فهرست مطالب
Iranian journal of immunology
Volume:2 Issue: 2, Spring 2005
- 60 صفحه،
- تاریخ انتشار: 1384/06/30
- تعداد عناوین: 8
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Pages 67-77Interferons (IFNs) are a family of small regulatory glycoproteins that play a central role in the defense against viral infections. Although IFNs have been initially discovered as antiviral factors، today they are known as an integral part of the cytokine network that affect a wide range of biological processes. IFNs exert their pleiotropic effects through their multisubunit cell surface receptors in a species specific manner that is believed to be controlled at the receptor and the post-receptor levels. Although IFN-mediated signaling and transcription activation of cellular gene expression is currently best understood in the context of the JAK-STAT signal transduction، additional IFNs signaling pathways may also act in certain conditions. The Janus family of tyrosine kinase (JAK) enzymes and two families of transcriptional regulators، signal transducer and activator of transcription (STATS) and IFN regulatory factors (IRFs)، are the principal components of the JAK-STAT pathway. Overlapping subsets of JAKS are involved in signaling by type I (IFN- /ß) and type II (IFN- IFNs، indicating that the receptor subunits confer specificity for activating particular JAK family members. A considerable cross talk can exist between separate signaling pathways. The emergence of new tools and approaches for study of IFNs signaling has been an exercise in coming to respect the level of complexity of IFNs system. For many years، IFNs have been satisfactorily used in many clinical trials. However، their serious side effects remain as the major concern in clinical use of IFNs. A better understanding of the exact mechanism involved in IFNs signaling pathways and the structure-function relationships of the IFNs system components will allow researchers to improve and expand the therapeutic potential of these naturally occurring molecules. IFNs actions are mediated through multiple signaling pathways. However، due to the space limitation، this review will focus primarily on the IFNs-mediated JAK-STAT pathway.
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Pages 78-86BackgroundPrevious studies have shown that Galectin-3، a member of lectin family، is expressed in developing cartilage in mouse embryo and also in growth plate of long bones.ObjectiveIn the present work، the expression pattern of Galectin-3 in normal and various grades of osteoarthritic (OA) human articular cartilage has been studied.MethodsUsing immunohistochemistry and standard western blotting، the in vivo and in vitro expression pattern of Galectin-3 in normal and OA human articular cartilage were assessed.ResultsImmunohistochemical studies showed a similar pattern of Galectin-3 expression in normal and mild OA but severe OA showed different strong expression in all zones of human articular cartilage.ConclusionIncreased expression pattern of Galectin-3 in advanced stages of OA may occur as a result of the imbalance of chondrocyte homeostasis that occurs in OA cartilage and provides a condition to modify normal chondrocyte to an OA chondroctye.
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Pages 87-90
Methods ResultsThe results of this investigation showed that the level of immunoglobulin IgG، IgM، IgA and IgE decreased post transplantation due to immunosuppressive drugs. CD3، CD4، CD8 T cells count، CD56 NK cells count and CD20 B cells count pre- and post-transplantation did not show any significant differences. The amount of IgE (220 vs. 462 IU/ml)، CD3 (62% vs. 69. 7%) and CD4 (35% vs. 41. 3%) cells increased in group II during rejection episode pre-transplantation. In addition، IgA increased pretransplantation in group I those without rejection episode in comparison with group II with a rejection episode. Forty five days post transplantation IgA (209 vs. 152 mg/dl)، IgG (1009 vs. 703 mg/dl) and CD20 (15% vs. 10%) increased in group I patients.ConclusionIt is suggestive that pre-transplantation increases IgE، CD3 and CD4 are predictive of acute rejection.
Vitiligo is an acquired skin disorder that selectively destroys melanocytes in epidermis with an unknown etiology.
To investigate the exon 1 A49G polymorphism of cytotoxic T lymphocyte antigen-4 (ctla-4) gene in vitiligo patients.
The A49G polymorphism was detected by Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) method in 101 patients and 208 normal healthy age/ethnicity matched individuals.
The frequencies of heterozygote genotypes in patients and controls were found to be 42 (41. 6%) of 101 and 85 (40. 9%) of 208، respectively. The frequencies of homozygote A and G genotypes were 49 (48. 5%) and 10 (9. 9%) in 101 patients، whereas، these frequencies in 208 control individuals were 103 (49. 5%) and 20 (9. 6%)، respectively. There was no significant difference between the genotype (P = 0. 98) and allele (P = 0. 86) frequencies of A49G polymorphism in patients and normal healthy individuals.
Our results indicate that in contrast to several immune mediated disorders، there is no association between ctla-4 A49G gene polymorphism and vitiligo.
Asthma is a chronic inflammatory disease with multifactorial and complicatedmechanisms. Elevated level of exhaled Nitric Oxide (NO) in asthma and other inflammatory lung diseases has led to many studies examining NO as a potential marker of airway inflammation.
This study was designed to determine the level of NO in Bronchoalveolar Lavage (BAL) fluid during early and late stages of asthmatic attack in mouse model.
In this study male BALB/c mice were used. The level of NO was determined in BAL fluid of asthmatic mice five minutes، six and sixteen hours after challenge with methacholine، as irritant and smoke and 5% ovalbumin as allergens، using colorimetric assay.
The level of NO increased upon exposure to all three irritants used in this study (52. 3 M for smoke and 49. 5 Mfor methacholine) as compared to 22. 8 M for the baseline. Our results showed that NO levels were increased during early phase of asthmatic condition and reached to its maximum level after six hours and decreased at the late stage of asthma (16hrs) possibly by activating a feedback regulatory loop. In addition، high level of NO led to the hypertrophy of smooth muscle that can account for the pathological changes associated with asthma.
Thus، NO is an inflammatory marker in asthma and its measurement، as a non-invasive method during asthmatic attack is suggested. A careful development of specific inhibitors for iNOS enzyme during asthmatic attack is also necessary.