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1

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
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2000
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vol. 48
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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.
2

Lack of association between Exon 1 CTLA-4 gene polymorphism A(49)G and multiple sclerosis in Polish population of the Lower Silesia Region

100%
Bocko D., Bilinska M., Dobosz T., Zoledziewska M., Suwalska K., Tutak A., Gruszka E., Frydecka I.
Archivum Immunologiae et Therapiae Experimentalis
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2003
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vol. 51
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issue 3
201-205
EN
Multiple sclerosis (MS) a chronic inflammatory demyelinating disease of the central nervous system (CNS) is believed to have a T-cell mediated autoimmune etiology. The cytotoxic T lymphocyte antigen 4 (CTLA-4) gene is a strong candidate for the involvement in autoimmune diseases because CTLA-4 plays an important role in downregulation of early and late stages of T cell activation and maintenance of peripheral T cell tolerance. To examine the genetic association of the CTLA-4 gene locus with MS, we analyzed exon 1 CTLA-4 gen polymorphism A(49)G in 102 unrelated Polish MS patients in Lower Silesia region and 101 age and sex matched healthy subjects. The distribution of CTLA-4 exon 1 A(49)G genotype, phenotype and allele frequencies did not differ between patients with MS and healthy subjects.
3

Macrophage migration inhibitory factor and its role in autoimmune diseases

100%
Denkinger C. M., Metz C., Fingerle-Rowson G., Denkinger M. D., Forsthuber T.
Archivum Immunologiae et Therapiae Experimentalis
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2004
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vol. 52
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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.
4

Genetics of experimental autoimmune encephalomyelitis in the mouse

100%
Andersson A., Karlsson J.
Archivum Immunologiae et Therapiae Experimentalis
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2004
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vol. 52
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issue 5
316-325
EN
Multiple sclerosis (MS) is an inflammatory, demyelinating disease in the central nervous system (CNS) affecting approximately 0.1% of the population in the northern part of the world. The factors behind the initiation of the inflammatory response are not known at present, but MS is considered as a complex disease depending on genetic as well as environmental factors. Experimental autoimmune encephalomyelitis (EAE) is the prevailing experimental rodent model for multiple sclerosis (MS). Disease is induced in genetically susceptible mice or rats by immunization with myelin proteins or peptides, which leads to an infiltration of leukocytes into the CNS. EAE has been subjected to investigations of genetic susceptibility to disease development. By the identification of genes predisposing to EAE, the hope is to get clues as to what genetic elements are also important in MS. To date, more than 25 Eae loci have been described in the mouse. The quantitative trait loci are linked to different disease traits and several show sex specificity. Here we discuss the current state of the genetics controlling susceptibility to EAE.
5

Review the paradigms of causality and treatment for autoimmune disease

88%
Cohen I. R.
Archivum Immunologiae et Therapiae Experimentalis
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2000
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vol. 48
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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.
6
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The value of magnetic resonance imaging in diagnosis and monitoring of treatment in multiple sclerosis

75%
Bekiesinska-Figatowska M., Walecki J., Stelmasiak Z.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 1
171-176
EN
We analysed MR examinations of 227 patients with multiple sclerosis. White matter hyperintensities in brain were found in 270 of them. The most frequently they were found in periventricular white matter (in 100% of cases), in subcortical localization (52.2%) and in the corpus collosum (44.4%). MR examination allows to estimate the activity of the disease on the basis of the presence of oedema around the plaques and their contrast enhancement with gadopentetate dimeglumine (Gd-DTPA). 17.8% of all cases showed the signs of the acute phase of MS. About one-third of all cases were accompanied by cortical brain atrophy (the most often seen in frontal lobes), subcortical brain atrophy was less frequent (one-sixth). In about two-third of all casese the corpus callosum atrophy was found. The analysis of follow-up MR examinations of 83 patients taking part in a double-blind placebo-controlled trial of new immunosupressive drug cladribine showed that patients from pacebo group were more compliant to any changes of plaques. Decrease of the plaques size was found mainly in women. No correlation between patients age and the plaques changes was established.
7

T cell chemokine receptor expression in human Th1- and Th2-associated diseases

75%
Campbell J. D., Hayglass K. T.
Archivum Immunologiae et Therapiae Experimentalis
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2000
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vol. 48
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issue 5
451-456
EN
The interaction between chemokines and their receptors is an important step in the control of leukocyte migration into sites of inflammation. Chemokines also mediate a variety of effects independent of chemotaxis, including induction and enhancement of Th1- and Th2---associated cytokine responses. Recent studies have shown that human Th1 and Th2 clones, activated under polarizing conditions with polyclonal stimuli in vitro, display distinct patterns of chemokine receptor expression: Th1 clones preferentially express CCR5 and CXCR3 while many Th2 clones express CCR4, CCR8 and, to a lesser extent, CCR3. These differential patterns of chemokine receptor expression suggest a mechanism for selective induction of migration and activation of Th1- and Th2-type cells during inflammation and, perhaps, normal immune homoeostasis. Studies have begun to examine T cell chemokine receptor expression in vivo to determine the relevance of these in vitro observations to human Th1 and Th2-associated diseases. In this review, we critically examine recent reports of T cell chemokine receptor expression in human autoimmune disorders (multiple sclerosis and rheumatoid arthritis) and atopic disorders (allergic rhinitis and asthma) which are believed to arise from inappropriate Th1- and Th2-dominated responses, respectively.
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