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1

Central nervous system and peripheral expression of CCL19, CCL21 and their receptor CCR7 in experimental model of multiple sclerosis

100%
Bielecki B., Jatczak-Pawlik I., Wolinski P., Bednarek A., Glabinski A.
Archivum Immunologiae et Therapiae Experimentalis
|
2015
|
tom 63
|
nr 5
2
Content available remote

Effect of natalizumab treatment on metalloproteinases and their inhibitors in a mouse model of multiple sclerosis

84%
Pyka-Fosciak G., Lis G. J., Litwin J. A.
Journal of Physiology and Pharmacology
|
2020
|
tom 71
|
nr 2
3

Effects of IFN-beta1a and IFN-beta1b treatment on the expression of cytokines, inducible NOS (NOS type II), and myelin proteins in animal model of multiple sclerosis

84%
Lubina-Dabrowska N., Stepien A., Sulkowski G., Dabrowska-Bouta B., Langfort J., Chalimoniuk M.
Archivum Immunologiae et Therapiae Experimentalis
|
2017
|
tom 65
|
nr 4
4

Epitope spreading: a mechanism for progression of autoimmune disease

84%
Tuohy V. K., Kinkel R. P.
Archivum Immunologiae et Therapiae Experimentalis
|
2000
|
tom 48
|
nr 5
5

The role of cytokines in experimental autoimmune encephalomyelitis

84%
Bettelli E., Nicholson L. B.
Archivum Immunologiae et Therapiae Experimentalis
|
2000
|
tom 48
|
nr 5
6

Association of CD45dimVLA-4plus cells with the NKT cell lineage and their selective expression of IL-13, IP-15, and CCR3 transcripts

84%
Matejuk A., Afentoulis M.
Archivum Immunologiae et Therapiae Experimentalis
|
2006
|
tom 54
|
nr 3
7

Genetics of experimental autoimmune encephalomyelitis in the mouse

84%
Andersson A., Karlsson J.
Archivum Immunologiae et Therapiae Experimentalis
|
2004
|
tom 52
|
nr 5
8
Content available remote

Mechanisms of immunological tolerance to the antigens of the central nervous system. Skin-induced tolerance as a new therapeutic concept

67%
Szczepanik M.
Journal of Physiology and Pharmacology
|
2011
|
tom 62
|
nr 2
The immune system is designed to recognize and eliminate foreign (non-self) antigens. At the same time, there are mechanisms protecting the organism from development of inappropriate immune responses that are harmful to ones own body (allergy, autoimmunity) and those that help to silence the inflammatory responses and allow their resolution. Tolerance to self-antigens is a result of central tolerance (negative selection) and various mechanisms of peripheral tolerance that include anatomical sequestration of self-antigens, deletion of peripheral autoreactive lymphocytes, the development of lymphocyte functional unresponsiveness and action of T regulatory (Treg) cells. This article summarizes current knowledge about mechanisms of immunological tolerance that protect from development of immune responses to self-antigens present in the central nervous system (CNS). Finally, it discusses the subject of skin-induced tolerance as demonstrated in an animal model of autoimmune disease of the CNS, experimental autoimmune encephalomyelitis (EAE). The potential clinical use of this approach to regulate disease will be discussed.
9

Gamma delta T cell positively regulate contact sensitivity (CS) reaction via modulation of INF-gamma, IL-12 and TNF-alpha production

67%
Strzępa A., Majewska-Szczepanik M., Szczepanik M.
Folia Biologica
|
2013
|
tom 61
|
nr 3-4
10

Autoimmune versus oligodendrogliopathy: the pathogenesis of multiple sclerosis

67%
Nakahara J., Aiso S., Suzuki N.
Archivum Immunologiae et Therapiae Experimentalis
|
2010
|
tom 58
|
nr 5
325-333
11

Immunohistochemical analysis of spinal cord components in mouse model of experimental autoimmune encephalomyelitis

67%
Pyka-Fosciak G., Stasiolek M., Litwin J. A.
Folia Histochemica et Cytobiologica
|
2018
|
tom 56
|
nr 3
12

Glutamate receptors antagonists attenuate neurological deficits and modulate neuroinflammation in Lewis rat subjected to experimental autoimmune encephalomyelitis

67%
Sulkowski G., Dabrowska-Bouta B., Chalimoniuk M., Lenkiewicz A., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Experimental autoimmune encephalomyelitis (EAE) is an animal model that mimics many aspects of multiple sclerosis (MS). Chronic or relapsing inflammation of the central nervous system results in the destruction of myelin sheath and cytokines play an important role in the pathogenesis of both MS and EAE. Myelin, oligodendrocytes and neurons are lost due to an inflammatory attack by leukocytes infiltrating the central nervous system (CNS) and releasing cytotoxic cytokines, anti CNS antibodies and large amounts of the excitatory neurotransmitter glutamate. Pharmacological studies have suggested that glutamate receptors mediate white matter injury in a variety of CNS diseases, including multiple sclerosis (MS). Memantine and amantadine are ionotropic glutamate receptors (iGluRs) antagonists. Memantine, a clinically applied drug with N-methyl-D-aspartate (NMDA) receptor antagonistic effects, dose-dependently ameliorates neurological deficits in Lewis rats subjected to experimental autoimmune encephalomyelitis (EAE). The aim of the present study was to investigate the effects of memantine and amantadine on the expression of proinflammatory cytokines such interleukin 1beta (IL-1β), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α) and various chemokines in the brain of EAE rats. Real-time Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western Blot were used to analyze the cytokine profile. We noticed increased expression of array of cytokines in experimental group when compared to the control. Dramatic increase of IL-1β, IL-6, TNF-α, and chemokines concentration corresponding to the intensity of neurological symptoms and loss of weight was observed in EAE rats. Administration of iGluR antagonists at an advanced stage of unremitting EAE resulted in amelioration of the disease. Cytokine analysis revealed that memantine significantly decreased the expression of interleukins: IL-6 (65%), IL-1β (60%) and TNF-α (45%) whereas treatment with amantadine reduced only the expression of IL-6 (60%) and TNF-α (15%) when compared to EAE animals. These results show that antagonists of iGlu receptors modulate the course of the disease by reducing the expression of proinflammatory cytokines thereby confirming the involvement of glutamate receptors into pathological mechanisms operating during EAE. This study was supported by grant nr NN401620038 from Polish Ministry of Science and Higher Education
13

Cerebral microvessels in rat subjected to EAE: Focus on pericytes and purinergic receptor P2X7

67%
Grygorowicz T., Lenkiewicz A., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Blood-brain barrier (BBB) is a structure that maintains central nervous system (CNS) homeostasis by isolating it from the normal blood flow. In physiological conditions BBB prevents CNS penetration by blood-derived molecules and is a barrier for the immune system. BBB is built by tight junctions between endothelial cells of microvessels, pericytes, and astroglial end-feets. Pericytes are very important part of BBB showing a great impact on properties of endothelial cells and BBB tightness. In pathological conditions (i.e. inflammation) the structure of BBB is loosened and cells of the immune system have a free access to the brain and the spinal cord. That is the main mechanism of pathogenesis in both multiple sclerosis (MS) and the rodent model of the disease – experimental autoimmune encephalomyelitis (EAE). Overactivation of purinergic receptor P2X7, is a possible mechanism leading to neurodegeneration observed during the course of MS/EAE. This receptor has two distinct functions: it participates in maturation and release of proinflammatory cytokines or can polymerase to create transmembrane pores which can drive cell to death by apoptosis or necrosis. Thus, we hypothesized that overactivation of this receptor on pericytes may lead to cell damage and/or loss of the protective function towards BBB. In this study we first analyzed status of BBB which was determined by expression of claudin 5 – a marker of BBB tightness – in correlation with the expression of P2X7R in microvessels’ fractions and brain sections of rats subjected to EAE. Using immunoblots and confocal microscopic method we found negative correlation between P2X7R and claudin 5 expression which decreased significantly in all examined time points of the disease, reaching the minimum level (45% and 70% of control) at days 2 p.i. and 4 p.i., respectively. Additionally, we present the results of pericytes features and P2X7R expression in microvessels in early time after EAE induction. Condition of pericytes was visualized by immunofluorescent staining against PDGFRβ (a marker protein). Semiquantitative level of this protein was measured using Western blot analysis of brain homogenates and isolated microvessels fraction. The pattern of observed changes suggests contribution of pericyte-located P2X7R on BBB state and the involvement of this receptor into pathological mechanisms connected with development of EAE.
14

Brain-derived neurotrophic factor in neuroimmunology: lessons learned from multiple sclerosis patients and experimental autoimmune encephalomyelitis models

67%
Luhder F., Gold R., Flugel A., Linker R. A.
Archivum Immunologiae et Therapiae Experimentalis
|
2013
|
tom 61
|
nr 2
15

Lactococcus lactis as a myelin antigen delivery system in experimental allergic encephalomyelitis treatment

67%
Kasarello K., Szczepankowska A. K., Kowalska Z., Kwiatkowska-Patzer B., Bardowski J. K., Lipkowski A. W.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Experimental Allergic Encephalomyelitis (EAE) is the animal model of Multiple Sclerosis (MS), human chronic and progressive autoimmunological disease that lead to neurodegeneration in Central Nervous System (CNS). Although there are some hypothesis, like genetic, environmental or viral factors involvement, cause and patophysiology of MS remains still unknown, and that is the reason why there is no sufficient MS treatment so far. Most common MS therapy is use of immunosupressive drugs, but that is not very effective and costs number of health complications. Also new targeted therapies are burdened with the risk of side effects, which may be even lethal. Therefore, the efficient alternative treatment is urgently needed. The autoimmune base of the disease directed treatment searching into immunological mechanisms. Few years ago we proposed application of animal spinal cord hydrolysate for inducing oral tolerance, which effect lies in reducing of immunoresponse for previously fed antigen. We presented the effectiveness of this type of treatment in EAE rat model. The success of oral tolerance with mixture of peptides stimulates us to development bacteria that may express active peptide related to myelin fragment. As far as it is known, that the dose of fed antigen is crucial in evoking oral tolerance, the aim of our study, was to investigate which dose or doses of Lactococcus lactis expressing myelin peptides is sufficient for EAE treatment. We used autolising strain of Lactococcus lactis, producing one of three myelin peptides, which are considered to be crucial in MS developement: Myelin Basic Protein (MBP aa85-97), Proteolipid Protein (PLP aa139- 151) or Myelin Oligodendrocyte Protein (MOG aa35-55). We mixed all three peptide variants, and made whole-cell extracts. For our experiments we used female Lewis rats (180–200 g), which were fed with ball-pointed needle with mixed bacteria extracts for 20 days. Doses of preparations ranged from 101 to 108 cells/rat/feeding suspended in 0.5 ml PBS. At the 10th day of feeding, EAE was evoked by hind paw injection of guinea pig spinal cord homogenate in Freund Adjuvant with Mycobacterium tuberculosis. During the whole experiment animals were weighted, and clinical symptomes were observed. The obtained results demonstrated, that the sufficient doses of Lactococcus lactis expressing myelin peptides, given orally to animals are 103 and 106 cells/rat/feeding. Further experiments including cytokine level measurement and microscopic observation of rats spinal cord are in progress.
16

17beta-estradiol treatment profoundly down-regulates gene expression in spinal cord tissue in mice protected from experimental autoimmune encephalomyelitis

67%
Matejuk A., Dwyer J., Hopke C., Vandenbark A. A., Offner H.
Archivum Immunologiae et Therapiae Experimentalis
|
2003
|
tom 51
|
nr 3
17

Post intoxicative therapeutic immunization with myelin oligodendrocyte glycoproteine [MOG 35-55] suppresses spontaneous regeneration of dopaminergic neurons injured with 1-methyl-4 phenyl-1,2,3,6-tetrahydropiridine [MPTP]

67%
Balkowiec-Iskra E., Kurkowska-Jastrzebska I., Joniec I., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2003
|
tom 63
|
nr 2
18

Myelin restoration: progress and prospects for human cell replacement therapies

59%
Potter G. B., Rowitch D. H., Petryniak M. A.
Archivum Immunologiae et Therapiae Experimentalis
|
2011
|
tom 59
|
nr 3
19

CD46 plasticity and its inflammatory bias in multiple sclerosis

59%
Ni Choileain S., Astier A. L.
Archivum Immunologiae et Therapiae Experimentalis
|
2011
|
tom 59
|
nr 1
20

Evidence that Fas and FasL contribute to the pathogenesis of experimental autoimmune encephalomyelitis

51%
Dittel B. N.
Archivum Immunologiae et Therapiae Experimentalis
|
2000
|
tom 48
|
nr 5
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