Full-text resources of PSJD and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl
Preferences help
Polish version English version Language
enabled [disable] Abstract
Number of results

Results found: 19

Number of results on page
first rewind previous Page / 1 next fast forward last

Search results

Search:
in the keywords:  AUTOIMMUNE DISEASE
help Sort By:

help Limit search:
first rewind previous Page / 1 next fast forward last
1

Role of SLAM-associated protein in the pathogenesis of autoimmune diseases and immunological disorders

100%
Furukawa H., Tohma S., Kitazawa H., Komori H., Nose M., Ono M.
Archivum Immunologiae et Therapiae Experimentalis
|
2010
|
vol. 58
|
issue 1
37-44
EN
Signaling lymphocytic activation molecule (SLAM)-associated protein (SAP) is an adaptor molecule containing a Src homology 2 (SH2) domain. SAP is expressed in T cells and natural killer (NK) cells and binds to the cytoplasmic domains of SLAM family receptors, resulting in the subsequent recruitment of Fyn. The SAP (SH2D1A) gene is located on the X chromosome and is responsible for X-linked lymphoproliferative disease, characterized by higher susceptibility to Epstein-Barr virus infection. The SAP-mediated signal is not only essential for the development of NKT cells, i.e. unconventional CD1d-restricted T cells with invariant V14 T cell receptors, but also for the regulation of the function of NK cells and conventional T cells. The role of SAP-mediated signaling in the induction of autoimmune diseases has been analyzed using animal models such as lupus, hepatitis, and graft-versus-host disease and is considered important in their pathogenesis in humans. In this review we highlight the current findings on SAP-mediated signaling in hematopoietic cells and discuss its importance in autoimmune diseases and immunological disorders.
2

The soluble CTLA-4 receptor: a new marker in autoimmune diseases

63%
Pawlak E., Kochanowska I. E., Frydecka I., Kielbinski M., Potoczek S., Bilinska M.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
|
vol. 53
|
issue 4
336-341
EN
A soluble form of cytotoxic T lymphocyte-associated antigen-4 (sCTLA-4) was recently found and shown to possess B7 binding activity. sCTLA-4 is generated by alternatively spliced mRNA. The mRNA encoding sCTLA-4 consists of 3 exons: exon 1 encodes a leader peptide, exon 2 the ligand binding domain, and exon 4 the cytoplasmic tail, but it lacks the transmembrane domain encoded by exon 3. The altered transcript is detected in resting CD4 and CD8 T cells and its expression is inhibited after 24?48 h of activation and returns to the prestimulation level after 72?120 h of activation. Low levels of sCTLA-4 have been detected in normal human serum and increased serum levels have been observed in several autoimmune diseases (e.g. Graves' disease, myasthenia gravis, systemic lupus erythematosus, and systemic sclerosis). The biological significance of increased sCTLA-4 serum level has not been clarified. On one hand, sCTLA-4 may bind B7 expressed on antigen-presenting cells and is thus able to interfere with the B7:CD28-mediated costimulation of T cell responses. On the other hand, sCTLA-4 may also be capable of interfering with B7:CTLA-4 interactions, thereby blocking the negative signal imparted via the full-length form of CTLA-4. This double-edged nature of B7 blocking by sCTLA-4 may result in different outcomes of the clinical course of disease.
3

Pregnancy, microchimerism, and autoimmune disease

51%
Nowakowska B.
Postępy Higieny i Medycyny Doświadczalnej
|
2002
|
vol. 56
|
issue 2
123-126
EN
Microchimerism is defined by the presence within an individual of a low level of cells derived from a different individual. The main, natural source of microchimerism is pregnancy. The migration of fetal cells into maternal blood during pregnancy has become an accepted fact. The maternal cells can also be found in the fetal circulation. Recent studies indicate that cells can persist in the maternal circulation for years after pregnancy. Maternal cells can also persist in het progeny. The autoimmune diseases are a diverse group of disorders. Many of them are of unknown etiology. Women are disproportionately affected by autoimmune disease and the incidence of some autoimmune disease in women peak following childbearing years. The integration of observation from differing fields of medicine has led to the consideration that microchimerism may be involved in the pathogenesis of some autoimmune diseases. Early results offer support for a potential role of microchimerism in SSc. The aim of this paper is to present current knowledge about this problem.
4

Emerging concepts in the molecular pathogenesis of systemic lupus erythematosus

51%
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.
5

Treatment of autoimmune disease: time for a paradigm shift?

51%
Mor F.
Archivum Immunologiae et Therapiae Experimentalis
|
2007
|
vol. 55
|
issue 1
13-18
EN
Current treatment of human autoimmune diseases (AIDs) was developed empirically and relies mostly on non-selective suppression of the immune system. Traditional non-selective immunosuppressants such as corticosteroids, cyclophosphamide, and methotrexate and more novel means such as monoclonal antibodies to CD3, CD4, or CD25 do not discriminate between pathogenic and beneficial T cells. Importantly, the severe side effects seen with current therapies are related to the fact that these treatments not only suppress the pathogenic disease-inducing cells, but also cells influential in combating infections and killing malignant cells. Severe infections and malignancies are the inevitable result of non-selective immune suppression. Many of the novel forms of therapy of AID were developed in experimental animals, and their translation to the human disease was associated with the revelation of unexpected and sometimes catastrophic side effects. These surprises underscore the major differences between the relative simplicity of the experimental model and the complexity of the human disease. How can this current state of treatment of AID be improved? Which principles should guide us in the design of new treatments? This review attempts to offer a new look at these questions.
6

Macrophage migration inhibitory factor and its role in autoimmune diseases

51%
Denkinger C. M., Metz C., Fingerle-Rowson G., Denkinger M. D., Forsthuber T.
Archivum Immunologiae et Therapiae Experimentalis
|
2004
|
vol. 52
|
issue 6
389-400
EN
After several decades of research into the macrophage migration inhibitory factor (MIF), its diverse actions in the immune system are yet to be fully revealed. What has become clear is that MIF plays an important role in both innate and adaptive immunity. However, while several pathways mediating the function of MIF in the immune system have been established, its role in pathogenic states such as autoimmune diseases has remained unresolved. MIF has been implicated in different autoimmune diseases, including rheumatoid arthritis, glomerulonephritis, and multiple sclerosis, but knowledge about the underlying cellular and molecular mechanisms is just emerging. However, overall it appears that the inhibition of its proinflammatory action is likely to be a successful new therapeutic strategy for some autoimmune diseases, possibly by reducing the need for steroids. As more aspects of the role of this cytokine in the pathogenesis of autoimmune diseases are elucidated, better strategies to target it therapeutically can be expected.
7

Molecular mimicry of bacterial polysaccharides and their role in etiology of infectious and autoimmunological diseases

51%
Korzeniowska-Kowal A., Witkowska D., Gamian A. S.
|
|
vol. 55
|
issue 2
211-232
EN
Molecular mimicry is one of the most important pathogenic factor of microorganism and is defined as a structural similarity of microbial molecules to host tissue contributing to the pathogenicity. Mimicry can be observed at the molecular, serological and functional level. In the review the infectious diseases have been discussed where the mimicry phenomenon may occurr, and also autoimmune disease where due to the molecular mimicry bacterial structures are potent to induce adverse immune reactions. The cross-reacting molecules mimicking the host structures comprise colominic acid, sialic acid containing capsular polysaccharides of Streptococcus group B, phosphocholine containing antigen, lipopolysaccharides of Campylobacter jejuni contributing in induction of Guillain-Barre syndrome or Lewis antigen containing lipopolysaccharides of Helicobacter pylori inducing gut carcinoma. Knowledge on the phenomenon of molecular mimicry is important when new conjugate vaccine has to be constructed, because great care should be paid not to induce autoantibodies with synthetic immunogen. Investigation of microbial factors reveal that many autoimmune diseases are of infection etiology.
8

Apoptosis-the programmed cell death

51%
Gora-Tybor J., Robak T.
Postępy Higieny i Medycyny Doświadczalnej
|
1994
|
vol. 48
|
issue 3
209-225
EN
Apoptosis is structurally distinct programmed cell death pathway.It takes place during embryogenesis, after withdrawal of the trophic hormones and in the course of normal tissue turnover.Defective regulation of apoptosis may play a very important role in the aetiology of cancer and other diseases.In this paper these and other problems concerning with apoptosis are reviewed.
9

Alterations in the expression of signal-transducing CD3? chain in T cells from patients with chronic inflammatory/autoimmune diseases

51%
Ciszak L., Pawlak E., Kosmaczewska A., Potoczek S., Frydecka I.
|
|
issue 6
373-386
EN
The CD3 zeta chain, a component of the T cell receptor (TCR)/CD3 complex, is considered to be a limiting factor in the assembly and transport of the TCR/CD3 complex to the cell surface and is crucial to receptor signaling function. Recent studies have demonstrated altered expression and function of this signal transduction molecule in T and natural killer cells in patients with chronic inflammatory/autoimmune diseases. In this review, current knowledge concerning the expression of CD3 zeta chain as well as the mechanisms responsible for abnormal expression of this molecule in systemic lupus erythematosus, rheumatoid arthritis, and childhood idiopathic nephrotic syndrome are summarized.
10

Biology of interleukin-6 (IL-6) and its significance in the pathogenesis of some diseases

51%
Robak T.
Postępy Higieny i Medycyny Doświadczalnej
|
1994
|
vol. 48
|
issue 5
565-588
EN
In the paper numerous activities of IL-6 toward various normal and neoplastic cells are reviewed.The role of this cytokine in pathophysiology of various disease including infections and inflammatory and autoimmune diseases as well as in leukaemias, lymphomas and other neoplastic diseases is presented.Potential clinical value of the IL-6 levels in the serum and the role of its recombinant form in the treatment of thrombocytopenia and some neoplastic diseases is also discussed.
11

Type I interferons as immunoregulatory molecules; implications for therapy in experimental autoimmune uveoretinitis

51%
Mizuguchi J., Takeuchi M., Usui M.
Archivum Immunologiae et Therapiae Experimentalis
|
2002
|
vol. 50
|
issue 4
243-254
EN
Clinical trials have shown that the type I interferon (IFN)-alpha/beta have some beneficial effects on organ-specific autoimmune disease, such as Behcet's diseases and multiple sclerosis, although the precise mechanims remain lergaly unresolved T helper cells (Th1)-mediated autoimmune response are involved in the initiation and/or progression of human uveitis, such as Behcet's disease. The animal model of experimental autoimmune uveoretinitis (EAU), characterized by a monophasic clinical course, has contributed to the understanding of the pathogenesis of human uveitis. Th1 producing IFN-gamma induce EAU development, while Th2 producing IL-4/IL-10 prevent the disease. However, depending on the cytokine milieu, the pro-inflammatory cytokine IFN-gamma may attenuate the autoimmune response and anti-inflammatory cytokine IL-4 exacerbates it. Chemokines also play a crucial role in EAU development, which might be resolved by Th2-mediated immune responses. The administration of IFN-alpha/beta prevents EAU development, accompanied by a dimished production of IFN-gamma/IL-10. Interestingly, however, IFN-alpha/beta also have some beneficial effects on patients with Th2-like phenotype in addition to Th1-like phenotypes. Thus, the immuno-modulatory action of IFN-alpha/beta may be dependent on the context of cytokine combination and/or their concentrations.
12

New target against inflammatory diseases: transglutaminase 2

51%
Kim S.-Y.
Archivum Immunologiae et Therapiae Experimentalis
|
2004
|
vol. 52
|
issue 5
332-337
EN
Transglutaminase (TGase) 2 is an enzyme that is widely used in many biological systems for generic tissue stabilization or immediate defense for wounds. Many reports showed that TGase 2 is aberrantly activated in tissues and cells and contributes to a variety of diseases, including neurodegenerative diseases and autoimmune diseases. In most cases, TGase 2 appears to be a factor in the formation of inappropriate proteinaceous aggregates that may be cytotoxic. However, in other cases, such as celiac disease, arthritis, lupus, and amyotrophic lateral sclerosis, TGase 2 is involved in the generation of autoantibodies. This suggests the possibility that inappropriate expression and/or presentation of TGase 2 to T cells might contribute to these diseases in genetically predisposed individuals. We and others have found that TGase 2 expression is also increased in the inflammation process. Furthermore, we also demonstrated a reversal of inflammation by TGase inhibition. This review will examine a possibility of TGase inhibitors as therapeutic agents in a variety of inflammatory diseases.
13

Immunotherapeutic approaches in ocular inflammatory diseases

51%
Kurup S. K., Chan C.-C.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
|
vol. 53
|
issue 6
484-496
EN
This comprehensive review discusses immunotherapeutic approaches to ocular inflammatory diseases, updates information provided in the literature, and presents clinical experiences with an emphasis on autoimmune uveitis at the National Eye Institute, United States. Current medical and surgical therapeutic approaches, including medications such as corticosteroids, anti-metabolites, alkylating agents, calcineurin and purine synthesis inhibitors, biologics as well as some anti-infectious agents, are reviewed along with new modalities and experimental approaches. Most immunosuppressive therapies have significant adverse effects. Physicians must be familiar with the pharmacology of the available drugs and aware of the philosophies behind the treatment.
14

Review extrathymic pathways of T cell differentiation

45%
Abo T.
Archivum Immunologiae et Therapiae Experimentalis
|
2001
|
vol. 49
|
issue 2
81-90
EN
It is known that the liver is a major hematopoietic organ at fetal stages, but the hematopoiesis of this organ ceases of birth. However, the liver is still found to comprise c-kit+ stem cells and gives rise to extrathymic T cells, NK cells, and even granulocytes after birth. Extrathymic T cells generated in the liver of mice are identified as intermediate TCR (TCRint) cells, which include the NK1.1+TCRint (i.e. NKT cells) and NK1.1-TCRint subsets. Although extrathymic T cells are few in number during youth, they increase in number with advancing age. The number and function of extrathymic T cells are also elevated under conditions of stress, infections, malignancy, pregnancy, autoimmune disease, chronic GVH diseases, etc. Under these conditions, the mainstream of T cell differentiation in the thymus, which produces conventional T cells, is inversely suppressed. Extrathymic T cells comprise self-reactive forbidden clones and mediate cytotoxicity against abnormal self-cells. Therefore, they might be beneficial for the elimination of such cells. However, over-activation of extrathymic T cells might be responsible for the onset of certain autoimmune disease.
15

Transcriptional regulation in thymic epithelial cells for the establishment of self tolerance

45%
Matsumoto M.
Archivum Immunologiae et Therapiae Experimentalis
|
2007
|
vol. 55
|
issue 1
27-34
EN
Thymic epithelial cells (TECs) play pivotal roles in the establishment of self tolerance through critical dialogue with developing thymocytes. Unique actions of two transcriptional regulators within TECs, NF-kB-inducing kinase (NIK) and an autoimmune regulator (AIRE), for the establishment of self tolerance have recently been highlighted by studies using a strain of mouse bearing a natural mutation of the NIK gene (aly mice) and gene-targeted mice, respectively. Previous studies have demonstrated essential roles of NIK downstream of the lymphotoxin-beta receptor (LTbetaR), which is essential for the development of secondary lymphoid organs; aly mice lack all lymph nodes and Peyer's patches because of the defective LTbetaR signaling. Additional roles of NIK in thymic organogenesis downstream of LTbetaR, mainly through the developmental regulation of TECs, have now emerged, although the corresponding ligand(s) for LTbetaR participating in this action have not been fully characterized. In contrast, AIRE, a gene responsible for the development of an organ-specific autoimmune disease that demonstrates monogenic autosomal recessive inheritance, contributes to the establishment of self tolerance probably by controlling the expression of self antigens through yet undetermined molecular mechanisms. Thus it is highly likely that a group of genes control self-tolerance within TECs through unique and coordinated actions, and that an understanding of this process would help to unravel the pathogenesis of autoimmune disease.
16

Review the paradigms of causality and treatment for autoimmune disease

45%
Cohen I. R.
Archivum Immunologiae et Therapiae Experimentalis
|
2000
|
vol. 48
|
issue 5
325-330
EN
A key concept in medicine is that rational therapy rests on accurate diagnosis; quite simply, therapy that is not tuned to the cause of the disease will not cure the patient. I do not mean to say that effective treatments cannot emerge from faulty diagnoses. In truth, much of our therapeutic ensemble is composed of drugs developed as a result of chance observation, random, screening, intuition, or pre-scientific tradition. Nevertheless, the way to effective therapy is best paved by understanding. Effects are inherent in their causes; so if we want to cure autoimmune diseases using the scientific method, we are obliged to inquire into their causes. By reducing the discordant complexity of the disease to the single cause that underlies it, we can hope to learn the most efficient way to manipulate the disease process. How do we identify a cause when we see one? Quite simply, a single cause is that which is both necessary and sufficient to produce the effect. Here, I explore the general paradigm of autoimmune causality, using multiple sclerosis as a specific example.
17

Peptide-based approaches to treat asthma, arthritis, other autoimmune diseases and pathologies of the central nervous system

45%
Hauff K., Zamzow C., Law W. J., De_Melo J., Kennedy K., Los M.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
|
vol. 53
|
issue 4
308-320
EN
In this review we focus on peptide- and peptidomimetic-based approaches that target autoimmune diseases and some pathologies of the central nervous system. Special attention is given to asthma, allergic rhinitis, osteoarthritis, and Alzheimer's disease, but other related pathologies are also reviewed, although to a lesser degree. Among others, drugs like Diacerhein and its active form Rhein, Pralnacasan, Anakinra (Kineret), Omalizumab, an anti-beta chain antibody 'BION-1', are described below as well as attempts to target beta-amyloid peptide aggregation. Parts of the review are also dedicated to targeting of pathologic conditions in the brain and in other tissues with peptides as well as methods to deliver larger molecules through the 'blood-brain barrier' by exploring receptor-mediated transport, or elsewhere in the body by using peptides as carriers through cellular membranes. In addition to highlighting current developments in the field, we also propose, for future drug targets, the components of the inflammasome protein complex, which is believed to initiate the activation of caspase-1 dependent signaling events, as well as other pathways that signal inflammation. Thus we discuss the possibility of targeting inflammasome components for negative or positive modulation of an inflammatory response.
18

Regulatory T cells: magic bullets for immunotherapy?

38%
Frey O., Brauer R.
Archivum Immunologiae et Therapiae Experimentalis
|
2006
|
vol. 54
|
issue 1
33-43
EN
In the past few years it has been become increasingly clear that T cells capable of actively suppressing immune responses are thought to be in part responsible for the maintenance of peripheral self tolerance. In healthy rodents and humans, CD4+ T cells constitutively expressing the interleukin (IL)-2 receptor -chain (CD25) are able to exert such suppressive function in vitro and in vivo. Despite great efforts in our understanding of the biology of such immunoregulatory T cells, there are still certain points incompletely understood. Although some authors suggest that immunoregulatory cytokines such as IL-10 or transforming growth factor b are critical for the suppressive effect of these cells, this is controversial and the exact molecular nature and the targets of suppression are largely unknown. Thus far, until regulatory T cells can be used for diagnostic or therapeutic purposes many questions have to be answered. In this review we summarize the current knowledge on the function and properties of this T cell subset and discuss their potential role in human autoimmune or chronic inflammatory diseases.
19

Treating autoimmune diseases through restoration of antigen-specific immune tolerance

38%
Wolfraim L. A.
Archivum Immunologiae et Therapiae Experimentalis
|
2006
|
vol. 54
|
issue 1
1-13
EN
The first line of treatment for many human autoimmune diseases involves the use of anti-inflammatory or immunosuppressive drugs such as prednisone or other steroids that not only suppress the underlying autoimmune disease, but lead to global suppression of the immune system. The sequelae of this approach include increased risk of infection, carcinogenesis, and osteoporosis. Moreover, such broad spectrum immunosuppression tends to have transient therapeutic benefit, as in many cases the disease becomes refractory to these drugs. There is a clear need for more specific means to restore immune tolerance to the specific autoantigens implicated in disease pathology. This review provides an overview of some of these newer, more specific therapeutic approaches to restoring immune tolerance to autoantigens, with an emphasis on those approaches that have been or will soon be tested in controlled clinical trials. Covered here are peptide- or protein-based therapeutics, oral tolerance, and cellular and gene therapy approaches to restoring antigen-specific immune tolerance.
first rewind previous Page / 1 next fast forward last
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.