bluuebunny/crossref_metadata_2025_split huggingface dataset:
Anchorage and Lymphocyte Function: Extracellular Matrix Substrata Control Morphogenesis and Interleukin Production but have Minor Effects on DNA Synthesis
Authors: SUNDQVIST K. G. , PEDARI L. , HAUZENBERGER D. 
Published: July 2006

Contact with collagen and fibronectin substrata triggers disruption of aggregates of activated lymphocytes, pseudopodia formation and migration of these lymphocytes onto the substrata. Monoclonal antibodies to the α4 and α5 chains of β1‐integrins inhibit cell substrate adhesion and aggregate disruption on fibronectin substrata. A rat monoclonal antibody to the β1‐integrin chain inhibits lymphocyte adhesion to collagen. Two‐dimensional (2D) and three‐dimensional (3D) collagen substrata have virtually the same capacity to abrogate lymphocyte aggregation. Fibronectin substrata trigger the initial phase(s) of aggregate disruption as effectively as collagen but the later part of the disruption process is relatively incomplete. Serum‐coated plastic does not cause aggregate disruption. These results indicate that disruption of lymphocyte aggregates is a specific event induced via cell surface receptors for extracellular matrix (ECM) components. A major difference between lymphocytes on 2D and 3D extracellular matrix substrata seems to be that the cells detach from the former whereas on the latter infiltration dominates over detachment. Collagen and fibronectin substrata are non‐mitogenic for lymphocytes but they can modulate lymphocyte activation induced by allogeneic cells and Con A. Thus, 3D collagen substrata augment and prolong such induced DNA synthesis, although they slightly delay entry into the S‐phase and decrease IL‐2 production. Collagen substrata, particularly in 3D form, also augment the DNA synthesis of preactivated lymphocytes above the magnitude on serum‐coated plastic. The nature of the substratum determines IL‐1 production. Accordingly, the spontaneous IL‐1 production by mononuclear cells is substantially lower on collagen substrata than on plastic surfaces coated with serum or BSA. However, factors which induce IL‐1 production (e.g. Con A or LPS) are more effective on collagen than on serum‐coated plastic.Abrogation of cell aggregation, induction of morphogenesis and motile behaviour as well as control of IL‐1 synthesis thus constitute major effects of ECM substrata on cells of the immune system. An additional but relatively minor influence of ECM substrata on these cells, as suggested by the present results, is exerted via modulation of DNA synthesis.
Organ‐Specific Regulation of Interferon‐γ, Interleukin‐2 and Interleukin‐2 Receptor during Murine Infection with Trypanosoma cruzi
Authors: ROTTENBERG M. E. , SUNNEMARK D. , LEANDERSSON T. , ÖRN A. 
Published: July 2006

We have studied the expression of IFN‐γ, IL‐2 and IL‐2 receptor (IL‐2R) at the mRNA and protein levels in spleen and lymph node cells from Trypanosoma crizi‐infected BALB/c mice. At 21 days post infection (dpi) (peak of parasitaemia), spleen cells stimulated with Con A for 16 h showed a reduced IFN‐γ, IL‐2 and IL‐2R mRNA production compared with non‐infected controls. Lymph node cells obtained at 4, 21 or 60 dpi produced similar amounts of IFN‐γ, IL‐2 or IL‐2R transcripts after mitogen stimulation as uninfected controls.Spleen cells obtained at 21 dpi showed a lower Con A proliferative response and IL‐2R expression compared with non‐infected controls, while the proliferation and IL‐2R expression of lymph node cells at 21 dpi was unaltered. Supernatantsfrom 48 h Con A‐stimulated spleen and lymph node cells from mice at 21 dpi had very low levels of IL‐2 but contained significantly higher levels of IFN‐γ compared with the supernatants of cells from non‐infected mice. The latter phenomenon correlates with an accelerated rate of IFN‐γ mRNA accumulation.
Cytokines and PGE2 Modulate the Phagocytic Function of the β‐Glucan Receptor in Macrophages
Authors: KONOPSKI Z. , SELJELID R. , ESKELAND T. 
Published: July 2006

Under serum‐free conditions the β‐glucan receptor of mouse macrophages mediates phagocytosis of β‐l,3‐D‐glucan‐coated microbeads (diameter 2 μm). IFN‐γ increases the phagocytic function of the β‐glucan receptor in a dose‐dependent manner, giving the plateau level at 100 U/ml. Maximum activity appears 9 h after addition of IFN‐γ to the cells. The effect disappears within 24 h. The effect of IFN‐γ may be a result of augmented receptor synthesis since treatment with cycloheximide reduces the phagocytosis.IL‐1 also increases the phagocytic function of the β‐glucan receptor giving a dose‐dependent response and with the plateau level reached at 10 U/ml. Maximum activity is found 4 h after addition of IL‐I to macrophages. The effect disappears within 24 h. TNF does not alter the phagocytic function of the β‐glucan receptor, but TNF together with IL‐1 prolongs the effect of IL‐1.PGE2 reduces the phagocytic function of the β‐glucan receptor. Maximum reduction is achieved with 8 ng/ml. Time‐course studies show the lowest phagocytic activity 9 h after addition of PGE2 to the cells.
Characteristics of IgA Antibodies Against HIV‐1 in Sera and Saliva from HIV‐Seropositive Individuals in Different Clinical Stages
Authors: MATSUDA S. , OKA S. , HONDA M. , TAKEBE Y. , TAKFMORI T. 
Published: July 2006

IgA antibodies were analysed in sera and saliva from 40 HIV‐1 seropositive individuals.The level of total IgA in serum was elevated according to the progress of the disease. IgA antibodies against p24 and gp160 were detected in the asymptomatic phase of infection. However, they declined in the symptomatic phases in contrast with IgG antibodies. Interestingly, three patients in the symptomatic phase who showed high levels of lgA antibodies were all in relatively good clinical condition. The IgG and IgA antibodies in saliva declined in the symptomatic phase. The level of IgG anti‐p24 antibodies in saliva correlated with that in serum, suggesting that IgG anti‐p24 antibodies in saliva originated from those in the serum. These results indicate that IgA antibodies are regulated independently from IgG antibodies and that the mucosal immune system is impaired early in the symptomatic phase of HIV infection, which starts with mucosal impairment. Detection of IgA antibodies may be useful for prognosis of the disease in HIV‐infected individuals. The results indicate also that treatment for the impaired IgA mucosal immune system should be taken into consideration.
Immune Modulatory Effects of Immunoglobulins on Cell‐Mediated Immune Responses In Vitro
Authors: KLAESSON S. , RINGDEN O. , MARKLING L. , REMBERGER M. , LUNDKVIST I. 
Published: July 2006

Intravenous Immunoglobulin (IVIG) at a concentration of 5 mg/ml, significantly inhibited mitogenic responses to phytohaemagglutinin (PHA), concanavalin A (conA) and pokeweed mitogen (PWM) by peripheral blood cells from healthy donors. No difference in inhibition by IVIG was seen when stimulating different T‐lymphocyte cell subsets. Inhibition by IVIG was dose‐dependent. An increased response was observed when IVIG was added more than 12 h after PHA compared to adding 1 h before [p= 0·05]. Intravenous immunoglobulin added to mixed lymphocyte cultures (MLC), reduced the median response by more than 60% (range 14–89%; P= 0·03) and almost completely abrogated the lymphocyte response to Staphylococcus aureus protein A (SPA), whose median inhibition was 94% (range 90–99%; P= 0·02).When comparing 12 different commercial IVIG preparations at a concentration of 2.5 mg/ml, the median inhibition of the PHA stimulation ranged from 4% to 35% and the MLC response from 0% to 66%. In the presence of IVIG the lymphocyte response to different herpes virus antigens was reduced by <50%. No difference in inhibitory effect was seen when comparing IVIG and cytomegalovirus (CMV) hyper Ig, but CMV negative Ig resulted in lower inhibition (P= 0·05].Three out of five IgG preparations (2.5 mg/ml) made from single donors inhibited PHA stimulation signifiantly more than commercial IVIG [P<0·05]. Mean inhibition was 61% compared to 35% Inhibition by pooled IgG from five donors was 56%. F(ab‘)2 fragments of IVIG inhibited the MLC response by more than 50% (range 34–75%), SPA stimulation by 97% (83–104%) and PHA stimulation by more than 30% (26–37%). One of two Fe preparations tested had an inhibitory effect, but the inhibition was less than that obtained with the F(ab')2 fragments [P= 0.04].These results further strengthen the notion that IVIG exerts its immune modulatory effect by binding to leukocyte surface receptors. A clear inhibition was obtained with concentrations corresponding to the serum levels obtained when IVIG is given 250–500 mg/kg bodyweight. F(ab')2 fragments have the same inhibitory effect as intact IgG molecules but the role of Fc fragments still remains unclear. Differences in the immunosuppressivc effect of various IVIG preparations may be associated with the method of preparation.
T‐Cell Stimulation Induced by Idiotypes on Monoclonal Immunoglobulins in Patients with Monoclonal Gammopathies
Authors: YI Q. , BERGENBRANT S. , ÖSTERBORG A. , ÖSBY E. , ÖSTMAN R. , BJÖRKHOLM M. , HOLM G. , LEFVERT A. K. 
Published: July 2006

The stimulation of peripheral blood mononuclear cells by purified autologous and/or allogeneic monoclonal IgG was studied in five patients with multiple myeloma (MM), nine patients with monoclonal gammopathy of undetermined significance (MGUS) and six healthy individuals.Single cells secreting IFN‐γ or IL‐2 were identified using an enzyme‐linked immunospot assay. Patients' cells were preferentially stimulated by autologous monoclonal IgG at low concentrations (1–100 pg/ml). while l00 ng/ml or higher stimulated T cells both from patients and, to a lesser degree, healthy individuals. This biphasic dose‐response of T‐cell stimulation by autologous monoclonal IgG was reproduced in all patients. The numbers of cells secreting IFN‐γ and IL‐2 in response to allogeneic IgG were significantly lower than the numbers obtained using autologous IgG in patients with MM and MGUS. Cells from healthy individuals were stimulated by allogeneic monoclonal IgG, but to a lesser extent.The results of this study support the presence of idiotype‐reactive T cells in patients with MM and MGUS and also may suggest a general but less pronounced T‐cell reactivity to monoclonal IgG among these patients.
Anti‐Interleukin‐2 Receptor Monoclonal Antibody Therapy Supports a Role for Thl‐Like Cells in HgCl2‐Induced Autoimmunity in Rats
Authors: DUBEY D. , KUHN J. , VIAL M. C. , DRUET P. , BELLON B. 
Published: July 2006

Brown‐Norway (BN) rats injected with HgCl2 develop an autoimmune disease characterized by a T dependent polyclonal B‐cell activation. Increase in major histocompatibility complex class II molecule expression on B cells concomitant with enhancement of serum IgE concentration supports the involvement of the T helper 2 (Th2)‐like subset in the induction of the disease. The mercury disease is autoreguiated and does not develop in Lewis (LEW) rats. Considering the reciprocal regulation, well defined in mice, between the Th1 and Th2 subsets, we addressed the role of the Thl‐like subset in this disease. Brown‐Norway and LEW rats injected with HgCl2 were treated wilh NDS61, a mouse anti‐ral‐IL‐2R MoAb that blocks mainly Th1 cells. Data reported herein show that: (1) HgCl2 treatment does not modify either the percentage of IL‐2R+ cells or IL‐2R expression in both BN and LEW rats; (2) treatment of BN rats with NDS61 MoAb does not modify the induction phase of the mercury disease but delays in parl the regulation phase; (3) such a treatment leads lo some immune abnormalities in LEW rals; (4) HgCl2 markedly potentiates the anti‐mouse Ig antibody response in BN rats which probably limits the effect of this treatment.This study supports a role for the Th1‐like subset in HgCl2‐induced auloimmunity in the rat.
Differences in the Rate of Intracellular Killing of Catalase‐Negative and Catalase‐Positive Listeria monocytogenes by Normal and Interferon‐Gamma‐Activated Macrophages
Authors: VAN DISSEL J. T. , STIKKELBROECK J. J. M. , VAN FURTH R. 
Published: July 2006

Intracellular killing of catalase‐positive bacteria by murine resident macrophages requires the presence of extracellular serum, whereas killing of catalase‐negative bacteria can occur in the absence of serum. To find out whether the intracellular killing of bacteria by rIFN‐γ‐activated macrophages also requires serum stimulation, we investigated the handling of ingested catalase‐negative and ‐positive Listeria monocytogenes by peritoneal macrophages of normal Swiss mice and mice injected i. p. with I × 104U rIFN‐γ 18 h earlier.In the absence of extracellular serum. rlFN‐γ‐activated macrophages killed ingested catalase‐negative Listeria more efficiently (P<0.01) than normal resident macrophages. Maximal killing of catalase‐negative bacteria by rlFN‐γ‐activated macrophages required an extracellular serum concentration of only 1.0 to 2.5% compared with the 10% needed by normal macrophages. No differences were observed in the rates of intracellular killing of catalase‐positive Listeria by rlFN‐γ‐activated and normal resident macrophages: both populations of macrophages required 10% extracellular serum for maximal killing of these bacteria, and killing was minimal in the absence of scrum. The rIFN‐γ‐activated macrophages displayed enhanced O2‐consumption after stimulation with phorbol myristate acetate and heat‐killed Listeria compared with macrophages from normal mice.These findings indicate that, under suboptimal stimulation by extracellular serum. rlFN‐γ enhances the intracellular killing of catalase‐negative Listeria which lack endogenous catalase acting as a scavenger of reactive oxygen intermediates. The mechanism underlying the enhancement is probably the amplification of the respiratory burst by IFN‐γ.
Identification of a Novel 27‐kDa Protein from Mycobacterium tuberculosis Culture Fluid by a Monoclonal Antibody Specific for the Mycobacterium tuberculosis Complex
Authors: RAMBUKKANA A. , DAS P. K. , KOLK A. H. J. , BURGGRAAF J. D. , KUIJPER S. , HARBOE M. 
Published: July 2006

Mycobacterium tuberculosis antigens inducing species‐specific immune responses are likely to be particularly important for serodiagnosis or for skin testing of tuberculosis. In the present study, we describe the characterization of two novel monoclonal antibodies (MoAbs) A3h4 (IgG2a) and B5gl (IgM) that are directed to M. tuberculosis 27‐kDa and 25‐kDa proteins respectively. Specificity analysis by immunoblotting using 20 different species of mycobacterial sonicates revealed that MoAb A3h4 was specific for M. tuberculosis complex alone while MoAb B5gl showed a limited cross‐reactivity. Direct comparison with previously characterized MoAbs revealed that these MoAbs A3h4 and B5gl defined new antigenic determinants of M. tuberculosis. By using M. tuberculosis complex‐specific MoAb A3h4 we have identified a distinct 27‐kDa protein in the M. tuberculosis H37Rv culture fluid. Since this MoAb did not bind to the previously characterized MPT44, MPT59, MPT45, MPT51 and MPT64 proteins as well as the 23‐kDa superoxide dismutase (SOD) protein of M. tuberculosis, we conclude that MoAb A3h4 recognizes a novel protein in the M. fuberculosis H37Rv culture fluid. Studies of the subccllular distribution of these MoAb‐reaetive proteins indicate that the MoAb A3h4‐reactive 27‐kDa protein is present not only in the culture fluid bnt also in the cytosol and the cell wall of M. tuberculosis. By contrast. B5gl‐reactive protein is mainly a cytosolic protein. When these MoAbs were tested in a previously established ELISA with intact mycobacteria derived from early cultures, only MoAb A3h4 showed the positive reactivity to mycobacteria belonging to the M. tuberculosis complex.In addition, during the present comparative studies of MoAbs we have also found that the previously described MoAb F116‐5, which is known to recognize the mycobacterial 23‐kDa SOD protein [17], cross‐reacted with the MPT44, MPT59, MPT45 and MPT51 secreted proteins but not with MPT64 and MPB70. These findings indicate that the family of four secreted proteins of M. tuberculosis share a common epitope with M. tuberculosis SOD protein.
IgA and IgG Subclass Deficiency in a Poor Population in a Developing Country
Authors: CASTRIGNANO S. B. , CARLSSON B. , CARNEIRO‐SAMPAIO M. S. , SÖDERSTRÖM T. , HANSON L. Å. 
Published: July 2006

The levels of IgG, IgG subclasses, IgM and IgA were determined in serum from 17 patients with IgA deficiency and severe or frequent infections, allergy and/or autoimmunity (median age 7 years, range 2–19), 11 healthy IgA‐deficient adults and 35 controls (median age 7 years, range 2–19). In serum from all groups IgG, IgM and IgA antibodies were determined against β‐lactoglobulin, E. coli O antigens and poliovirus type 1 antigen. In saliva of 15 IgA‐deficient patients and 12 of the controls IgG, IgM and secretory component‐carrying antibodies against E. coli O antigens and poliovirus type I were determined. The majority of the studied individuals lived under poor socio‐economic conditions in Brazil, with consequent heavy microbial exposure. One IgA‐deficient patient with rheumatoid arthritis also had IgG2 deficiency but no infectious problems. Four out of the 35 controls without any obvious infectious problems were found with IgA or IgG subclass deficiency. One of the 11 healthy IgA‐deficient adults was low in the IgG2 subclass, one in IgGl and one in IgG3.Those with symptomatic IgA deficiency had significantly higher serum IgG than the controls, especially in the age group 6–11 years. This latter group also had significantly increased serum IgG 1 and IgG2 levels when compared with the age‐matched controls. Salivary IgM antibodies to E. coli and poliovirus antigens were significantly higher among the symptomatic IgA‐deficient individuals than among the controls. It is not clear at present whether these increased Ig levels are secondary to frequent infections and/or part of mechanisms that may compensate for the IgA deficiency.
Experimental Allergic Bronchopulmonary Aspergillosis in the Mouse: Immunological and Histological Features
Authors: WANG J. M. , DENIS M. , FOURNFER M. , LAVIOLETTE M. 
Published: July 2006

C57BL/6 mice treated with intranasal instillation of 100 μg of Aspergillus antigen three times a week developed a pulmonary eosinophilia, observed in the bronchoalveolar lavage (BAL) and on hislopatholo‐gical examination. At week 3, the instillation of Aspergillus antigen provoked a 10‐fold increase in the BAL cell number and eosinophils were the predominant inflammatory cells (66.4′%,). Histopathological findings showed focal alveolar lesions with pcribronchial and perivascular infiltration of lymphoid cells, numerous eosinophils, epithelioid cells, and granulomus with giant cells. Increases in total IgF. and IgG1 levels in BAL fluid (33‐fold and 14‐fold) and serum (67‐fold and 8‐fold) were observed also (P<0.05). IgGl specific to Aspergillus fumigatus (Af) was detected only in the antigen‐treated mice.At 12 weeks, there was a persistent but less intense eosinophilia both in BAL and on histopathological examination accompanied by steadily elevated total IgE and total FgGl and a higher level of specific IgGl‐Af in BAL fluids and sera. No bronchocentric granulomatosis, mucoid impaction nor bronchiecta‐sis could be observed.Data from the study described here showed that in mice repeated exposure to Aspergillus antigen leads to a strong inflammatory pulmonary response, characterized by remarkable pulmonary eosinophilia and elevations of total IgE, total IgG 1 and specific TgG1‐Af in both BAL and serum, which are the hallmarks of human allergic bronchopulmonary aspergillosis also. However, this inflammation did not induce the chronic histological features of the human disease.
Signal Transduction via MHC Class‐I Molecules in T cells
Authors: Tscherning T. , Claësson M. H. 
Published: July 2006

SUMMARYThe data reviewed in this paper, suggest that besides their role in presentation of antigenic pcptides to T cells, MHC‐I molecules may play an important role in the fine‐tuning of signal transmission across the cell membrane by their associations with a variety of cell‐surface receptors regulating cell growth and differentiation.
Functional and Biochemical Properties of a Mouse Placental Immunoregulatory Factor
Authors: BOBÉ P. , BLEUX C. , KANELLOPOULOS‐LANGEVIN C. 
Published: July 2006

The authors have a long standing interest in immune regulations which control the absence of rejection of a semi‐allogeneic fetus by the mother. A previous work described a soluble 40 kDa factor extracted from mouse placenta and capable of inhibiting secondary immune responses in vivo. The present paper reports the following on its mode of action in vivo: (1) it is active even in a fully allogeneic host; (2) it can be administered i. v. or i. p. along with antigen; and (3) the injections of factor and antigen must not be more than 2 days apart for maximum efficacy. Moreover, the results of the study described here indicate also that this factor is a concanavalin A‐binding giycoprotein, sensitive to heat and pronase, and different from interleukin 10 (IL‐10).Thus, this placental factor appears to be different from previously described immune regulators such as IL‐10 and could contribute significantly to immune regulations at the level of the placenta.
IgM and IgG Subclass Distribution of Human Anti‐Ro/SSA 60 kDa Autoantibodies
Authors: WAHREN M. , RINGERTZ N. R. , PETTERSSON I. 
Published: July 2006

The Ro/SSA and La/SSB antigens are common targets for autoantibodies found in the sera of patients with Sjögren's syndrome and SLE. The anti‐Ro/SSA and anti‐La/SSB antibodies often appear together but are not cross‐reactive. This paper describes the humoral autoimmune response to the Ro/SSA 60 kDa protein moiety with respect to the presence of IgM and IgG1‐4 antibodies. IgM antibodies to the Ro 60 kDa protein coexisted with IgG anti‐Ro 60 kDa antibodies in nearly half of the sera. A similar fraction also contained IgM anti‐La/SSB antibodies. The frequency of sera with IgM antibodies of both specificities was that expected from random overlap.A predominating igGl anti‐Ro 60 kDa response was found in all patients, but anti‐Ro 60 kDa antibodies of the other IgG subclasses were present also in a high number of sera. This is in contrast to the reported IgG subclass distribution of anti‐La/SSB antibodies.Mapping of IgM and IgG 1–4 antibody recognition of different parts of the Ro 60 kDa protein was also performed. IgM and IgGl‐4 antibodies of all sera reacted with the central part of the Ro 60 kDa protein, encompassing amino acid residues 181–320.