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1

Investigation of serum cytokine levels and cytokine production in whole blood cultures of paranoid schizophrenic patients

100%
Kaminska T., Wysocka A., Marmurowska-Michalowska H., Dubas-Slemp H., Kandefer-Szerszen M.
Archivum Immunologiae et Therapiae Experimentalis
|
2001
|
vol. 49
|
issue 6
439-446
EN
There is some evidence that the pathophysiology of schizophrenia is related to changes in the innate and adaptive immune systems. In an attempt to define a potential immunological dysfunction in schizophrenia, we measured the serum levels of several cytokines in the sera of 24 patients with paranoid schizophrenia and investigated the cytokine production in whole blood assays after stimulation in vitro with virus (Newcastle disease), phytohemagglutinin (PHA) or bacterial lipopolysaccharide (LPS) and compared them with healthy, normal controls. A significant increase of IL-6, IL-8 and IFN- gamma levels, but a decreased IL-10 level were observed in the sera of patients with schizophrenia. No significant changes in the serum levels of IL-2, IL-4, IFN-alpha and TNF-alpha were detected in these patients. When cytokine production in vitro was examined, a significant defect in PHA-induced IL-2, IL-4 and IFN-gamma, and in virus-induced IFN-alpha production, but no significant alterations in LPS-induced IL-6, IL-10 and TNF-alpha production were observed. In summary, increased serum levels of some cytokines such as IL-6, IL-8 and IFN-gamma indicate an activation of the inflammatory response in schizophrenia, while the in vitro assay indicates significant changes in the Th1 (decreased production of IL-2 and IFN-gamma) and Th2 (decreased production of IL-4) cell system responses. The role of the defective IFN-apha production in the regulation of the imbalance between Th1 and Th2 cell system responses is suggested.
2

Lack of relationship between serum content of MBL, sCD14, anti-PPD and anti-Hsp65 IgG, and ingestion of Mycobacterium bovis BCG bacilli by phagocytes

100%
Paziak-Domanska B., Bonar A., Kowalewicz-Kulbat M., Klink M., Kowalski M., Karhukorpi J., Karttunen R., Jurkiewicz M., Rozalska B., Rudnicka W.
Archivum Immunologiae et Therapiae Experimentalis
|
2002
|
vol. 50
|
issue 5
337-344
EN
Prophylactic vaccination against tuberculosis (TB) with a live attenuated strain of Mycobacterium bovis Bacille Calmett?e-Gerin (BCG) has been used worldwide. However, TB remains one of the most significant diseases of humans and animals. Better understanding of the mechanisms of human immunity to mycobacteria is essential for development of new vaccines and estimation of their efficacy. In this study we determined the levels of known humoral mediators of mycobacterial phagocytosis - mannose binding lectin (MBL), soluble CD14 (sCD14), antibodies of IgG class against mycobacterial purified protein derivative (PPD) and mycobacterial Hsp65 antigen, in the sera from healthy young volunteers vaccinated with BCG and presenting positive and negative Mantoux responses to PPD. Than we asked a question as to whether macrophages and polymorphonuclear leukocytes (PMNs) from the individuals with positive (TT(+)) and negative (TT(-)) tuberculin tests differ by the ability to ingest mycobacteria. Also we were looking for a relation between the intensity of mycobacterial ingestion by phagocytes in the medium with autologous sera containing different concentration of MBL, sCD14 andf anti-mycobacterial IgG. We found no significant differences between the investigated parameters for TT(+) and TT(-) volunteers. Our result suggest that ability of macrophages and PMNs to ingest mycobacteria depends on an individual intrinsic capacity of phagocytes.
3

Pathogenic immunity in Theiler?s virus-induced demyelinating disease: a viral model for multiple sclerosis

100%
Kim B. S., Palma J. P., Inoue A., Koh C.-S.
Archivum Immunologiae et Therapiae Experimentalis
|
2000
|
vol. 48
|
issue 5
373-380
EN
Multiple sclerosis involves inflammatory immune responses in the central nervous system and is considered as an autoimmune disease potentially associated with viral infection. The majority of experimental models rely heavily on the autoimmune components since similar diseases can be induced following immunization with various myelin antigens. A very attractive alternative model is the Theiler?s murine encephalomyelitis virus-induced demyelinating disease. This disease is primarily a CD4+ T cell-mediated, inflammatory demyelinating disease, induced following viral infection. Virus-specific inflammatory Th1 cell responses, rather than cytotoxic T lymphocyte response, play a critical role in the pathogenic immune responses. The major pathogenic epitopes have been identified and these are correlated with a Th1 type response to the epitopes following viral infection. In addition, the initial virus-specific immune response is followed by the autoimmune responses to myelin antigens. Assessment of cytokines produced locally in the CNS during the course of disease suggests involvement of inflammatory cytokines in the disease. Furthermore, the manipulation of inflammatory cytokine levels by administration of either recombinant cytokines or antibodies to the cytokines strongly influences the induction and/or progression of disease, supporting the importance of these inflammatory cytokines in this virus-induced demyelinating disease.
4

All roads lead to Rome: pathways of NKT cells promoting asthma

100%
Jinquan T., Li W., Yuling H., Lang C.
Archivum Immunologiae et Therapiae Experimentalis
|
2006
|
vol. 54
|
issue 5
335-340
EN
NKT cells are the prominent manipulator in asthma development. Asthmatic NKT cells migrate from thymus, spleen, liver and bone marrow into blood vessels, and then concentrate in airway bronchi mucosa. This recruitment is dependent on high expression of CCR9 and engagement of CCL25/CCR9. NKT cells promote asthma in two different pathways. One is an indirect pathway. NKT cells contact with CD3+ T cells and induce them secreting large quantity of Th2 cytokines (IL-4, IL-13), which requires the participation of dentritic cells and the synergic signaling of CCL25/CCR9 and CD226. The other is a direct pathway. Circulating asthmatic NKT cells selectively highly express Th1 cytokines . Once reached airway epithelium, most NKT cells shift to Th2-bias, highly expressing IL-4, IL-13, but not IFN-alpha. Both pathways lead to airway hyperresponsiveness and inflammation, asthma development. Comparing to the well documented suppressive regulatory T cells, CD4+CD25+ T cells, NKT cells perform as a novel active regulator in asthma. These recent understanding of NKT cells performance in the development of asthma might unveil new therapy targets and management strategies for asthma.
5

Cytokine production by human leukocytes with different expressions of natural antiviral immunity and the effect of antibodies against interferons and TNF-alpha

100%
Orzechowska B., Antoszkow Z., Siemieniec I., Lorenc M., Jatczak B., Blach-Olszewska Z.
Archivum Immunologiae et Therapiae Experimentalis
|
2007
|
vol. 55
|
issue 2
111-117
EN
Introduction: Two activities of innate antiviral immunity were studied: the resistance of human peripheral blood mononuclear cells (PMBCs) ex vivo to viral infection and the production of cytokines. Materials and Methods: Samples of blood were taken from healthy blood donors and from persons with frequent infections of the upper respiratory system. PMBCs were isolated by gradient centrifugation. Vesicular stomatitis virus (VSV) was used as the indicatory virus to infect PMBCs. The cytokines: IFN, TNF, and IL-6 were titrated by biological methods and IL-10 by ELISA. Results: Blood donors were divided for two groups: those with VSV-resistant and those with VSV-sensitive PMBCs and secretion of cytokines by them was compared. The resistant PMBCs produced more cytokines than the sensitive ones. A statistically significant difference, was found only in the case of the IFNs. To examine the contribution of IFNs and TNF in maintaining resistance, leukocytes from both groups were treated with specific anti-cytokine antibodies. The authors' previous study showed that the elimination of spontaneous IFN-alpha IFN-beta, IFN-gamma, and TNF-alpha from resistant leukocytes resulted in increased VSV replication This indicates the important role of cytokines. In VSV-sensitive PMBCs, anti-IFN-alpha showed the opposite effect (decreased virus replication). In the absence of spontaneous IFN-alpha, disturbances in cytokine production were observed. Conclusions: Complete resistance of PMBC to VSV infection is accompanied by higher cytokine release, The paradoxical effect of anti-IFN-alpha on virus replication in leukocytes sensitive to viral infection may be attributed to changes in the cytokine profile balance, i.e. high TNF production by VSV-infected leukocytes and a complete reduction of IL-6 production.
6

Mycobacterium-specific human CD8 T cell responses

100%
Klein M. R., Fox A.
Archivum Immunologiae et Therapiae Experimentalis
|
2001
|
vol. 49
|
issue 5
379-390
EN
Tuberculosis (TB) remains a global health problem. There is an intense effort to identify correlates of protective immunity and to design new TB vaccines. CD8 T cells are thought to play a significant role in controlling Mycobacterium tuberculosis infection. Relatively little has been published about the antigens and epitopes targeted by mycobacteria-specific CD8 T cells. Here we present an update of our 1999 overview of human CD8 T cell epitopes in mycobacterial antigens and discuss related issues relevant to TB diagnosis and vaccine development.
7

Effect of outer membrane proteins from Shigella humoral immunity induced in mice by SRBC

100%
Czarny A., Witkowska D., Mulczyk M.
Archivum Immunologiae et Therapiae Experimentalis
|
1992
|
vol. 40
|
issue 2
129-134
EN
Shigella flexneri outer membrane proteins (OMP) which had been earlier found to exert immunomodulatory effect on cell mediated immune response were also found to act as immunomodulator of the humoral immune response. Effects of OMP were investigated in the experiments in vitro and in vivo, where the level of humoral immune response measured as the number of plaque-forming cells (PFC) to SRBC in the spleen was evaluated. We demnostrate that small doses of OMP stimulate, whereas higher doses suppress the humoral immunity.
8

HLA-DR antigens in children with mumps meningitis

100%
Matej H., Kacprzak-Bergman I., Pacynska J., Nowakowska B., Kalamarz M.
Archivum Immunologiae et Therapiae Experimentalis
|
1992
|
vol. 40
|
issue 2
117-118
EN
the frequency of HLA-DR antigens was studies in 54 patients with mumps meningitis, and in two control groups. The first control group comprised 333 rondomely chosen subjects while the second group was composed of 46 subjects who have passed mumps without meningitis. The DR5 antigen was more frequent in patients than in the second control group with relative risk of 2,4 and significance at the level of p smaller than 0.05. The p value became insignificant after the correction for the number of antigens investigated.
9

The cGMP synthesis and PKG1 expression in murine lymphoid organs

100%
Kurowska E., Kobialka M., Ziolo E., Strzadala L., Gorczyca W. A.
Archivum Immunologiae et Therapiae Experimentalis
|
2002
|
vol. 50
|
issue 4
289-295
EN
Numerous reports indicate that cyclic 3',5' guanosine monophosphate (cGMP) is involved in the regulation of immune processes. However, the mechanisms responsible for the synthesis of this nucleotide and its signaling pathways in immune cells are still not well recognized. The aim of our study was to establish: 1) which form of guanylyl cyclase synthesizes cGMP in murine lymphoid organs and 2) whether the same organs express the isoforms PKG1alpha and/or PKG1beta of protein kinase G, known as a possible target for synthesized cGMP. Cells isolated from thymus, lymph nodes, and spleen were treated with activators (SNP, ANP, CNP, STa) of soluble or particulate cyclases. Sodium nitroprusside (SNP) elevated intracellular cGMP 2-fold in thymic and lymph node cells and about 10-fold in spleen cells. Atrial natriuretic peptide (ANP) caused modest but statistically significant increases of cGMP in cells of all the organs. Additionally, spleen cells elevated their cGMP content about 2-fold in response to C-type natriuretic protein (CNP). In cellular homogenates of all the analyzed organs, the antibody anti-PKG1beta stained the 78 kDa band corresponding to the molecular mass of PKG1. Only homogenates of spleen cells were stained by the antibody recognizing PKG1alpha. Our results indicate that in all the investigated organs, cGMP may be synthesized mainly by soluble guanylyl cyclases in response to nitric oxide. The modest increase of cGMP upon stimulation by ANP suggests that in all these organs either exist only a small subpopulation of cells that express particulate cyclase GC-A or GC-A is expressed at very low level. In spleen cells, however, cyclase GC-B appears to be the more active enzyme. Elevated cGMP concentration may in turn activate PKG1beta in thymus, lymph node, and spleen cells and also PKG1alpha in spleen cells.
10

Phagocyte NADPH oxidase: a multicomponent enzyme essential for host defenses

100%
El-Benna J., Dang P. M.-C., Gougerot-Pocidalo A.-M., Elbim C.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
|
vol. 53
|
issue 3
199-206
EN
Phagocytes such as neutrophils and monocytes play an essential role in host defenses against microbial pathogens. Reactive oxygen species (ROS), such as superoxide anion, hydrogen peroxide, the hydroxyl radical, and hypochlorous acid, together with microbicidal peptides and proteases, constitute their antimicrobial arsenal. The enzyme responsible for superoxide anion production and, consequently, ROS generation, is called NADPH oxidase or respiratory burst oxidase. This multicomponent enzyme system is composed of cytosolic proteins (p47phox, p67phox, p40phox, and rac1/2) and membrane proteins (p22phox and gp91phox, which form cytochrome b558) which assemble at membrane sites upon cell activation. The importance of this enzyme in host defenses is illustrated by a life-threatening genetic disorder called chronic granulomatous disease in which the phagocyte enzyme is dysfunctional, leading to life-threatening bacterial and fungal infections. Also, because ROS can damage surrounding tissues, their production, and thus NADPH oxidase activation, must be tightly regulated. This review describes the structure and activation of the neutrophil NADPH enzyme complex.
11

Abnormalities in the handling of intracellular bacteria in Crohn's disease: a link between infectious etiology and host genetic susceptibility

100%
Glasser A.-L., Darfeuille-Michaud A.
Archivum Immunologiae et Therapiae Experimentalis
|
2008
|
vol. 56
|
issue 4
237-244
EN
The etiology of Crohn's disease (CD) is still poorly understood, but recent advances have highlighted the importance of the innate immune system and the critical relationship between the gut flora and the intestinal mucosa. Several combinations of genetic factors predisposing to CD have been described, with the most significant replicable associations including genes for intracellular receptors of bacterial cell walls (NOD2/CARD15) and for bacterial clearance and antigen processing via autophagy (ATG16L1 and IRGM). One theoretical link between susceptibility genes NOD2/CARD15, ATG16L1, and IRGM is that CD is primarily induced by the presence of a dysfunctional immunological response to persistent infection by intracellular bacterial pathogens such as Mycobacterium avium subspecies paratuberculosis or adherent-invasive Escherichia coli, both first-rank candidates on the basis of host genetic susceptibility, which concerns impaired functions in the defense against intracellular bacteria.
12

Histamine receptor expression on peripheral blood lymphocytes is influenced by specific and nonspecific activation

100%
Zak-Nejmark T., Kraus-Filarska M., Malolepszy J., Jankowska R., Jutel M., Nowak I. A., Nadobna G.
Archivum Immunologiae et Therapiae Experimentalis
|
2000
|
vol. 48
|
issue 2
107-110
EN
Histamine is a physiological mediator which exerts both effector and regulatory functions through its receptors on various cells. The aim of the study was to investigate changes in histamine receptor expression on peripheral blood lymphocytes affected by stimulation with both specific and nonspecific stimuli. Lymphocytes were obtained from both healthy and allergic subjects. Cells were incubated with various allergens (mixed grass pollen, Lolium perenne, Dermatophagoides pteronyssinus 1, bee venom, phospholipase A2) and nonspecific (fMLP, PMA/ionomycin, LPS) stimuli. The percentage of histamine-binding cells was determined with a fluorescence microscope after incubation with histamine-fluorescein. In control subjects histamine binding after stimulation with allergens was not significantly changed. In contrast, in allergic subjects stimulation with specific allergens resulted in significantly increased histamine binding. Nonspecific stimulation caused increased histamine binding to lymphocytes in both allergic subjects and healthy controls. We conclude that specific and nonspecific activation of lymphocytes is associated with increased expression of histamine receptors.
13

Time-dependent observations of secretion marker levels in nasal secretion after histamine and methacholine provocations

100%
Pupek M., Mikulewicz W., Mielnik J., Batycka B., Katnik-Prastowska I.
Archivum Immunologiae et Therapiae Experimentalis
|
2003
|
vol. 51
|
issue 4
259-265
EN
Nasal provocation tests with histamine and methacholine were carried out in 25 healthy men on an effort to assess the dynamic changes of albumin, total IgA, secretory IgA and lactoferrin concentrations in the nasal secretion. The trials were performed with 0.5, 1, and 4 mg of histamine and 8, 16, 32 mg of methacholine. Each dose of histamine or methacholine was sprayed into a nose every second day, and with two days interval between two provocating agents. The nasal secretions were collected after saline spraying only forming baseline group and after 3, 10 and 15 minutes of the challenge agent administration. The baseline levels presented the following values: for albumin 257? 230 mug/ml, secretory IgA 608 ? 379 mug/ml, total IgA 1025 ? 423 mug/ml, and lactoferrin 213 ? 156 mug/ml. The increase of albumin level after nasal provocation, particularly significant after histamine administration (to 3713 ? 2311 mug/ml), indicates the incessant protein plasma leaking from the blood circulation to the nasal secretion. After administration of both provocating agents there was the significant gradual decrease of secretory IgA level, even below the baseline value. After the 2nd and the 3rd doses of methacholine and histamine spraying the concentration of secretory IgA decreased 2-3 times and was found to be 200-300 mug/ml, respectively. Also, lactoferrin concentration values decreased gradually after the 2nd and 3rd doses of methacholine and histamine to level close the baseline value. These observations suggest time and dose dependent, a non-specific dysfunction of local immunity response after nasal provocations.
14

Neurokinin receptors: relevance to the emerging immune system

100%
Kang H. S., Trzaska K. A., Corcoran K., Chang V. T., Rameshwar P.
Archivum Immunologiae et Therapiae Experimentalis
|
2004
|
vol. 52
|
issue 5
338-347
EN
The adult bone marrow (BM) is the major site of the emerging immune system. Hematopoiesis is the process whereby immune cells are generated from a finite number of hematopoietic stem cells. Hematopoiesis is regulated by soluble mediators and intercellular interactions. A major regulatory mechanism of hematopoiesis involves bidirectional crosstalk with the neural system. This communication mainly occurs by the release of neurotransmitters from innervated fibers. The neurotransmitters interact with specific receptors on BM resident cells and release other hematopoietic regulators such as cytokines. Together, the neurotransmitters and cytokines form a complex network to regulate hematopoiesis. Among BM resident cells, the stromal cells are particularly relevant for two reasons: 1) they represent non-neural sources of neurotransmitters, and 2) stromal cells express specific receptors for neurotransmitters. This review focuses on the hematopoietic effects of neurotransmitters belonging to the tachykinins. The two major tachykinins focused in this review are substance P and neurokinin (NK)-A, 11 and 10 amino acid peptides. In BM, the tachykinins interact with two major NK receptors: NK-1 and NK-2. These two receptors appear to limit tachykinin-mediated effects on hematopoiesis. The central roles of NK receptors within a network comprising of cytokines and tachykinins are reviewed.
15

Nuclear import of arachidonate 5-lipoxygenase

100%
Brock T. G., Healy A. M.
Archivum Immunologiae et Therapiae Experimentalis
|
2000
|
vol. 48
|
issue 5
481-486
EN
Leukotrienes are lipid messenger molecules that are secreted by leukocytes to orchestrate a rapid and prolonged immune response. The enzyme 5-lipoxygnease catalyzes the rate-limiting first two steps in the synthesis of leukotrienes from arachidonic acid. Although it has long been known that 5-lipoxygenase moves from the cytoplasm to a membrane following activation, it has only recently been recognized that the enzyme may shuttle into and out of the nucleus before activation. The regulation of this movement of soluble 5-lipoxygenase between the cytoplasm and the nucleoplasm, as well as its impact on 5-lipoxygenase action, leukotriene synthesis and cell function, is only now being elucidated. This review details the state of our understanding of the nuclear import of 5-lipoxygenase and its potential importance in immunity.
16

Effect of cardiopulmonary bypass on neutrophil activity in pediatric open-heart surgery

100%
Pasnik J., Siniewicz K., Moll J., Moll J. A., Baj Z., Sysa A., Zeman K.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
|
vol. 53
|
issue 3
272-277
EN
The nature of the participation of neutrophils in the post-cardiopulmonary bypass (CPB) inflammatory response is not very clear. The aim of our study was to investigate alterations in neutrophil phagocytic activity and adhesion molecule expression on these cells in children during and after CPB. Twenty-one children aged 6?33 months with congenital heart disease, scheduled for primary corrective surgery, were enrolled. The expressions of CD11b adhesion molecules and Fcg receptor on neutrophils and their phagocytic activity were evaluated. The studied markers were sequentially measured before, at the initiation of, and after CPB. During the course of the operation, CD11b molecule expression on neutrophils showed a slight elevation at the start of CPB (876.5104.8 mean fluorescence intensity, MFI, vs. 768.1178.2; p=0.0047), followed by a significant decrease to 689.01166.7 MFI after completion of the procedure. The expression of CD11b molecule on neutrophils measured at the end of CPB inversely correlated with the duration of CPB (r= ?0.68, p=0.00059). The expression of CD16 antigen dropped significantly at the start of CPB (1164.6307.3 MFI vs. 1327.4345.3 MFI; p=0.0007) and remained decreased until the end of CPB (814.0198.1 MFI). These findings suggest that the characteristics of the neutrophil response to cardiac surgery appear to depend on many factors. We demonstrated a link between the duration of CPB and adhesion molecule expression on neutrophils.
17

Mechanisms of mouse T lymphocyte-induced suppression of the IgG2ab allotype and T lymphocyte tolerance to IgG2ab

100%
Majlessi L., Bordenave G.
Archivum Immunologiae et Therapiae Experimentalis
|
2001
|
vol. 49
|
issue 6
407-416
EN
In mice of the Igha immunoglobulin allotypic haplotype we found, the presence of T lymphocytes with an inherent inhibitory activity against the expression of the IgG2ab allotype (IgG2a of the Ighb immunoglobulin allotypic haplotype). This constitutive anti-IgG2ab T lymphocyte activity can be enhanced in vivo by what we called 'sensitization', which usually consists of one or two intravenous injections of B splenocytes from Ighb congenic mice. When injected at birth, the resulting anti-IgG2ab T splenocytes induce, with 100% success, total, specific and chronic (but experimentally reversible) suppression of IgG2ab in Igha/b F1 hybrid mice prepared by mating Igh congenic mice. Even if restricted to IgG2ab expression, this experimental model, which deals with an unambiguous case of T cell-mediated down-regulation of immunoglobulin production, provides a clear and powerful tool to dissect finely the behavior of the partners (T and B lymphocytes) intervening in regulation within the immune system. For example, we observed that CD4 T lymphocytes were necessary to obtain full recruitment of anti-IgG2ab CD8 T lymphocytes during the sensitization, that suppression induction in anti-IgG2ab T splenocytes of newborn recipients required cooperation between CD4 and CD8 T lymphocytes, and that CD8 T lymphocytes were essential for suppression maintenance. We showed that this suppression was not characterized by an accumulation of B lymphocytes containing the allotype they could not secrete or Cgamma2ab mRNA they could not translate. The recipient's immune system was not involved in the suppession maintenance; this was done by donor T lymphocytes, which ensured the chronicity of IgG2ab suppression throughout the recipient's life. We demonstrated that the mechanism of this suppression implied an MHC-restricted presentation by target B lymphocytes of Cgamma2ab peptides to the T cell receptor (TCR) of anti-IgG2ab T lymphocytes. Notwithstanding the requirement of a CD4-CD8 T lymphocyte cooperation during the induction phase, we functionally determined that the suppression induction implicated an MHC class I-, but not class II-restricted interaction. We also demonstrated the existence in vivo of alternative or concomitant use of perforine- and Fas-mediated cytotoxicity pathways in this T cell-induced IgG2ab suppression. Thus this suppression did not imply silencing IgG2ab production, but B lymphocyte destruction by CD8 T lymphocytes. Always using our suppression model, we demonstrated that an agonistic anti-CD40 treatment helps in recruiting CD8 cytotoxic T lymphocytes, involved in immune regulatory functions and that CD40 expression on Ighb B lymphocytes confronted with CD8 T lymphocyte effectors only operating via the Fas pathway was involved in the total suppression of IgG2ab expression. The selection and maintenance of such normal T cell activity against the IgG2ab allotype in mice of different genetic backgrounds remain somewhat enigmatic. Indeed, we did not observe any similar activity against other immunoglobulin allotypes or isotypes. The intestinal flora had no influence on the emergence of this anti-IgG2ab T lymphocyte activity, as it was untouched in germ-free Igha mice when compared with normal Igha mice. More recently, this model offered an opportunity to study problems pertaining to immune tolerance. For instance, we showed that the genetic elements involved in the building of anti-IgG2ab TCR were available in Igha and Ighb mice of different genetic backgrounds, but that somatic constraints, namely the perinatal presence of IgG2ab, effectively prevented their acquisition, while its absence led to their spontaneous emergence. Consequently, we were able to induce anti-IgG2ab T lymphocytes into a tolerance state by injecting Igha mice with soluble IgG2ab during the perinatal period. However, the full T lymphocyte tolerance obtained in this manner was not definitively acquired, as it had reversed spontaneously when investigated 3 to 6 months after the end of tolerogen treatment, even when this treatment had been prolonged from the perinatal period to 9 months of age. The mechanisms (induction and reversion) of this tolerance involves the physical elimination or the irreversible inactivation of the natural anti-IgG2ab T lymphocyte clones and their resurgence, from bone-marrow precursors, as long as the thymus remains operational, but not the establishment of a reversible, functional unresponsiveness (anergy) or an active, cell-mediated inhibition of anti-IgG2ab T clones. We attempted to elucidate, in Ighb mice, whether the natural T lymphocyte unresponsiveness to IgG2ab involved a central tolerance mechanism and to identify the type of tolerogen implicated in this tolerogenesis. The experiments principally showed that this natural T lymphocyte tolerance to IgG2ab was mediated by a thymic mechanism; that the capacity to induce it was gradually acquired by Ighb thymuses and was most probably due to potentially IgG2ab-producing/presenting cells, progressively colonizing the developing thymus; and that a significantly decreased postnatal Cgamma2ab gene transcription correlated with the emergence of anti-IgG2ab T lymphocytes in Igha/b F1 (postnatally deprived of their B lymphocyte compartment), which subjected them to autoimmune IgG2ab-allotype suppression.
18

Emerging concepts in the molecular pathogenesis of systemic lupus erythematosus

100%
Nambiar M. P., Juang Y.-T., Tsokos G. C.
Archivum Immunologiae et Therapiae Experimentalis
|
2002
|
vol. 50
|
issue 1
35-46
EN
Systemic lupus erythematosus is a prototypic autoimmune disease that predominantly afflicts women during child-bearing age. The disease is characterized by the production of autoantibodies and immune complexes in association with a diverse array of clinical manifestations. Investigation into the etiopathogenesis has been directed at identifying the genes that provide susceptibility to the disease, the complex cellular and cytokine aberrations and the biochemical abnormalities that are responsible for them. Understanding the immune cell signaling and gene transcription abnormalities will help us tailor new strategies for efficient biotherapy of the disease.
19

Immunological properties of mesenchymal stem cells and clinical implications

100%
Patel S. A., Sherman L., Munoz J., Rameshwar P.
Archivum Immunologiae et Therapiae Experimentalis
|
2008
|
vol. 56
|
issue 1
1-8
EN
The rapid evolution of experimental data has acknowledged the critical relevance of immune biology in stem cell research. It appears that efficient transfer of stem cells to patients requires robust analyses of the immune properties as well as the responses of the stem cells to immune mediators. This review discusses the biology of adult human mesenchymal stem cells (MSCs) in the context of immunology. MSCs are pluripotent, self-renewing cells with the potential for tissue regeneration, for example the repair of bone, cartilage, tendon, ligament, skeletal muscle, and cardiac muscle. MSCs have also been shown to transdifferentiate into cells of ectodermal origin, such as neurons. MSCs are located in perfused areas of adult bone marrow, whereas hematopoietic stem cells are located in poorly perfused areas of the same organ. MSCs show bimodal, i.e. anti-inflammatory and immune-enhancing, immune responses. MSCs also regulate immune responses such as the regulation of antibody production by B cells, alterations in T cell subtypes, and immune tolerance of allogeneic transplants. MSCs also have the potential for gene delivery. This review explores the diverse clinical potential for MSCs and discusses the limitations and advantages of their immunomodulatory properties.
20

Natural and genetically engineered viral agents for oncolysis and gene therapy of human cancers

100%
Sinkovics J. G., Horvath J. C.
Archivum Immunologiae et Therapiae Experimentalis
|
2008
|
vol. 56 Sup
|
issue 6
3-59
EN
Based on personal acquaintances and experience dating back to the early 1950s, the senior author reviews the history of viral therapy of cancer. He points out the difficulties encountered in the treatment of human cancers, as opposed by the highly successful viral therapy of experimentally maintained tumors in laboratory animals, especially that of ascites carcinomas in mice. A detailed account of viral therapy of human tumors with naturally oncolytic viruses follows, emphasizing the first clinical trials with viral oncolysates. The discrepancy between the high success rates, culminating in cures, in the treatment of tumors of laboratory animals, and the moderate results, such as stabilizations of disease, partial responses, very rare complete remissions, and frequent relapses with virally treated human tumors is recognized. The preclinical laboratory testing against established human tumor cell lines that were maintained in tissue cultures for decades, and against human tumors extricated from their natural habitat and grown in xenografts, may not yield valid results predictive of the viral therapy applied against human tumors growing in their natural environment, the human host. Since the recent discovery of the oncosuppressive efficacy of bacteriophages, the colon could be regarded as the battlefield, where incipient tumor cells and bacteriophages vie for dominance. The inner environment of the colon will be the teaching ground providing new knowledge on the value of the anti-tumor efficacy of phage-induced innate anti-tumor immune reactions. Genetically engineered oncolytic viruses are reviewed next. The molecular biology of viral oncolysis is explained in details. Elaborate efforts are presented to elucidate how gene product proteins of oncolytic viruses switch off the oncogenic cascades of cancer cells. The facts strongly support the conclusion that viral therapy of human cancers will remain in the front lines of modern cancer therapeutics. It may be a combination of naturally oncolytic viruses and wild-type viruses rendered oncolytic and harmless by genetic engineering, that will induce complete remissions of human tumors. It may be necessary to co-administer certain chemotherapeutic agents, advanced cancer vaccines, or even immune lymphocytes, and targeted therapeuticals, to ascertain, that remissions induced by the viral agents will remain complete and durable; will co-operate with anti-tumor host immune reactions, and eventually will result in cures of advanced metastatic human cancers. Key words: naturally oncolytic viruses viral oncolysates, human cancer immunity, interaction of resident viral flora with the oncolytic virus, oncosuppressive bacteriophages, genetically engineered oncolytic viruses .
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