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1

ETS transcription factors and regulation of immunity

100%
Gallant S., Gilkeson G.
Archivum Immunologiae et Therapiae Experimentalis
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2006
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vol. 54
|
issue 3
149-163
EN
The ETS family is a diverse group of transcription factors that control the expressions of genes that participate in an array of cellular activities, ranging from mitosis to apoptosis. As a consequence of regulating these processes, most ETS factors are oncogenic. However, there is growing evidence that ETS factors are also essential to regulation of the immune system. Of the 29 recognized ETS factors, nine are known to regulate genes involved in immunity, including Ets1, Ets2, GABP, Fli1, Elf1, MEF, ESE1, PU.1, and SpiB. These ETS factors typically activate the transcription of genes associated with pathogen and tumor defense, but several also demonstrate ability to repress transcription. Ets1 and PU.1 appear to have the greatest impact on immunity, primarily through their control of immune cell development. Alterations of Fli1 and Elf1 expression are associated with autoimmunity, emphasizing the role of ETS factors as not only positive, but also negative regulators of immunity. This review summarizes the roles of ETS factors in development of the immune system, defense against pathogens and malignancies, and self-tolerance.
2

Regulation of local immunity by airway epithelial cells

80%
Mayer A. K., Dalpke A. H.
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2007
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vol. 55
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issue 6
353-363
EN
Epithelial cells are the first line of defense against invading microbial pathogens. They are important contributors to innate mucosal immunity and generate various and sophisticated anti-microbial defense mechanisms, including the formation of a tight barrier and secretion of anti-microbial substances as well as inflammatory mediators. To provide these active defense mechanisms, epithelial cells functionally express various pattern-recognition receptors. Toll-like receptors have been shown to recognize conserved microbial patterns mediating inducible activation of innate immunity. Mucosal surfaces, however, are prone to contact with pathogenic as well as non-pathogenic microbes and, therefore, immune-recognition principles have to be strictly regulated to avoid uncontrolled permanent activation. This review will focus on mechanisms by which epithelial cells regulate mucosal immune responses, thus creating an organ-specific microenvironment. This includes local adaptations in microbial recognition, regulation of local immune homeostasis, and modulation of antigen-presenting cells and adaptive immune responses. These regulatory mechanisms serve the special needs of controlled microbial recognition in mucosal compartments.
3

The biology and pathology of hypoxia-ischemia: an update

80%
Clarkson A. N., Sutherland B. A., Appleton I.
Archivum Immunologiae et Therapiae Experimentalis
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2005
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vol. 53
|
issue 3
213-225
EN
After an hypoxic-ischemic (HI) insult, a multi-faceted complex cascade of events occurs that ultimately causes cell death and neurological damage to the central nervous system. The various cascades include, amongst others: immunological changes, such as the activation of the complement system and the generation of antibodies; increased inflammation through the actions of pro-inflammatory cytokines and chemokines; the production of reactive oxygen species leading to oxidative stress; and diminished mitochondrial function leading to the activation of apoptotic pathways and subsequent alteration in the function of neurons within the contralateral hemisphere. This review addresses the immunological aspects following HI, the role of various cytokines (both pro-inflammatory and anti-inflammatory) and chemokines after the induction of HI. In addition, the role of free radicals in producing HI-induced neurodegeneration and the contribution that mitochondrial dysfunction has in neuronal apoptotic cell death will be discussed. This review also covers the changes that the previously assumed 'internal control', the contralateral hemisphere, undergoes due to HI and describes the difficulties associated with therapy intended to prevent neuronal injury associated with HI.
4

Uncovering the differences between T cell tolerance and immunity

80%
Vella A. T.
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|
vol. 48
|
issue 5
331-338
EN
In the last two decades T cell function has been analyzed in vitro from many different angles with a great deal of attention dedicated to the basic requirements of activation. During this time a compendium of information has been collected and has proven to be invaluable. Paradoxically very little is known about T cell activation and function in vivo. In the last decade a number of models have been developed which allow the tracking of Ag-activated T cells in vivo and these studies have been instrumental in advancing the field of T cell biology. In particular, a new and emerging paradigm of T cell immunity is evolving.
5

The immunity in Toxoplasma gondii infections

80%
Dlugonska H.
Postępy Higieny i Medycyny Doświadczalnej
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2000
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vol. 54
|
issue 1
52-66
EN
The immunity in Toxoplasma gondii infections The article presents selected data concerning pathogenesis, clinical manifestations, natural and specific resistance and vaccines against T. gondii infections. Toxoplasma gondii protozoan has been recognized as one of the most successful parasites infecting any nucleated cell of human individuals and most warm-blooded animals. The infection causes life-threatening disease in individuals with defective immunity such as fetuses, AIDS patients and transplant recipients. In immunocompetent humans toxoplasmosis is usually asymptomatic. Following an acute phase of infection characterized by systemic spread of rapidly dividing tachyzoites, bradyzoites encyst in various host tissues (brain, muscles) and may persist there lifelong. Toxoplasmosis in controlled by vigorous cell-mediated immune response capable of killing infected cells and parasites. As shown in the mouse experimental model natural killer cells (NK) are critical for the resistance at the early stage of primary infections, whereas adaptive immunity depends on T lymphocytes. Both CD4+ Th1 and CD8+ Tc1 lymphocytes are believed to mediate protection by producing of IFN-?, a pitoval cytokine that induces anti-Toxoplasma effector mechanisms in macrophages.
6

Studies of immunity in mice immunized with outer membrane proteins of Hafnia

80%
Witkowska D., Czarny A., Mulczyk M.
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vol. 40
|
issue 2
119-124
EN
Nonspecific protection induced in mice after administration outer membrane proteins of Hafnia alvei against infection with homologue and heterologous bacteria was transferred into other mice with lymphocytes isolated from spleens of mice immunized with outer membrane proteins. It was also found that mice sensitized with outer membrane proteins derived from H. alvei or with living bacteria induced in animals delayed hypersensitivity (DTH) in homologous and heterologous systems. The observed type of hypersensitivity was transferable to normal mice by lymphocytes obtained from donor animals which were previously sensitized with OMP. The experiments revealed that immunity induced with outer membrane proteins of Hafnia alvei is cell-mediated.
7

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

80%
Czarny A., Witkowska D., Mulczyk M.
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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

Roles of galectin-3 in immune responses

80%
Chen H. Y., Liu F.-T., Yang R.-Y.
Archivum Immunologiae et Therapiae Experimentalis
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2005
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vol. 53
|
issue 6
497-504
EN
Galectins are a family of animal lectins with conserved carbohydrate-recognition domains for b-galactoside. Galectin-3 is the only family member that is composed of a glycine/proline-rich N-terminal repeated sequence and a C-terminal carbohydrate-binding domain. Multiple functions of galectin-3 have been reported, depending on its location. Extracelluar galectin-3 can bind to cell surface through glycosylated proteins and thereby trigger or modulate cellular responses such as mediator release or apoptosis. Intracellular galectin-3 has been reported to inhibit apoptosis, regulate the cell cycle, and participate in the nuclear splicing of pre-mRNA. Recent studies have revealed that galectin-3 is expressed in a variety of cell types in the immune system, constitutively or in response to microbial invasion. These studies implicate galectin-3 in both innate and adaptive immune responses, where it participates in the activation or differentiation of immune cells. This review summarizes the roles of galectin-3 in the immune system and discusses the possible underlying mechanisms.
9

Modulation of pulmonary innate immunity during bacterial infection: animal studies

70%
Schultz M. J., van_ d. P. T.
Archivum Immunologiae et Therapiae Experimentalis
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2002
|
vol. 50
|
issue 3
159-168
EN
Both the increasing number of immunocompromised patients susceptible to pneumonia, and the development of bacterial resistance are significant problems related to the treatment of pneumonia. The primary outcome of treatment for pneumonia is to tip the balance to a successful host response. An ideal approach would be the combination of immunomodulation and conventional antimicrobial therapy for the treatment of pneumonia. It is of increasing importance to understand the components of innate immunity, before immunomodulatory therapy can be applied to patients. Much of our knowledge of the role of alveolar macrophages, cytokines and chemokines in the pathogenesis of pneumonia is derived from animal studies on experimental pneumonia. This article summarizes current information on the role of an alveolar macrophage (AM) and AM-derived mediators in host defense against pneumonia.
10

DNA Tumor Vaccines

70%
Wlazlo A. P., Ertl H. C. J.
Archivum Immunologiae et Therapiae Experimentalis
|
2001
|
vol. 49
|
issue 1
1-12
EN
A new generation of vaccines are being developed to induce immune responses that fight off infectious agents, or erradicate cancerous cells. The new vaccines are based on a plasmid vector, which in transfected mammalian cells cause constitutive high-level expression of the target antigen. Expression of the target antigen, in turn, can induce a full-range of immunologic responses, including cell-mediated killing, cell-mediated cytokine release and the production of antigen-specific antibodies. Through molecular techniques, these nucleic acid vaccines can enhanced to increase target antigen expression and faciliatate antigen presentation. Additionally, genetic adjuvants expressed simultaneously with the target antigens can induce the immune responses to disease-associated antigens. The ease with which these genetic vaccines can be generated and the potency of their ability to generate immune-mediated responses make them highly effective, which creates hope for developing effective treatment and prevention of various diseases, most notably cancer.
11

Immune phenomena in echinoderms

61%
Glinski Z., Jarosz J.
|
|
vol. 48
|
issue 3
189-193
EN
Advances in biochemistry and molecular biology have made it possible to identify a number of mechanisms active in the immune phenomena of echinoderms. It is obvious that echinoderms have the ability to distinguish between different foreign objects (pathologically changed tissues, microorganisms, parasites, grafts) and to express variable effector mechanisms which are elicited specifically and repeatably after a variety of non-self challenges. The molecular and biochemical basis for the expression of these variable defense mechanisms and the specific signals which elicit one type of effector mechanism are not, however, yet well known. The high capacity of coelomocytes to phagocytose, entrap and encapsulate invading microorganisms is a valid immune cell-mediated mechanism of echinoderms. The entrapped bacteria, discharged cellular materials and disintegrating granular cells are compacted and provoke the cellular encapsulation reaction. Moreover, humoral-based reactions form an integral part of the echinoderm defense system against microbial invaders. Factors such as lysozyme, perforins (hemolysins) vitellogenin and lectins are normal constituents of hemolymph, while cytokines are synthesized by echinoderms in response to infection.
12

Surfactant proteins SP-A and SP-D in human health and dis

61%
Kishore U., Lopez B. A., Kamran M. F., Saxena S., Singh M., Sarma P. U., Madan T., Chakraborty T.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
|
vol. 53
|
issue 5
399-417
EN
Surfactant proteins A (SP-A) and D (SP-D) are lung surfactant-associated hydrophilic proteins which have been implicated in surfactant homeostasis and pulmonary innate immunity. They are collagen-containing C-type (calcium-dependent) lectins, called collectins, and are structurally similar to mannose-binding protein of the lectin pathway of the complement system. Being carbohydrate pattern-recognition molecules, they recognize a broad spectrum of pathogens and allergens via the lectin domain, with subsequent activation of immune cells via the collagen region, thus offering protection against infection and allergenic challenge. SP-A and SP-D have been shown to be involved in viral neutralization, clearance of bacteria, fungi, and apoptotic and necrotic cells, the down-regulation of allergic reaction, and the resolution of inflammation. Studies on single-nucleotide polymorphism, protein levels in broncho-alveolar lavage, and gene knock-out mice have clearly indicated an association between SP-A and SP-D and a range of pulmonary diseases. In addition, recent studies using murine models of allergy and infection have raised the possibility that the recombinant forms of SP-A and SP-D may have therapeutic potential in controlling pulmonary infection, inflammation, and allergies in humans.
13

Immune-endocrine interactions of the hypothalamus-pituitary-thyroid axis: integration, communication and homeostasis

61%
Armstrong M. D., Klein J. R.
Archivum Immunologiae et Therapiae Experimentalis
|
2001
|
vol. 49
|
issue 3
231-237
EN
The immune and neuroendocrine systems are two essential physiological components of mammalian organisms. Although each is primarily committed to a set of tasks involved, on the one hand, in the protection from infection and disease, and on the other hand, in the regulation of metabolism and other physiological activities, there is also evidence indicating that active and dynamic collaborations exist between those systems in the execution of their designated functions. These interactions occur at many stages of embryonic and neonatal development, and they are a continual part of the normal homeostatic balance needed to maintain health. The present review discusses various historical and contemporary perspectives of immune-endocrine interactions involving the hypothalamus-pituitary-thyroid axis, and offers a hypothesis of how this aspect of the neuroendocrine system participates directly in the immune response to antigenic challenge, infection and disease.
14

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

61%
Sinkovics J. G., Horvath J. C.
|
|
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 .
15

Stress and immunity: minireview.

61%
Plytycz B., Seljelid R.
Folia Biologica
|
2002
|
vol. 50
|
issue 3-4
181-189
EN
Stress, a state of threatened homeostasis, may be induced by various physical or psychological factors (stressors), including antigenic stimulation. Stressful experiences may affect both physical/psychological well being and immune functioning of humans and animals; the ongoing immune reaction may affect other physiological functions and psychological comfort. The molecular basis of these effects involves a network of multidirectional signalling and feedback regulations of neuroendocrine- and immunocyte-derived mediators. The consecutive stages of the multistep immune reactions might be either inhibited or enhanced owing to the previous and/or parallel stress experiences, depending on the kind of stressor and the animal species, strain, gender, or age. Therefore, the final results of stress-induced alteration of immune reactions are difficult to predict. The effect of a particular stressor on immune functions varies according to the previous stress experience of the individual (e.g. social confrontation, sterile saline injection) while various stressors may act in the same or in opposite ways on the same immune parameter. In general, the efficacy of immune response depends on the neuroendocrine environment on which it is superimposed. Conversely, neural and endocrine responses depend on the concurrent immune events upon which they are superimposed. It seems that the consequences of stress on the immune functioning are generally adaptive in the short run but can be damaging when stress is chronic.
16

Eicosanoid regulation of pulmonary innate immunity post-hematopoietic stem cell transplantation

61%
Ballinger M. N., McMillan T. R., Moore B. B.
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2007
|
vol. 55
|
issue 1
1-12
EN
Hematopoietic stem cell transplantation (HSCT) is a therapeutic option for a number of malignant and inherited disorders. However, the efficacy of this therapy is limited by a number of serious infectious and noninfectious complications. Pulmonary infections represent a significant cause of morbidity and mortality post-HSCT and can occur both pre- and post-hematopoietic reconstitution. Susceptibility to Gram-negative bacterial infections despite full hematopoietic engraftment suggests that innate immunity remains impaired months to years post-HSCT. This review will describe the process and complications of HSCT and will summarize what is known about innate immune reconstitution post-HSCT. Data from the literature as well as our own laboratory will be presented to suggest that an eicosanoid imbalance characterized by over-production of prostaglandins and under-production of leukotrienes leads to impaired lung phagocyte function post-HSCT. Of therapeutic interest, strategies which limit production of prostaglandins can improve pulmonary host defense in animal HSCT models, which suggests that this may also be beneficial for human HSCT recipients.
17

CD1 molecules: mechanisms of lipid antigens presentation

51%
Mikulska J.
Postępy Higieny i Medycyny Doświadczalnej
|
2003
|
vol. 57
|
issue 6
649-667
EN
This review summarizes the status of our knowledge on the structure, expression and function of CD1 proteins. An endosomal and non-endososomal pathways of CD1 antigen presentation are also described.
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