bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differential effects of CD45 CD45R and CD45R0 monoclonal antibodies in modulating human B cell activation
Authors: DEANE D L , HARVEY E , STEEL C M 
Published: July 2010

SUMMARYWe have examined the effect of monoclonal antibodies (MoAbs) to different epitopes of the leucocyte common antigen (LCA). CD45, on anti-human immunoglobutin-primed B cell activation. Binding of MoAbs to restricted epitopes present on CD45 glycoproteins of 180 kD and 220 kD (designated CD45R0 and CD45R. respectively) was found to promote B cell proliferation in the presence of T cells. CD45 MoAbs reactive with ‘public’ determinants on all four constituent members of the LCA family (180, 190, 205, and 220 k D) had either little effect or inhibited the basal B cell response to anti-immunoglobulin priming. Simultaneous immunonuorcsccnt analysts of 5-broinodeoxyuridinc incorporation and the expression of CD19 (B cell specific) or CD2 (T cell specific) identified the majority of responder cells as B lymphocytes. CD45R MoAbs significantly enhanced the B cell response to sub-optimal concentrations of interleukin-2. CD45 and CD45R0 MoAbs failed to elicit a similar response. Antibody to the interleukin-2 receptor (anti-Tac) partially blocked the CD45R-driven. T cell-dependent B cell proliferation.
The complement-inhibiting protein, Protectin (CD59 antigen), is present and functionally active on glomerular epithelial cells
Authors: ROONEY I A , DAVIES A , GRIFFITHS D , WILLIAMS J D , DAVIES M , MERI S , LACHMANN P J , MORGAN B P 
Published: July 2010

SUMMARYProtectin (CDS9 antigen) is a 20-kD phosphatidyl-inositol-linked membrane protein that inhibits formation of the membrane attack complex (MAC) of complement on homologous cells. Although the antigen has been identified in a number of human tissues, until recently a functional role had been demonstrated only in circulating cells. Using immunofluorescence techniques we have shown the presence of protectin on human glomerular epithelial cells (GEC) in culture and on GEC, tubular epithelial cells and endothelial cells in frozen sections of normal human renal cortex. In addition, we present evidence that this protein functions in protection of GEC from homologous complement: cultured cells incubated with the Fab2 fragment of a monoclonal anti-protectin antibody were markedly more susceptible to killing by homologous serum than were cells in the absence of Fab2 anti-protectin. These findings suggest that this protein may be important in the maintenance of glomerular integrity in vivo, and may be of relevance in certain renal diseases.
Characterization of three monoclonal antibodies to membrane co-factor protein (MCP) of the complement system and quantification of MCP by radioassay
Authors: CHO S-W , OGLESBY T J , HSI B-L , ADAMS E M , ATKINSON J P 
Published: July 2010

SUMMARYMCP is a widely distributed regulatory glycoprotein of the complement system which binds C3b and C4b and has factor I-dependent co-factor activity. Monoclonal antibodies raised to lymphocytes (E4.3), chorionic microvilli (GB24) and an embryonal carcinoma cell line (TRA-2–10) recognize MCP (CD46). GB24 inhibited both the binding of MCP to its ligand iC3 and co-factor activity; E4.3 and TRA-2–10 did not. The binding of GB24 to cells bearing MCP was not cross-inhibited by E4.3 or TRA-2–10, but TRA-2–10 blocked binding and displaced pre-bound E4.3. Using these antibodies, we developed a radioassay for quantifying the number of MCP molecules/cell. Human peripheral blood mononuclear (PBMC) and polymorphonuclear cells (PMN) had about 10000 MCP/cell; platelets had about 600/cell, and no MCP was found on erythrocytes. Neoplastic hematopoietic cell lines, of myelocytic and T lymphocytic origin, had several-fold more (20–60000) molecules/cell than peripheral blood cells or B cell lines (about 12000). Malignant epithelial cell lines, HeLa (about 100000/cell) and HEp-2 (about 250000/cell) had the highest MCP expression of any cells examined. These monoclonal antibodies—especially GB24, which blocks MCP function–and the direct binding assay will facilitate the further analysis of the biology of this complement regulatory protein.
Autoantibodies to the URNP particles: relationship to clinical diagnosis and nephritis
Authors: REICHLIN M , VAN VENROOIJ W J 
Published: July 2010

SUMMARYPrecipitating autoantibodies to the URNP particles were used to select 80 patients, and were further characterized by immunoblotting and quantitative ELISA. These immunochemical results have been related to clinical diagnosis, the frequency of nephritis, and Raynaud's phenomenon. Autoantibodies to the 70-kD polypeptide of the Ul RNP particle were present in 16 out of 19 patients with mixed connective tissue disease (MCTD) and in 27 out of 61 patients with systemic lupus erythematosus (SLE). The ratio of anti-U1 RNP/Sm by ELISA and the frequency of antibody to 70-kD protein were directly related to the frequency of Raynaud's phenomenon and inversely related to the frequency of nehritis.
Increased CDS-positive B lymphocytes in type I diabetes
Authors: MUÑOZ A , GALLART T , VIÑAS O , GOMIS R 
Published: July 2010

SUMMARYCD5+ B lymphocytes have been implicated in the production of polyspecific and monospecific antibodies that bind self-antigens, and increased proportions of this B cell subset occur in patients with some autoimmune diseases. We investigated the proportion of peripheral blood CD5+ B lymphocytes in type I diabetic patients. Compared with 18 age-matched healthy subjects. 11 out of 28 (39.2%) type I diabetic patients had increased proportions of circulating CD5+ B lymphocytes with no alterations in the numbers of circulating B and T lymphocytes. Although all patients with increased CD5 B lymphocytes also had serum islet cell antibodies and/or insulin autoantibodies. the occurrence of increased proportions of CD5+ B lymphocytes and scrum autoantibodies was not significantly correlated. Increased proportions of CD5+ B lymphocytes was not related to the time elapsed since the clinical onset of diabetes. In addition, regardless of being increased or normal, the proportion of CD5+ B lymphocytes appeared as a relatively constant phenotype after 1 year of follow-up studies at 3-month intervals in eight patients. Although the significance of these findings remains to be established, the possibility exists that CD5+ B cells play a role in the pathogenesis of type I diabetes.
Induction of tumour necrosis factor-alpha during haemodialysis. Influence of the membrane type
Authors: CHOLLET-MARTIN S , STAMATAKIS G , BAILLY S , MERY J P , GOUGEROT-POCIDALO M A 
Published: July 2010

SUMMARYSome of the secondary clinical effects induced by long-term haemodialysis in patients with end-stage renal failure have been related to an increased production of interleukin-1 (IL-1). We investigated the role of another cytokine which shares a number of biological properties with IL-1, tumour necrosis factor-alpha (TNF-α). In long-term haemodialysed patients, we found at the beginning of the dialysis increased plasma TNF-α levels and enhanced monocyte capacity to produce TNF-α spontaneously ex vivo. Non-haemodialysed uraemic patients also presented increased plasma TNF-α levels. During dialysis with cellulose acetate (CA) or polysulphone (PS) membranes, plasma TNF-α levels and the spontaneous and lipopolysaccharide-induced production of TNF-α by monocytes remained at predialysis levels. In contrast, when cuprophane membranes were used, there was a significant increase in plasma TNF-α levels and in both spontaneous (10-fold) and lipopolysaccharide-induced (seven-fold) ex vivo TNF-α production by monocytes. These results suggest that monocytes are stimulated during haemodialysis with the poorly biocompatible cuprophane membrane.
Programmed cell death (apoptosis) in lymphoid and myeloid cell lines during zinc deficiency
Authors: MARTIN S J , MAZDAI G , STRAIN J J , COTTER T G , HANNIGAN B M 
Published: July 2010

SUMMARYThree human cell lines of lymphoid (Molt-3 and Raji) or myeloid (HL-60) origin were maintained in vitro under zinc-sufficient or zinc-deficient conditions. Under these conditions, cell proliferation, viability and mode of death (apoptotic or necrotic) were assessed. All three cell types decreased their proliferative capacity and viability under conditions of zinc deficiency. Cell death in the HL-60 and Raji cultures occurred primarily via apoptosis, while most cells in zinc-deficient Molt-3 cultures died via necrosis. Apoptosis in zinc-deficient cultures of HL-60 and Raji cells was characterized by a slow decline in culture viability as cells with condensed and fragmented nuclear DNA appeared. These morphological changes were accompanied by an increase in cell buoyant density, which allowed separation of viable apoptotic cells from their non-apoptotic counterparts by means of percoll step-density gradients. Necrosis in zinc-deficient Molt-3 cultures was characterized by rapid loss of cell culture viability as these cells underwent direct lysis. Intact necrotic cells were easily identified by the flocculated state of their chromatin as well as the decreased basophilia of their cytoplasm. Analysis of DNA from apoptotic HL-60 and Raji cells revealed that internucleosomal DNA degradation, indicative of endogenous endonuclease activation, had occurred, whereas the nuclear DNA of necrotic Molt-3 cells remained relatively unfragmented. The different modes of cell death evoked may reflect the relative sensitivities of cells of these lineages to zinc levels in vivo.
Lack of T cell oligoclonality in enzyme-digested synovial tissue and in synovial fluid in most patients with rheumatoid arthritis
Authors: VAN LAAR J M , MILTENBURG A M M , VERDONK M J A , DAHA M R , DE VRIES R R P , VAN DEN ELSEN P J , BREEDVELD F C 
Published: July 2010

SUMMARYThe dominant presence or specific T-cell populations in the rheumatoid joint as detected by Southern blot analysis of T cell receptor (TCR) gene rearrangements would indicate local antigen recognition and T cell proliferation. We therefore studied TCR β chain gene rearrangements using a Cβ2 probe in paired samples of T cell populations from synovial tissue and peripheral blood (n= 6) as well as synovial fluid (n= 16) and peripheral blood (n = 18) of patients with rheumatoid arthritis (RA). Peripheral blood mononuclear cells from healthy donors (n= 7) served as a control. T cells were studied directly after isolation or after non-specific expansion with OKT3 monoclonal antibody (MoAb) and T cell growth factor (TCGF). DNA samples were digested with EcoRI and Hind III to detect rearrangements to Cβ1 and Cβ2, respectively. Extra bands were detected in all EcoRI-digested DNA samples prepared from both freshly isolated and non-specifically expanded T cell populations of patients and healthy donors, possibly representing ‘common’ (V-) D-J rearrangements. Dominant rearrangements were found in only two out of 16 synovial fluid T cell populations (one freshly isolated and one expanded) and not in peripheral blood or synovial tissue derived T cell populations. No extra bands were detected in HindIII-digested DNA samples. To investigate the effect of in vitro culture techniques on rearrangement patterns we studied DNA samples prepared from synovial tissue T cells obtained both by outgrowth from tissue with TCGF or by enzyme digestion and subsequent expansion either with TCGF or with OKT3 MoAb and TCGF. Whereas the latter T cell population yielded ‘common’ rearrangements, the former T cell populations yielded different dominant rearrangements. These data indicate that oligoclonality of the T cell populations in synovial tissue and synovial fluid of patients with RA is a rare event. The data also show the influence of in vitro culture techniques on the result of TCR gene rearrangement analysis.
La/SSB ribonucleoprotein levels increased in transformed cells
Authors: ROTHER R P , THOMAS P S 
Published: July 2010

SUMMARY
Autoantibodies to the La/SSB ribonucleoprotein are commonly found in patients with Sjögren's syndrome. Previous studies have shown that La/SSB accumulates in cells shortly after viral infection. We have extended these studies by investigating levels of the La/SSB antigen in virally and spontaneously transformed cell lines (contact-insensitive and tumourigenic) relative to their non-transformed counterpart cell lines (contact-sensitive and non-tumourigenic). Transformed BALB/ 3T12-3 and KNRK fibroblasts were visibly brighter by immunofluorcscence assay than non-transformed BALB/3T3 and NRK fibroblasts respectively, when reacted with anti-La/SSB specific sera. This was confirmed by flow cytometry, as La/SSB levels were elevated in the transformed counterparts of the same cell lines. An anti-Sm monoclonal antibody and normal human serum reacted with these cell lines failed to show a significant increase by flow cytometry. Finally, a two-fold increase in the La/SSB antigen was demonstrated in cell lysates of these cell lines by a capture ELISA. These data show that La/SSB is elevated in transformed cell lines compared with non-transformed counterpart cell lines and suggest that this increase is not restricted to viral transformation.
Induction of type II collagen-specific antibody production in blood lymphocyte cultures of Rhesus monkeys (Macaca mulatto) with collagen-induced arthritis using the immobilized native antigen
Authors: HART B A T , BOTMAN C A D , BAKKER N P M 
Published: July 2010

SUMMARYPeripheral blood mononuclear cells (PBMC) from Rhesus monkeys previously immunized with bovine type II collagen to induce arthritis were cultured with the same antigen. Because the native protein is poorly soluble in culture medium a healing step is often used. The antigen in this form induced PBMC proliferation, but epitopes for the induction of antibody production and arthritis were lost. To keep the native protein intact it was coated on affigel beads. With the immobilized antigen specific antibody production could be induced.
Predominance of IgGl and IgG4 subclasses of anti-neutrophil cytoplasmic autoantibodies (ANCA) in patients with Wegener's granulomatosis and clinically related disorders
Authors: BROUWER E , TERVAERT J W COHEN , HORST G , HUITEMA M G , VAN DER GIESSEN M , LIMBURG P C , KALLENBERG C G M 
Published: July 2010

SUMMARYIn view of the supposed hypersensitivity, the elevated levels of IgE, and the occurrence of eosinophilia reported in Wegener's granulomatosis and related conditions, we studied the IgG subclass distribution of ANCA directed against a 29-kD serine protease and myeloperoxidase (MPO) in 41 untreated ANCA-positive patients with several forms of active vasculitis and/or glomerulonephritis. We found that both 29-kD ANCA and MPO ANCA were predominantly of the IgG1 and IgG4 subclass in all groups of patients. The additional presence of IgG3 subclass was associated with renal involvement. We compared the subclass distribution of ANCA with that of total IgG subclass levels, and with the IgG subclass distribution of antibodies to cytomegalovirus (CMV) as a persistent endogenous antigen and antibodies to tetanus toxoid (TT) as an exogenous recall antigen. Total levels of IgG4 were elevated in the majority of the patients together with elevated IgG1 levels. Antibodies to CMV and TT, however, had the same subclass distribution as found in normals and did not show enhanced IgG4 expression. ANCA belong predominantly to the IgG1 and IgG4 subclass, which may suggest that the production of ANCA is related to recurrent exposition to the antigen(s) involved, possibly as part of a hypersensitivity reaction.
Decreased expression of complement receptor type 2 (CR2) on neoplastic B cells of chronic lymphocytic leukaemia
Authors: TOOZE J A , BEVAN D H 
Published: July 2010

SUMMARYNeoplastic cells from 49 patients with B cell chronic lymphocytic leukaemia (B-CLL) were studied and compared with normal peripheral and tonsillar B cells using CD2I monoclonal antibodies. Membrane expression of CR2 was quantified by calibrated flow cytometry and by binding analysis with radiolabelled antibody. Both assays indicate that B-CLL cells express only 30% of the CR2 found on normal B cells. These findings are further evidence of the aberrant phenotype of B-CLL cells.
Increased frequency of the null allele at the complement C4b locus in autism
Authors: WARREN R P , SINGH V K , COLE P , ODELL J D , PINGREE C B , WARREN W L , WHITE E 
Published: July 2010

SUMMARY
Associations between C4 deficiency and autoimmune disorders have been found over the past several years. Since autism has several autoimmune features, the frequencies of null (no protein produced) alleles at the C4A and C4B loci were studied in 19 subjects with autism and their family members. The autistic subjects and their mothers had significantly increased phenotypic frequencies of the C4B null allele (58% in both the autistic subjects and mothers, compared with 27% in control subjects). The siblings of the autistic subjects also had an increased frequency of the C4B null allele, but this increase was not significant. The fathers had normal frequencies of this null allele. All family members had normal frequencies of the C4A null allele, all normal C4A and C4B alleles and all BF and C2 alleles.
Changes in natural killer cell phenotype in patients with post-viral fatigue syndrome
Authors: MORRISON L J A , BEHAN W H M , BEHAN P O 
Published: July 2010

SUMMARYWe analysed peripheral blood CD56+ natural killer (NK) cell subsets in 23 carefully characterized patients with post-viral fatigue syndrome (PFS), compared with 19 healthy controls, using fluorochrome-conjugated, specific monoclonal antibodies and the FACScan. We found significantly increased percentages of CD56+ and especially CD56bright NK cells in PFS patients. We also found significantly increased percentages of CD56+ high affinity interleukin-2 (IL-2) receptor (CD25)+ and CD56+ transferrin receptor (CD71+) subsets of cells, most of which also stained brightly for CD56. Also, we found an increased percentage of CD56+ CD3+ cells, many of which stained brightly for CD56, although there was no increase in the percentage of CD56- CD3+ T cells in these patients. These observations, in conjunction with very low percentage of CD56- CD25+ cells, suggest that there is a preferential involvement of this minor subset of CD56+ CD3+ T cells in PFS. Finally, a decreased percentage of CD56+ Fc gamma receptor (CD16)+ NK cells was identified, which suggests a reduced capacity for antibody-dependent cellular cytotoxicity in PFS patients. Subsets of CD56+ NK cells co-expressing CD2, CD4 or CD8 did not show any significant difference between PFS patients and healthy controls. These phenotypic changes provide laboratory evidence of immunological abnormalities in this syndrome, and, we suggest, may be consistent with persistent viral infection.
Expression of CD45R0 (UCHL1) by CD4+ and CD8+ T cells as a sign ofin vivoactivation in infectious mononucleosis
Authors: MIYAWAKI T , KASAHARA Y , KANEGANE H , OHTA K , YOKOI T , YACHIE A , TANIGUCHI N 
Published: July 2010

SUMMARYCD4SR0 (UCHL1), a member of leucocyte common antigen family, is expressed largely on previously activated or memory T cells. We examined CD45R0 expression of T cell subpopulations in patients with Epstein-Barr virus (EBV) induced infectious mononucleosis (IMN) as a sign of in vivo activation. Consistent with the notion that activated CD8+ T cells expand in acute IMN, the majority of CD8+ T cells in patients with acute IMN expressed CD45R0 to the similar extent to HLA-DR expression. Most CD4+ T cells in these patients also demonstrated marked expression of CD45R0 as well as HLA-DR antigens, compared with age-matched controls. Expression of CD45R0 by CD4+ T cells in patients with acute IMN was more notable than their HLA-DR expression. While predominant CD8+ T cells resulted in decreased percentages of CD4+ T cells, CD4+ T cells expressing CD4SR0 were shown to be significantly elevated in absolute number. The results suggest that both CD4+ and CD8+ T cells may be activated by stimulation with EBV infection. The appearance of two T cell subpopulations expressing CD4SR0 in acute IMN implies their immunoregulatory roles in the control of EBV-infected cells.
Modulation ofMycobacterium aviumgrowthin vivoby cytokines: involvement of tumour necrosis factor in resistance to atypical mycobacteria
Authors: DENIS M 
Published: July 2010

SUMMARYThe protective mechanisms associated with resistance to atypical mycobacteria infections are not clear. In an effort to broaden our understanding of the mechanisms involved, susceptible mice were infected with a virulent strain of M. avium and various treatments were applied so as to modify the course of the disease. Treatment with an antiserum against tumour necrosis factor-alpha (TNF-α) significantly enhanced the experimental infection, as judged by enumeration of colony-forming units (CPU) in the spleens and livers of infected mice, suggesting a role for TNF-α in resistance to M. avium. In other sets of experiments, recombinant cytokines were directly infused into infected mice. Infusion of recombinant interferon-gamma (IFN-γ) did not modify the experimental infection significantly, and infusion of interleukin-2 was also without effect. Injection of TNF-α enhanced resistance in susceptible animals, as seen by a reduction in the viable bacilli recovered from the spleens and livers. In a final set of experiments, we demonstrate that combinations of cytokines may induce strong resistance against M. avium, namely injection of 1 μg of interleukin-lα and 1 μg of TNF-α at 5-day intervals which was seen to eradicate M. avium in both spleens and livers of susceptible BALB/c mice. Overall, our results suggest that induction of protection against M. avium by treatment with cytokines may be feasible, and that TNF-α may be a pivotal molecule in resistance to M. avium.
Analysis of the human T cell responsiveness to purified antigens ofLeishmania:lipophosphoglycan (LPG) and glycoprotein 63 (gp 63)
Authors: MENDONÇA S C F , RUSSELL D G , COUTINHO S G 
Published: July 2010

SUMMARYThe responsiveness of peripheral blood lymphocytes from 15 cutaneous leishmaniasis patients and five healthy volunteers to purified surface antigens of Leishmania was studied. The following purified antigens were independently used as stimuli for lymphocyte proliferation in vitro: lipophosphoglycan of L. braziliensis, (Lb-LPG), lipophosphoglycan of L. mexicana (Lm-LPG), glycoprotein 63 of L. braziliensis (Lb-gp 63) and glycoprotein 63 of L. mexicana (Lm-gp 63). Among six patients tested with Lb-gp 63 and Lm-gp 63, two borderline responses and two positive responses were observed, respectively, all the others being negative. Lb-LPG and Lm-LPG induced positive responses in all patients tested (11 with Lb-LPG and five with Lm-LPG). A positive dose-response correlation was observed in the responses of the patients to both Lb-LPG and Lm-LPG. Significant differences (P&lt;0.01) were found between the two groups (patients and healthy subjects) with regard to the responses to Lb-LPG. The proliferating cells after stimulation with Lb-LPG were shown to belong to the CD4+ T cell subset by flow cytometry. However, the following evidence suggests that the T cell responses were not induced by LPG itself but rather by protein contaminants in the LPG preparations: a highly purified Lb-LPG batch that had undergone additional purification induced positive responses in cells from only three out of six patients and a proteinase K-treated Lb-LPG batch did not stimulate any positive response among the same six patients.