bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lymphocyte Subsets in the Blood
Authors: WESTERMANN J. , SCHWINZER R. , JECKER P. , PABST R. 
Published: June 2006

Removal of the largest single lymphoid organ, the spleen, leads to an increase in severe infections. To prevent this, transplantation of splenic fragments can be performed, which may, however, cause an increase in CD8+ lymphocytes in the blood of these patients. This is controversial since in the clinical situation it is often difficult to account for the different age of the patients, the time point after the operation and many other factors known to influence the number of lymphocyte subsets.Using a well‐defined animal model, B, T, CD4+, and CD8+ lymphocytes were determined preoperatively in adult rats. Then, either sham splenectomy, splenectomy, or splenic autotrans‐plantation was performed and the animals were followed up for 15 months after the operation.The surgical procedure itself, the site of blood sampling and ageing all influenced the number of lymphocyte subsets profoundly. Furthermore, giving the data as relative or absolute numbers leads to different results.Splenectomy caused lymphocytosis, due to a significant increase in B and CD8+ lymphocytes, as did splenic autotransplantation, which indicates that the number of lymphocyte subsets in the blood should not be used to argue in favour of or against splenic autotransplantation.This study demonstrates that the number of lymphocyte subsets in the blood is influenced by many factors and therefore should be determined in a highly standardized fashion.
Low T‐ and B‐Cell Reactivity is an Apparently Paradoxical Request for Murine Immunoprotection Against Streptococcus mutans
Authors: SOARES R. , FERREIRA P. , SANTAREM M. M. G. , DA SILVA M. TEIXEIRA , ARALA‐CHAVES M. 
Published: June 2006

C57BL/6 mice thymectomized as adults or depleted of CD4+ cells were much less susceptible than intact conventional mice to the B‐cell mitogenic and specific immunosuppressive effects of a protein designated as F5′EP‐Sm secreted by Streptococcus mutans. These mice were also considerably more resistant to infection by these bacteria than intact individuals. The immunosuppressor effect of F5′EP‐Sm was also abrogated, however, in conventional intact mice when immunized intraperitoneally against heat‐inactivated F5′EP‐Sm. On the other hand, resistance to bacterial infection could be achieved by immunization of conventional intact C57BL/6 mice against heat‐inactivated F5′EP‐Sm by intraperitoneal or intradermal routes even when the animals were infected 3 months after immunization and even when the immunization procedure did not include Freund's adjuvant, which was the case with the intradermal route. Interestingly, the protection against the bacterial infection was accompanied by only a minor increase in specific serum antibodies against F5′EP‐Sm.These results are discussed in the context of adequate strategies for immunoprotection against Streptococcus mutans and other micro‐organisms which are secretors of substances that share both B‐cell mitogenic and immunosuppressive properties and which are thus able to suppress the immune response by overstimulation of the immune system of the host.
Fine Specificity and Isotype Expression of Anti‐PC Antibodies in BALB/c, MRL/Mp‐1pr/1pr, and −+/+ Mice at Different Ages
Authors: GERBER V. E. , PONNAPPAN U. , HEUSSER C. H. , CINADER B. , BLASER K. 
Published: June 2006

The MRL/Mp congenic mouse strains develop autoimmune disease with age. We have investigated age‐ and autoimmune‐related changes in fine specificity, isotype spectra and T15 idiotype expression of the anti‐phosphorylcholine (PC) response in BALB/c, MRL/Mp −+ and ‐lpr congenic mice and in (BALB/c x MRL/Mp‐lpr) F1 hybrids. Two groups of anti‐PC antibodies with distinct fine specificity are elicited in the memory response. Group I antibodies recognize the PC moiety and express the T15 idiotype. Antibodies of group II are specific for phenyl‐phosphorylcholine and are found predominantly in the memory response. In the MRL/Mp‐lpr and −+ strains only a minor population of antibodies expresses the T15 idiotype at all ages. However, a third group of antibodies was observed which binds to PC‐coated proteins and to Diplococcus pneumoniae R‐36A. This binding was not inibited by PC‐chloride and appeared mainly in the memory response at old age. The isotype distribution among anti‐PC antibodies was similar in all strains analysed. In the initial response primarily μ, γ3 and γ1 isotypes were produced, while in the memory response γ1 was dominant.Thus autoimmune defects and ageing result in altered anti‐PC antibody and idiotype profile, probably related to altered states in both the T‐ and B‐cell compartments.
Zinc Ions Inhibit Factor I‐Mediated Release of CR1‐Bound Immune Complexes and Degradation of Cell‐Bound Complement Factors C3b and C4b
Authors: JEPSEN H. H. , TEISNER B. , SVEHAG S. E. 
Published: June 2006

ZnCl2 exerted a dose‐dependent inhibition of citrate‐phosphate dextrose (CPD) plasma‐induced release of 125I‐labelled BSA‐anti‐BSA immune complexes (IC) bound to complement receptor lype I (CRl. CD35) in human whole blood. Maximal inhibition was observed at 10mM of ZnCl2.Furthermore, the release of IC bound to erythrocyte (E)‐CRI by purified factor I. factor Ideficient serum plus purified factor I. or normal human. Serum was reduced by approximately 90%, 64%, and 52%, respectively, in the presence of 10 mM ZnCl2.The effect of ZnCl2 on factor 1‐mediated degradation of cell‐bound C3b/C4b was also investigated employing CPD blood or E from a factor I‐deficient donor. These cells expressed covalently bound C3b and C4b as demonstrated by a simple agglutination technique. Upon incubation of CPD whole blood with purified factor I. or of E wilh purified factor I or normal CPD plasma, the C‐fragments were cleaved and the cells were no longer agglutinated by antibodies to C3c and C4c. The presence of ZnCl2 prevented Ihis factor 1‐mediaied degradation of C3b and C4b, as evidenced by the unaffected agglutination of the cells by the antibodies.We conclude that ZnCl2 inhibited factor I aclivity since: (1) release of complementpreopsonized IC from E‐CR 1 by purified factor I was markedly inhibited (90%) in the presence of ZnCl2, (2) preincubation of the cells with ZnCl2 caused only a moderate inhibition (32 38%) of the IC release, and (3) degradation by purified factor I of covalently cell‐bound C3 band C4b was abrogated in the presence of 10 mM ZnCl2.
Secretory Component‐Binding Properties of Normal Serum IgM
Authors: BOUVET J.‐P. , PILLOT J. , ISCAKI S. 
Published: June 2006

Our aim was to investigate why serum IgM is poorly transferred into secretions in normal subjects. Indeed, the low IgM level in secretions contrasts with the eapacity of monoclonal IgM to bind to secretory component (SC), but it is not well established to what extent normal serum IgM can do so.The mean SC affinity was studied with a polyclonal IgM preparation from 250 normal subjects and with a representative pool of 100 different monoclonal IgM. The SC‐binding percentages varied as a function of the IgM/SC molar ratio according to a common hyperbolic curve, with similar association constants: Ka= 4.19 ± 2.61 × 107 M‐1 (polyclonal pool) and Ka= 5.8 0 ± 2.73 × 107 (monoclonal pool). It thus appears that the large difference in IgM concentrations between blood and secretions cannot be due to an SC‐binding defect of serum IgM, but is probably explained by its low diffusion from blood to the extravascular compartment, compartment.
Quantitation of Antibody‐Secreting Cells in the Blood after Vaccination with aHaemophilus influenzaeType b Conjugate Vaccine
Authors: BARINGTON T. , HEILMANN C. , ANDERSEN V. 
Published: June 2006

The human B‐lymphocyte response to proiein‐conjugated polysaccharide antigens has not previously been studied at the cellular level. In order to do so, we developed and evaluated haemolytic plaque‐forming cell assays detectingHaemophilus influenzaetype b (Hib) capsular polysaccharide‐specific antibody‐secreting cells (AbSC) of the isotypes IgM, IgG, and IgA. The appearance of AbSC in the blood after vaccimation of adults with diphtheria toxoid‐conjugated Hib polysaccharide was investigated. AbSC were detected from post‐vaccination day 5 to day 14.IgA was the predominant isotype among these cells. IgM AbSC peaked slightly earlier (median day 7) than IgG and IgA AbSC (both day 8). On post‐vaccination day 8 ihe numbers of AbSC were: IgA. 1217/106mononuclear cells (median); IgG, 211; and IgM, 30 (n= 11). Similar isotype distribution has earlier been found after vaccination with pure capsular polysaccharides from Hib and pneumococci. The predominance of IgA AbSC in response to both conjugate and pure polysaccharide vaccines is probably due to reactivation of the same clones of IgA‐committed memory B cells originally primed at the mucosa by natural exposure to the polysaccharide or cross‐reacting antigens.
Alteration of Idiotypic Connectivity in Prenatally Tolerized Neonatal Mice*
Authors: ZÖLLER M. 
Published: June 2006

Prenatal tolerization with trinitrobenzenesulphonic acid (TNBS) leads lo expansion of trinitrophenyl (TNP)‐specific B cells, the majority of which become refractory to stimulation during postnatal development [60]. One possible explanation could be that they belong to the repertoire of naturally activated B cells which are limited in expansion after antigenic stimulation due to a high degree of idiotypic connectivity [42]. To evaluate this hypothesis, 59 thymus‐ and 490 spleen‐derived B‐cell hybribomas from 6‐day‐old prenatally untreated and prenatally TNBS‐treated mice were tested for reactivity against 33 arbitrarily chosen clones derived from the same fusions, 17 being derived from control and 16 from tolerized litters. Two major points could be deduced:

Idiotypic connectivity, including connectivity of TNP‐ and anti‐TNP‐reactive monoclonal antibodies (MoAb), was maintained after prenatal tolerization. This accounted for thymus‐ and spleen‐derived MoAb.
Only TNP‐ and anli‐TNP‐reaclive MoAb derived from prenalally untreated and prenatally tolerized mice displayed significantly distinct idiotypic profiles. Differences were pronounced, especially with thymus‐derivcd MoAb.

Thus, TNP‐specilic B cells in prenatally tolerized newborns do not behave like B cells of adult mice stimulated by external antigen, but rather like a part of the naturally activated, ldiotypically connected B‐cell repertoire of the newborn. This could explain B‐ccI! unresponsiveness at older age as a consequence—at least partly—of their high idiotypic connectivity.
Histological and Immunohistochemical Characterization of Joint Inflammation and Flare‐up Reactions Induced by Cloned MT4 +,Lyt‐2−T cells
Authors: KLASEN I. S. , LADESTEIN R. M. T. , GRANDIA A. A. , VAN DER KWAST TH. H. , BENNER R. 
Published: June 2006

This report describes the histological and immunohistochemical characterization of joint inflammations and flare‐up reactions in mice induced by cloned MT4+, Lyt‐2− T cells. The T‐cell clone used was specific for the antigen methylated bonne serum albumin (mBSA) and was inoculated locally into a joint together with the antigen. The histological examination was performed in methylmethacrylate sections, and the various cell types were quantified m distinct regions of the knee joint. The infiltrates consisted predominantly or granulocytes admixed with small numbers of histiocytes. Few lymphocytes were present, while plasma cells were not found. Fibrosis was prominent in the later stages of the inflammation.Immunohistochemical analysis of total unfixed, non‐decalcified sections using monoclonal antibodies revealed the presence of T cells which were predominantly of the helper phenotype. sporadic B cells, and a considerable number of la‐positive cells. Macrophages were scattered throughout the infiltrate. The synovial lining was shown to express Ia antigens and to contain cells that stained with macrophage markers Cell clusters were found including helper T (Th) cells, some B cells, and Ia‐positive cells.These results are in line with immunohistological examinations in other arthritis models and resemble the early events in human rheumatoid arthritis. The data indicate that activated helper T cells are required and sufficient to give rise to the inflammatory infiltrates that are characteristic of the inflammations and exacerbations in human rheumatoid arthritis.
Tumour Necrosis Factor Alpha (TNF‐α) and Interleukin 6 in a Zymosan‐Induced Shock Model
Authors: VON ASMUTH E. J. U. , MAESSEN J. G. , VAN DER LINDEN C. J. , BUURMAN W. A. 
Published: June 2006

TNF plays a central role in septic shock induced by endotoxin or Gram‐negative bacteria. Zymosan can elicit a septic shock‐like syndrome in rodents in the absence of endotoxin. TNF and IL‐6 release in mice treated with zymosan was investigated. One hour after intraperitoneal zymosan injection, maximal TNF levels were measured in serum, followed by IL‐6 peak levels 1 h later. Treatment with a monoclonal antibody against TNF lowered zymosan‐induced mortality from 63 to 11.6%, while maximal IL‐6 levels were lowered by about 40%.Mechanisms triggering zymosan‐induced cytokine release in murine macrophages were analysed in vitro. Cytokine release was only slightly triggered by uncoated zymosan particles. Thirty‐nine per cent of TNF release by macrophages appeared to be triggered by zymosan‐bound activated complement. Maximal TNT release also required the presence of natural antibodies against zymosan and zymosan‐activated scrum. In contrast, maximal 11–6 release was reached upon stimulation with zymosan‐activated serum only, while the presence of zymosan particles lowered this response.We conclude that TNF is a crucial mediator m zymosan‐induced shock. TNF release can be induced by different immunological pathways, without the need for the direct presence of endotoxins. Although IL‐6 release during septic shock is partly dependent on TNF. in vitro trigger mechanisms for IL‐6 and TNF differ remarkably.
Dynamics of Blood Components and Peritoneal Fluid during Treatment of Murine E. coli Sepsis with β‐1,3‐D‐polyglucose Derivatives
Authors: RASMUSSEN L.‐T. , FANDREM J. , SELJELID R. 
Published: June 2006

The influences of pretreatmeni with β‐1.3‐D‐polyglucose derivatives on levels of cytokines and arachidonic acid metabolites in body fluids in experimental peritonitis in mice are reported. Peritonitis was induced by an intraperitoneal injection of 108 live Escherichia coli. Pretreated animals survived the infection, untreated animals died about 12 h after inoculation with E. coli.Levels of IL‐l in plasma and peritoneal fluid, measured by cytotoxicity assay of the HT‐2 cell line, increased significantly during the first 48 h after intraperitoneal treatment with β‐1.3‐D‐polyglucose‐derivalized microbeads (GDM) or soluble, animated /β‐1,3‐D‐polyglucose (AG). After subsequent challenge with E. coli. the levels of IL‐1 were significantly lower than in untreated animals. There was no increase in levels of TNF after treatment with GDM or AG, measured by cytotoxicity assay of the WEHI clone 13 cell line. After challenge with E. coli. TNF in plasma and peritoneal fluid was significantly lower compared with untreated animals. Both PGE2; and LTB4. measured by radioimmunoassay kits, were increased in peritoneal fluid alter treatment with GDM and AG. After challenge with E coli. PGE2 and LTB4 in peritoneal fluid increased to about half the concentration of infected control animals. Intraperitoneal injection of indomethacin to pretreated animals resulted in increased levels of IL‐l and TNF‐ and decreased levels of PGE2; following challenge with E. coli. The levels of IL‐1 and TNF remained elevated until the animals died after about 12 h.These studies demonstrate that the raised levels of arachidonic acid metabolites after pretreatment with GDM or AG seem to inhibit the otherwise lethal elevation of IL‐1 and TNF in body fluids which is seen in untreated animals.
Monoreactive and Polyreactive Rheumatoid Factors Produced by in Vitro Epstein‐Barr Virus‐Transformed Peripheral Blood and Synovial B Lymphocytes from Rheumatoid Arthritis Patients
Authors: BURASTERO S. E. , CUTOLO M. , DESSI V. , CELADA F. 
Published: June 2006

The CD5 membrane molecule, initially identified as an exclusive T‐cell marker, also defines a phenotypically and functionally distinct B‐lymphocyte population. In normal individuals, CD5+ B cells are committed to secrete‘natural’polyreactive (auto)antibodies, that is antibodies, mainly IgM, endowed with multiple antigen‐binding capabilities, including rheumatoid factor (RF) activity. At variance with this, in rheumatoid arthritis (RA) as well as in other autoimmune conditions, monoreactive autoantibodies binding with high affinity and specificity to a given self antigen have been isolated and the cells from which they originate differently related to the CD5+ B‐lymphocyte subset.Here, we studied the proportions of CD5+ B cells and the characteristics, in terms of polyreactivity and monoreactivity, of RF produced by B lymphocytes in RA patients with classified disease activity. Our results suggest that patients with a more severe disease activity have higher proportions of CD5+ B cells and higher frequencies of B lymphocytes committed to secrete RF, with the characteristics of polyreactive antibodies. On the other hand, we did not find a significant difference between the proportions of peripheral B cells producing monoreactive RF in patients with high‐ versus patients with low‐activity RA. However, in two highly active RA patients, we found that synovial fluid, compared with peripheral blood, was significantly enriched for (IgG and IgA) monoreactive RF‐producing B cells.
Experimental Studies of Immunologically Mediated Enteropathy
Authors: FELSTEIN M. V. , MOWAT A. MCI. 
Published: June 2006

We have attempted to investigate the relative roles of specific cytotoxic T lymphocytes (CTL) and allospecific suppressor T cells (T5) in the systemic and intestinal manifestations of acute graft‐versus‐host reaction (GvHR) in mice.Treatment adult (C57Bl/10xDBA/2)F1 (BDF1) mice with the suppressor cell‐specific toxin 2'‐deoxyguanosine (dGuo) inhibited the weight loss and mortality which normally occur after induction of GvHR and C57BI donor cells. dGuo also delayed the development of a destructive enteropathy as typified by jejunal villus atrophy. Paradoxically, dGuo completely prevented villus atrophy during an acute GvHR in neonatal (CBA × BALB/c)F1 hosts, despite having only a slight ability to inhibit the systemic disease. In both models. dGuo had no effect on the generation of splenomegaly or anti‐host CTL. and dGuo‐treated mice with GvHR actually had increased proliferative alterations in the intestine, as assessed by crypt hyperplasia, In parallel. dGuo prevented the loss of NK cells which normally occurs in acute GvHR.Thus dGuo inhibits many of the destructive features of systemic and intestinal GvHR without affecting the development of CTL. We conclude that a dGuo‐sensitive mechanism causes the transition from a proliferative to a destructive GvHR.
Tγδ Cell Subsets in Cord and Adult Blood
Authors: SMITH M. D. , WORMAN C. , YÜKSEL F. , YÜKSEL B. , MORETTA L. , CICCONE E. , GROSSI C. E. , MACKENZIE L. , LYDYARD P. M. 
Published: June 2006

A minor population of T cells expresses a heterodimeric antigen receptor composed of y and A chains (TcR‐1). In blood from adults, two subsets of Tγδ cells can be identified by the monoclonalantibodies (MoAb) BB3 and A13. Little is known about the distribution and markers of these subsets early in life. We have therefore examined both the frequencies of these cells in cord blood and their expression of the cytotoxicity‐associated marker serine esterase (SK). using immunocytochemical techniques.Our data show lower percentages of TcR‐1+ cells in the blood of newborns compared with that in adults. However, the ratio of the Al3+/BB3 cells was significantly higher in cord than in adult blood. Whereas virtually all the adult TcR‐1+ cells in blood were SE‐positive. only a small proportion of the cord blood cells earned ibis enzymes. This was; restricted lo the BB3+ Tγδ ‐cell subset in the cord.Our data suggest different characteristics of the TcR‐1+ cells in blood from newborns compared with adult blood, and study of the functions of the different subsets, e.g. cytotoxicity. will be important in understanding their particular role in immunity.
Fcγ Receptor Heterogeneity in the Human Placenta
Authors: KRISTOFFERSEN E. K. , ULVESTAD E. , VEDELER C. A. , MATRE R. 
Published: June 2006

Fc receptors for IgG, FcRI (CD64), FcRII (OD32), and FcRIII (CD 16) in human placenta were studied by indirect immunohistochemistry using avidin biotin‐peroxidase complexes For the sunning of cryostat sections. The MoAb 32.2 against FcRI stained cells in the loose connective tissue of the placental villi. The MoAb IV3 (FcRII) and C1KM5 (FcRII) also stained stromal cells and in addition stained the endothelium of the placental villi. The MoAb anti‐Leu‐11b against FcRIII and BID6 against a 40‐kDa FcR from placenta stained both stromal cells and endothelium as well as the fetal trophoblasts lining the villi. The MoAb 3G8 (FcRIII) also stained trophoblasts and stromal cells but did not stain the endotheliumThe heterogeneity of FcR expression on human placenta is established. The function of the different receptors is still unclear.
Effects of Isoprinosine Treatment of HIV‐Positive Patients on Blood Mononuclear Cell Subsets, NK‐ and T‐Cell Function, Tumour Necrosis Factor, and Interleukins 1, 2, and 6
Authors: PEDERSEN B. K. , TVEDE N. , DIAMANT M. , GERSTOFT J. , HANSEN M. BAGGE , HAAHR P. M. , HØRDING M. , KAPPEL M. , KLOKKER M. , SØEBERG B. , SKINHØJ P. 
Published: June 2006

The immunomodulatory drug isoprinosine has been found to delay the occurrence of opportunistic infections in HIV‐infected individuals. To elucidate the mechanism of action, eight HIV‐positive, healthy patients were treated with isoprinosine, 3 g/day for 28 days; six patients received no treatment but were examined in parallel, and two patients were withdrawn. All patients had blood collected just before the start as well as on days 14 and 28 of isoprinosine treatment.Isoprinosine significantly enhanced the lymphoproliferative response after stimulation with phytohaemagglutinin (PHA) and purified derivative of tuberculin (PPD), while isoprinosine had no effect on the following immune parameters: the expression of surface markers on blood mononuclear cells including CD2, CD3, CD4, CD8, CD14, CD19, CD20, CD25, leu‐8, and HLA‐DR. Furthermore isoprinosine did not influence the ability of interleukin 2 (IL‐2) to stimulate the proliferation of lymphocytes or the natural killer (NK) cell activity either unstimulated or stimulated in vitro with alpha interferon (IFN‐α), IL‐2. or indomethacin. Neither did isoprinosine affect the in vitro production of (IL‐1) α or β, IL‐2, IL‐6. or tumour necrosis factor (TNF).