with PPD using a monoclonal antibody-PPD heteroconjugale. Cell-free supcrnatants produced by PPD-stimulated T lymphocyte clones were however highly cytostatic for the two tumour targets when assayed over 48–72 h. In this study we have demonstrated good litres of tumour necrosis factor (TNF) and interferon-gamma (IFN-γ) in the supernatants. which accounted for their observed cylostatic activity on the tumour targets. The high level of cylostasis seen with the B16 melanoma using the supernatants could be attributed to their sensitivity to the cytostatic activity of IFN-γ; the lower levels of cytostasis seen with the IFN-γ-resistant MC6A target was the result of IFN-γ increasing the sensitivity of this target to TNF. Antibodies to IFN-γ were able to neutralize the majority of the cytostatic activity of the supernatants on both targets, consistent with the role demonstrated for this lymphokine.
Bacteroides gingivalis-specificserum IgG and IgA subclass antibodies in periodontal diseases
Authors: OGAWA T , KUSUMOTO Y , HAMADA S , McGHEE J R , KIYONO H 
Published: July 2010

SUMMARYThe level of serum IgM, IgG and IgA antibodies including IgG1. IgG2, IgG3, IgG4, IgA1 and IgA2 subclass-specific antibodies to Bacteroides (Porphyromonas) gingivalis fimbriae and to lipopolysaccharide(LPS) were analysed in paiients with different forms of periodontal disease (PD) and control subjects by ELISA. Among PD subjects, sera obtained from adult periodonitis (AP). rapidly progressive periodontitis (RPP) and gingivitis contained high litres of fimbriae-specific IgG antibodies (7500–15000 ELISA units) followed by IgA (90–700 units) and IgM (30–90 units). In contrast, sera from localized juvenile periodontitis (LJP) subjects exhibited much lower titres of fimbriae-specific IgG (89 ± 11 units), IgA (31.5 units) and IgM (17 ± 3 units) antibodies. A similar response pattern was also seen in sera from normal subjects aged 35–41 years who practice normal oral hygiene, while sera of younger adults (aged 18–24) with superior hygiene did not have any antigen-specific antibodies. Analysis of IgG subclass anti-fimbriae responses revealed that the major response was IgG3 followed by IgG1, IgG2 and IgG4 in AP, RPP and gingivitis. Although lower, a similar pattern of IgG subclass titre was seen in LJP and normal subjects aged 35–41 years. When IgA subclass responses were measured in AP and RPP, higher titres of the fimbriae-specific response were noted with IgAl when compared with IgA2. However, lower but approximately equal levels of fimbriae-specific IgAl and IgA2 titres were seen in other PD groups. When anti-B. gingivalis LPS-specific responses were measured, the sera of AP patients contained high levels of IgG antibodies (2265 ± 224 units) followed by IgA (411 ± 90 units) and IgM (214 ± 56 units). Further. IgG anti-LPS responses were mainly IgG2 followed by IgG4. IgG3 and IgGI. For IgA subclass responses, higher titres of anti-LPS-specific antibodies were noted in IgA2 subclass over IgAl. These results showed that higher anti-B. gingivalis antibody responses occur in PD when compared with healthy individuals and protein and lipid-carbohydrate antigens of B. gingivalis induce distinct patterns of antigen-specific IgG and IgA subclass responses.
Macrophage procoagulant activity as an assay of cellular hypersensitivity to gluten peptides in coeliac disease
Authors: DEVERY J M , GECZY C L , DECLARLE D , SKERRITT J H , KRILLIS S A 
Published: July 2010

SUMMARYGluten and casein digests were tested for their ability to induce a cellular immune response on peripheral blood mononuclear cells (PBM) obtained from coeliac patients as well as healthy volunteers and disease control patients using the macrophage procoagulant assay. PBM from coeliac patients who had been on a gluten-free diet for less than 2 years responded strongly to gluten peptides, while coeiiac patients at diagnosis or who had maintained a strict gluten-free diet for longer than 5 years showed weaker responses. PBM from healthy volunteers did not respond to gluten or casein peptides, whereas those from patients with Crohn's disease displayed weak reactivity to gluten and casein peptides. Our study using the macrophage procoagulant assay confirms previous findings that lymphoid cells from patients with coeliac disease exhibit a specific cellular immune response to gluten. This assay represents an alternative measure for cell-mediated immunity and is technically much simpler than the previously described leucocyte migration inhibition assay. Macrophage procoagulant activity is measured using a simple plasma recalcification time assay or spectrophotometrically using commercially available chromogenic substrates.
Soluble interleukin-2 receptor and soluble CD8 in liver cirrhosis and obstructive jaundice
Authors: WAGNER F , ASSEMI C , LERSCH C , HART R , CLASSEN M 
Published: July 2010

SUMMARYActivated lymphocytes secrete soluble interleukin-2 receptor (sIL-2R); CD8-positive lymphocytes secrete soluble CD8 (sCD8). Liver dysfunction in cirrhosis and obstructive jaundice is known to result in depressed cellular immunity. To evaluate whether this is due to real inactivation of the immune system, we measured sIL-2R and sCD8 in the serum of 46 patients with liver cirrhosis, 25 patients with obstructive jaundice, 32 patients with alcoholic liver disease without evidence of cirrhosis, 23 healthy persons and 43 patients with unrelated disease. sIL-2R in patients with cirrhosis (mean ± s.e.m. 1499.140 U/ml) and obstructive jaundice (1517 ± 204) was significantly increased compared with healthy subjects (363 ± 29) and patients with unrelated diseases (685 ± 92); sCD8 was significantly increased in patients with cirrhosis (737 ± 63) but not in patients with obstructive jaundice (419 ± 32) compared with healthy subjects (322 ± 23) and patients with unrelated diseases (375 ± 22). No difference was found between patients with cirrhosis due to alcohol abuse (n= 15) and chronic hepatitis B (n = 6). The Child-Pugh score had no significant influence on the sIL-2R or sCD8 value. In obstructive jaundice, sIL-2R correlated with alkaline phosphatase as marker of cholestasis (r= 0.43). These data show that in spite of the apparent depressed cellular immune defense both in liver cirrhosis and obstructive jaundice there is a general activation of the immune system but the CD8+ cell compartment is only activated in liver cirrhosis. The great changes of sIL-2R and sCD8 in liver dysfunction are important for the interpretation of studies using these serum proteins as markers for immune activation.
Interpretation of blocking activity in maternal serum depends on the equation used for calculation of mixed lymphocyte culture results
Authors: PARK M I , EDWIN S S , SCOTT J R , BRANCH D WARE 
Published: July 2010

SUMMARY
Immunosuppressive blocking factors in maternal serum are usually determined by inhibition of mixed lymphocyte cultures (MLC), but reports on the importance of these factors for successful pregnancy are conflicting. Here we measured serum blocking activity in men, non-pregnant nulliparous women, non-pregnant multiparous women, women with normal pregnancies, and in women who had had recurrent spontaneous abortions and were treated with leucocyte immunizations. Three different equations were used for calculation of blocking activity: blocking effect index (BEI); stimulation index (SI); and blocking index (BI). By all three methods of calculation, significantly lower levels of blocking activity were noted for men and women compared with pregnant women and multiparae. In the patients with a history of recurrent spontaneous abortions blocking activity as determined by BEI and BI increased into the positive range after treatment with infusions of third-party donor leucocytes in a statistically significant number of women (P &lt; 0.05). However, blocking activity as determined by BEI had a higher predictive value for successful pregnancy than did that determined by BI or SI. Our data suggest that the equation used for calculating BEI is superior to other methods for the determination of blocking activity when monitoring the response to leucocyte immunization in women with recurrent spontaneous abortion. However, these results also cast doubt on the importance of blocking antibodies in histories of recurrent abortion, since pregnancies occurred in the absence and spontaneous abortions occurred in the presence of blocking activity.
Antibody repertoire against culture filtrate antigens in wild house mice infected withMycobacterium bovisBCG
Authors: HUYGEN K , PALFLIET K , JURION F , LENOIR C , VAN VOOREN J-P 
Published: July 2010

SUMMARYWild house mice (Mus domesticus) captured in a Flemish pigsty were infected intravenously with 4 × l06 viable units of Mycobacterium bovis BCG and examined by Western blot analysis for IgG secretion against BCG culture filtrate (CF) antigens. Wild mice showed a marked individual variation in antibody pattern when tested 4, 6 and 8 weeks after infection. Some animals reacted to a wide range of antigens and others only to a limited number. Most wild mice recognized preferentially antigens with molecular weight of 24 kD, 32 kD, 37–38–40 kD, 65 kD and 82 kD, i.e. the major CF antigens known to be recognized by sera from BCG-infectcd inbred laboratory strains, BALB/c, DBA/2, CBA/Ca and C57BL/6. The 32-kD fibronectin-binding protein and the 65-kD heat-shock protein appeared as very immunodominant in wild mice. Furthermore, about 20–25% of the mice reacted strongly with a unique antigen of 35 kD estimated molecular weight, to which the tested inbred laboratory mice did not respond. Monitoring the size of the bacterial population in the spleen indicated that the BCG inoculum did not replicate in wild mice, suggesting that the Bcgr allcle is expressed in this population.