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[Analysis of polymorphism of the interleukin-4 gene of healthy and HIV-infected persons]

https://arctichealth.org/en/permalink/ahliterature7401
Source
Zh Mikrobiol Epidemiol Immunobiol. 2001 Nov-Dec;(6):28-32
Publication Type
Article
Author
V I Konenkov
M V Smol'nikova
V A Kozlov
S V Sennikov
L P Siziakina
E. Taleb
Author Affiliation
Institute of Clinical Immunology, Siberian Branch, Russian Academy of Medical Sciences, Novosibirsk, Russia.
Source
Zh Mikrobiol Epidemiol Immunobiol. 2001 Nov-Dec;(6):28-32
Language
Russian
Publication Type
Article
Keywords
Adolescent
Adult
Alleles
Cells, Cultured
Comparative Study
Concanavalin A - pharmacology
English Abstract
European Continental Ancestry Group
HIV Infections - genetics - immunology
Homozygote
Humans
Interleukin-4 - biosynthesis - genetics
Leukocytes, Mononuclear - drug effects - immunology
Male
Middle Aged
Polymorphism, Genetic
Promoter Regions (Genetics) - genetics
Sex Factors
Statistics, nonparametric
Abstract
The distribution of the allel variants of the promoter area (C = 590T) of the interleukin-4 (IL-4) gene in HIV-infected and relatively healthy representatives of the Caucasoid population has been studied. The relationship between the genotypes of this polymorphism and the production of IL-4 by mononuclear cells of peripheral blood as well as distribution of IL-4 genotypes among males and females is analyzed. The occurrence of the homozygous combination of the allel variant C/C of the promoter of IL-4 has been shown to prevail almost twofold over the occurrence of the variant C/T among healthy donors and HIV-infected patients. Sexual differences play an essential role in the character of inheriting the allel variants of the genes of IL-4, the presence of the homozygous variant C/C or T/T being a risk factor of HIV infection in males. As revealed in this study, in the peripheral blood of healthy donors mononuclear cells having genotype C/C differ from cells with the heterozygous variant C/T in higher spontaneous production of IL-4 and, simultaneously, in lower capacity for the activation of its production in response to stimulation with mitogen. In HIV-infected patients mononuclear cells differ in higher spontaneous production of IL-4 in comparison with controls. We may thus infer that the human genotype controlling the initial level of the production of IL-4 by lymphocytes Th2 may influence the intensity of antibody production in the process of infection.
PubMed ID
11881490 View in PubMed
Less detail

Conjugates of ovalbumin and monomethoxypolyethylene glycol abolish late allergic responses and decrease IL-4 and IL-5 mRNA expression in the rat.

https://arctichealth.org/en/permalink/ahliterature9604
Source
Pulm Pharmacol Ther. 2003;16(6):361-9
Publication Type
Article
Date
2003
Author
J-P Lavoie
K. Maghni
R. Taha
X-X Yang
G M Lang
A H Sehon
Q A Hamid
J G Martin
Author Affiliation
Department de Sciences Cliniques, Faculté de Médecine Vétérinaire, Université de Montréal, 3200 Sicotte CP5000, St-Hyacinthe, Que., Canada J2S 7C6. jean-pierre.lavoie@umontreal.ca
Source
Pulm Pharmacol Ther. 2003;16(6):361-9
Date
2003
Language
English
Publication Type
Article
Keywords
Animals
Asthma - drug therapy - metabolism - physiopathology
Bronchoalveolar Lavage Fluid - chemistry - cytology
Bronchoconstriction - drug effects
Histamine - analysis
Interferon Type II - biosynthesis - genetics
Interleukin-4 - biosynthesis - genetics
Interleukin-5 - biosynthesis - genetics
Ovalbumin - administration & dosage - immunology - therapeutic use
Polyethylene Glycols - administration & dosage - therapeutic use
RNA, Messenger - biosynthesis
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Abstract
The purpose of this study was to test the therapeutic potential of monomethoxypolyethylene glycol (mPEG) conjugated-allergen using a rodent model of allergic asthma. Previously, this conjugate has been shown to possess the dual capacity of inducing long-term ovalbumin (OA)-specific suppression of the antibody response and inactivating rat mast cells that have been sensitized with murine IgE to OA. Ovalbumin sensitized and challenged Brown Norway rats were studied. Fourteen days after sensitization, a test group of six rats received mPEG-OA solution intratracheally and were challenged 30 min later with aerosolized OA. Another group of seven sensitized rats was similarly challenged with OA 30 min after intratracheal administration of normal saline. A group of six sensitized rats received mPEG-OA solution intratracheally but were challenged with normal saline. Another group of seven sensitized rats received mPEG-BSA solution intratracheally and were challenged 30 min later with aerosolized OA. A final group of five unsensitized rats were neither challenged nor medicated intratracheally. Pulmonary resistance was measured before and for 8 h following inhalation challenge. mPEG-OA treatment had an inhibitory effect on the allergic late airway response, but the early response was not significantly altered. Both mPEG-OA and mPEG-BSA reduced the total cells, eosinophils and neutrophils, in bronchoalveolar lavage and decreased the expression of IL-4, IL-5 and IFN-gamma mRNA. In conclusion, mPEG-OA can prevent the development of allergen-induced late airway responses and reduce airway Th2-type cytokine expression whereas mPEG conjugated to an irrelevant antigen (BSA) is anti-inflammatory but does not affect the late response.
PubMed ID
14580928 View in PubMed
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The effects of CD8+gammadelta T cells on late allergic airway responses and airway inflammation in rats.

https://arctichealth.org/en/permalink/ahliterature57418
Source
J Allergy Clin Immunol. 2003 Sep;112(3):547-55
Publication Type
Article
Date
Sep-2003
Author
Susumu Isogai
Alexandra Rubin
Karim Maghni
David Ramos-Barbon
Rame Taha
Yasuyuki Yoshizawa
Qutayba Hamid
James G Martin
Author Affiliation
Meakins Christie Laboratories, Department of Medicine, McGill University, 3623 St Urbain, Montreal, Quebec, Canada H2X 2P2.
Source
J Allergy Clin Immunol. 2003 Sep;112(3):547-55
Date
Sep-2003
Language
English
Publication Type
Article
Keywords
Adoptive Transfer
Allergens - administration & dosage
Animals
CD8-Positive T-Lymphocytes - immunology
Cytokines - biosynthesis - genetics
Eosinophilia - immunology
Immunoglobulin E - blood
Interferon Type II - biosynthesis - genetics
Interleukin-4 - biosynthesis - genetics
Male
Models, Immunological
Ovalbumin - administration & dosage - immunology
RNA, Messenger - genetics - metabolism
Rats
Rats, Inbred BN
Receptors, Antigen, T-Cell, gamma-delta - metabolism
Research Support, Non-U.S. Gov't
Respiratory Hypersensitivity - etiology - immunology
T-Lymphocyte Subsets - immunology
Abstract
BACKGROUND: Gamma-delta (gammadelta) T cells regulate immune responses to foreign protein at mucosal surfaces. Whether they can modify allergen-induced early (EAR) and late airway responses (LAR) is unknown. OBJECTIVE: We have tested the hypothesis that the CD8+ subtype of gammadelta T cells decreases allergen-induced LAR and airway eosinophilia in the rat. METHODS: Brown Norway rats were administered, intraperitoneally, 3.5 x 10(4) lymph node CD8+gammadelta T cells from naive or sensitized rats. The recipients were sensitized to ovalbumin (OVA) in Al(OH)(3) 3 days after cell transfer and challenged with aerosolized OVA 14 days later. Serum IgE was measured before allergen challenge. After challenge, lung resistance was monitored for 8 hours and then bronchoalveolar lavage (BAL) was analyzed for eosinophil major basic protein (MBP), IL-4, IL-5, IL-13, and IFN-gamma messenger RNA-expressing cells. RESULTS: gammadelta T cells from naive donors significantly decreased LAR in OVA-challenged sensitized rats, whereas MBP(+) eosinophils were decreased by both gammadelta T cells from naive and sensitized donors. EAR and serum IgE levels were unchanged. The expression of IL-4, IL-5, and IL-13 by BAL cells of gammadelta T cell recipients was attenuated compared with OVA-challenged controls. This was accompanied by an increase in the expression of IFN-gamma. CONCLUSIONS: Our results are consistent with a suppressive role of CD8+gammadelta T cells on allergic airway responses. However, only gammadelta T cells from naive donors inhibit LAR.
PubMed ID
13679814 View in PubMed
Less detail

Gold is a T cell polyclonal activator in BN and LEW rats but favors IL-4 expression only in autoimmune prone BN rats.

https://arctichealth.org/en/permalink/ahliterature14023
Source
Eur J Immunol. 2001 Aug;31(8):2266-76
Publication Type
Article
Date
Aug-2001
Author
M. Savignac
A. Badou
C. Delmas
J F Subra
S. De Cramer
P. Paulet
G. Cassar
P. Druet
A. Saoudi
L. Pelletier
Author Affiliation
INSERM U28, IFR 30 CHU Purpan, Toulouse, France.
Source
Eur J Immunol. 2001 Aug;31(8):2266-76
Date
Aug-2001
Language
English
Publication Type
Article
Keywords
Animals
Antibodies, Monoclonal - immunology - pharmacology
Autoimmunity - drug effects - immunology
B-Lymphocytes - drug effects - immunology
CD8-Positive T-Lymphocytes - drug effects - immunology - metabolism
Calcium - metabolism
Calcium Signaling - drug effects
Chlorides - pharmacology
Gene Expression Regulation - drug effects
Gold - pharmacology
Gold Compounds - pharmacology
Immunoglobulin E - immunology
Immunoglobulin G - immunology
Interferon Type II - biosynthesis - genetics - immunology
Interleukin-4 - biosynthesis - genetics - immunology
Lymphocyte Activation - drug effects
Phosphorylation - drug effects
RNA, Messenger - genetics - metabolism
Rats
Rats, Inbred BN
Rats, Inbred Lew
Research Support, Non-U.S. Gov't
Spleen - cytology - drug effects - immunology
T-Lymphocytes - drug effects - immunology - metabolism
Th2 Cells - drug effects - immunology - metabolism
Abstract
Gold salts are beneficial in the treatment of rheumatoid arthritis but may induce immune-mediated disorders in predisposed patients. Gold salts induce Th2-dependent autoimmunity in Brown-Norway (BN) rats but not in Lewis (LEW) rats. The aim of this study was to define molecular targets of gold salts and to approach why LEW rats are resistant. Gold salts act on early steps of transduction in T cells from BN and LEW rats since they trigger tyrosine phosphorylation of numerous proteins including p56(lck) and a calcium signal which results in IL-4 and IFN-gamma expression by BN and LEW T cells. However, the IL-4 response was favored in BN spleen cells in vitro and in vivo. IFN-gamma, produced in part by CD8(+) cells, contributes to the resistance of LEW rats since gold salt-injected LEW rats receiving anti-CD8 or anti-IFN-gamma mAb displayed the parameters characteristics of gold salt-induced Th2 autoimmunity although to a lesser extent than in BN rats. Gold salts transduce a signal in BN and LEW spleen cells resulting in IL-4 and IFN-gamma gene transcription with a preferential IL-4 response in BN rats, a Th2-prone strain, while IFN-gamma contributes to the resistance of LEW rats.
PubMed ID
11477538 View in PubMed
Less detail

IL-4 gene expression up-regulated by mercury in rat mast cells: a role of oxidant stress in IL-4 transcription.

https://arctichealth.org/en/permalink/ahliterature14058
Source
Int Immunol. 2001 Mar;13(3):297-304
Publication Type
Article
Date
Mar-2001
Author
Z. Wu
D R Turner
D B Oliveira
Author Affiliation
Division of Renal Medicine, St George's Hospital Medical School, Cranmer Terrace, London SW17 0RE, UK.
Source
Int Immunol. 2001 Mar;13(3):297-304
Date
Mar-2001
Language
English
Publication Type
Article
Keywords
Animals
Antioxidants - pharmacology
Autoimmunity
Cells, Cultured
Gene Expression Regulation - drug effects
Gene Expression Regulation, Leukemic - drug effects
Glutathione - pharmacology
Hydrogen Peroxide - pharmacology
Interleukin-4 - biosynthesis - genetics
Leukemia, Basophilic, Acute - pathology
Mast Cells - drug effects - metabolism
Mercuric Chloride - pharmacology
Neoplasm Proteins - biosynthesis - genetics
Oxidative Stress
Promoter Regions (Genetics)
Rats
Rats, Inbred BN
Reactive Oxygen Species
Research Support, Non-U.S. Gov't
Reverse Transcriptase Polymerase Chain Reaction
Spleen - cytology
Th2 Cells - immunology
Transcription, Genetic - drug effects
Transfection
Tumor Cells, Cultured - drug effects
Abstract
In the Brown Norway (BN) rat, chemical compounds [mercuric chloride (HgCl2), D-penicillamine or gold salts] induce a T(h)2-dominated autoimmune syndrome with tissue injury in the form of a vasculitis and arthritis. An early phase of vasculitis in the model occurs within 24 h of an injection of HgCl2, is alphabeta T cell independent and involves the mast cell. In addition, HgCl2 induces IL-4 mRNA in mast cells from BN rats. Our recent work has demonstrated that the balance of oxidative/antioxidative influences plays an important role in the modulation of mast cell function (degranulation) in chemically induced autoimmunity. The aim of this study was to determine, in mast cells, whether oxidative status influences IL-4 transcription and translation, which is required for the development of a T(h)2 response. Exposure of the mast cell line RBL-2H3 to HgCl2 enhanced both IL-4 mRNA and its promoter activity. Oxidative stress by hydrogen peroxide mimicked the effects of HgCl2 in enhancing IL-4 promoter activity. The enhancement of IL-4 gene expression by HgCl2 was significantly reduced by antioxidants (both sulphydryl and non-sulphydryl containing). The same pattern of regulation was also observed on IL-4 protein expression in the mast cells. These data suggest a novel mechanism of IL-4 transcriptional up-regulation by oxidative stress. Our results provide evidence to support our hypothesis that alterations in intracellular reactive oxygen species production modulate both IL-4 gene expression and mast cell function.
PubMed ID
11222498 View in PubMed
Less detail

IL-4, IL-5 and IFN-gamma mRNA expression in pulmonary lymphocytes in equine heaves.

https://arctichealth.org/en/permalink/ahliterature15211
Source
Vet Immunol Immunopathol. 2004 Jan;97(1-2):87-96
Publication Type
Article
Date
Jan-2004
Author
Marie-Eve Cordeau
Philippe Joubert
Oday Dewachi
Qutayba Hamid
Jean-Pierre Lavoie
Author Affiliation
Faculté de Médecine Vétérinaire, Université de Montréal, 3200 Sicotte, St-Hyacinthe, Que., Canada J2S 7C6.
Source
Vet Immunol Immunopathol. 2004 Jan;97(1-2):87-96
Date
Jan-2004
Language
English
Publication Type
Article
Keywords
Animals
Bronchoalveolar Lavage Fluid - cytology - immunology
Female
Horse Diseases - genetics - immunology - metabolism
Horses
In Situ Hybridization - veterinary
Interferon Type II - biosynthesis - genetics - immunology
Interleukin-4 - biosynthesis - genetics - immunology
Interleukin-5 - biosynthesis - genetics - immunology
Lung Diseases, Obstructive - genetics - immunology - metabolism - veterinary
Male
RNA, Messenger - biosynthesis - blood - genetics
Research Support, Non-U.S. Gov't
Respiratory Function Tests - veterinary
Respiratory Hypersensitivity - genetics - immunology - metabolism - veterinary
Statistics, nonparametric
Abstract
Heaves is a common condition of horses of cold climate that is characterized by small airway inflammation and obstruction following exposure of susceptible horses to moldy hay and straw. It has been shown that helper T lymphocytes (Th) orchestrate the inflammatory response in asthma and in various animal models of allergic lung diseases by the release of Th2-type cytokines. Results of previous studies indicate that a predominant expression of Th2-type response by airway cells may also be present in heaves. To evaluate the temporal mRNA expression of Th1 (IFN-gamma) and Th2 (IL-4, IL-5) type cytokines in heaves and their relationship to clinical disease, we studied the pulmonary mechanics and cytokine mRNA expression (IL-4, IL-5 and IFN-gamma) in bronchoalveolar lavage lymphocytes of horses with heaves (n=6) and control (n=6) before and after 24h and 9 days of continuous natural inhalation challenge. Starting 24h after challenge horses with heaves, but not control horses, had a significant increase in pulmonary elastance and the number of lymphocytes expressing mRNA for IL-4 and IL-5. These changes were further increased at 9 days, at which time the number of cells positive for IFN-gamma mRNA was decreased. In this study we have shown that BAL lymphocytes of horses with heaves during clinical exacerbation have a predominant Th2-type cytokine response and that this response coincides in time with the presence of airway obstruction.
PubMed ID
14700540 View in PubMed
Less detail

Local cytokine messenger ribonucleic acid expression and in vitro allergic late phase responses in Brown-Norway rats.

https://arctichealth.org/en/permalink/ahliterature15744
Source
Eur Respir J. 1998 Mar;11(3):630-5
Publication Type
Article
Date
Mar-1998
Author
E M Minshall
R J Dandurand
Q. Hamid
D H Eidelman
Author Affiliation
Meakins-Christie Laboratories, Montreal Chest Institute Research Center, Royal Victoria and Montreal General Hospitals, McGill University, Quebec, Canada.
Source
Eur Respir J. 1998 Mar;11(3):630-5
Date
Mar-1998
Language
English
Publication Type
Article
Keywords
Animals
Antigens - immunology
Asthma - immunology - metabolism - physiopathology
In Situ Hybridization
Interferon Type II - biosynthesis - genetics
Interleukin-2 - biosynthesis - genetics
Interleukin-4 - biosynthesis - genetics
Lung - immunology - metabolism
Ovalbumin - immunology
RNA, Messenger - genetics
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Time Factors
Abstract
The events subsequent to antigen challenge in allergic asthmatics involve the synthesis of pro-inflammatory cytokines. However, little is known how cytokine gene activation prior to allergen challenge may influence this series of events, nor how cytokine gene expression is related to antigen-induced alterations in lung function. Using a novel in vitro explant technique, we hypothesized that the local expression of cytokines influenced the development of antigen-induced late-onset airway responses, and that alterations in cytokine messenger ribonucleic acid (mRNA) expression were associated with antigen-induced changes in airway luminal area. Explants were prepared from excised lungs of ovalbumin-sensitized Brown-Norway rats. Airways were challenged by direct application of ovalbumin or an irrelevant control antigen. Cryostat sections of explants were used for in situ hybridization and mRNA for interleukin (IL)-2, IL-4 and interferon (IFN)-gamma were detected using radiolabelled probes. We found that the presence of high numbers of cells expressing IFN-gamma and IL-2 mRNA within the airways attenuated the development of antigen-induced late airway responses in sensitized rat lung explants. Furthermore, we observed that cytokine mRNA for IL-4 was significantly increased following allergen exposure in sensitized lung explants exhibiting late airway responses. This study implicates the local expression of interferon-gamma and interleukin-2 messenger ribonucleic acid in the failure of sensitized rat lung explants to exhibit late airway responses, and provides evidence linking local interleukin-4 messenger ribonucleic acid expression to the sequelae of events occurring as a result of antigen exposure within the airways.
PubMed ID
9596114 View in PubMed
Less detail

Oxpentifylline inhibits tumor necrosis factor-alpha mRNA transcription and protects against arthritis in mercuric chloride-treated brown Norway rats.

https://arctichealth.org/en/permalink/ahliterature14326
Source
Eur J Immunol. 1995 Oct;25(10):2899-906
Publication Type
Article
Date
Oct-1995
Author
P D Kiely
K M Gillespie
D B Oliveira
Author Affiliation
Department of Medicine, University of Cambridge School of Clinical Medicine, GB.
Source
Eur J Immunol. 1995 Oct;25(10):2899-906
Date
Oct-1995
Language
English
Publication Type
Article
Keywords
Animals
Arthritis - chemically induced - immunology - pathology - prevention & control
Autoimmune Diseases - chemically induced - immunology - pathology - prevention & control
Cecal Diseases - chemically induced - immunology - pathology - prevention & control
Disease Models, Animal
Humans
Immunoglobulin E - biosynthesis - genetics
Interleukin-4 - biosynthesis - genetics
Mercuric Chloride - toxicity
Pentoxifylline - pharmacology - therapeutic use
RNA, Messenger - biosynthesis - genetics
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Tumor Necrosis Factor-alpha - biosynthesis - genetics
Vasculitis - chemically induced - immunology - pathology - prevention & control
Abstract
The phosphodiesterase inhibitor oxpentifylline (OXP) has a number of potentially important immunomodulatory actions which include a selective inhibition of the Th1 subset of CD4+ cells in vitro and inhibition of tumor necrosis factor (TNF)-alpha mRNA transcription. In vivo, it has a dramatic protective effect against experimental allergic encephalomyelitis. In this animal model, tissue injury is associated with both a Th1 response and with TNF-alpha production, either of which could be targets for the protective action of OXP. In an attempt to clarify the relative importance of the Th cell subsets and TNF-alpha in pathogenesis, we investigated the effect of OXP on a Th2 model of T cell-dependent disease, mercuric chloride (HgCl2)-induced autoimmunity in the Brown Norway rat. The effects of OXP on the Th1:Th2 response, TNF-alpha mRNA transcription in spleen and ankle joints, and on the incidence and severity of arthritis and cecal vasculitis have been examined and the effects in vivo have been compared with those of a soluble TNF receptor-IgG1 fusion protein (sTNFR) that neutralizes rat TNF-alpha. In two separate experiments, OXP significantly enhanced unstimulated levels of splenic interleukin-4 (IL-4) mRNA (median 62%, of an artificial IL-4 mRNA construct, vs. 36.5% in controls) and in one experiment, exaggerated the total IgE response to HgCl2. OXP inhibited HgCl2-induced TNF-alpha mRNA transcription in spleen and ankle joints. In three separate experiments, OXP had a significant protective effect against arthritis, with the mean incidence reduced from 100% to 30% and mean peak score reduced from 7.2 to 2.59 (experiments 1 and 2). The protection against arthritis was indistinguishable from that produced by sTNFR. There was no such protection against cecal vasculitis with either OXP or sTNFR. These results demonstrate that OXP induces a shift towards a Th2 response, inhibits TNF-alpha mRNA transcription locally in joint and systemically in spleen, and has a protective effect against arthritis similar to that produced by sTNFR in the HgCl2-treated BN rat. We conclude that TNF-alpha is a critical cytokine in the pathogenesis of arthritis but not cecal vasculitis in this model, and that inhibition of TNF-alpha transcription is the most important mode of action of OXP in this situation. OXP may be a potential therapeutic agent in the treatment of other arthritides, such as human rheumatoid arthritis, in which TNF-alpha has been implicated in pathogenesis.
PubMed ID
7589090 View in PubMed
Less detail

Reactive oxygen species in the initiation of IL-4 driven autoimmunity as a potential therapeutic target.

https://arctichealth.org/en/permalink/ahliterature15178
Source
Curr Pharm Des. 2004;10(8):899-913
Publication Type
Article
Date
2004
Author
Z. Wu
I A M MacPhee
D B G Oliveira
Author Affiliation
Department of Cellular and Molecular Medicine-Renal Medicine, St. George's Hospital Medical School, Cranmer Terrace, London SW17 0RE, UK. zwu@sghms.ac.uk
Source
Curr Pharm Des. 2004;10(8):899-913
Date
2004
Language
English
Publication Type
Article
Keywords
Adjuvants, Immunologic - genetics
Animals
Antioxidants - pharmacology
Autoimmune Diseases - immunology - therapy
Autoimmunity - immunology - physiology
Humans
Interleukin-4 - biosynthesis - genetics - immunology
Oxidative Stress - immunology
Reactive Oxygen Species - immunology - metabolism
Research Support, Non-U.S. Gov't
Th1 Cells - immunology
Th2 Cells - immunology
Transcription, Genetic
Abstract
Helper T-lymphocytes have been shown to differentiate into two mutually regulatory subsets. Cells primarily secreting interleukin-2 (IL-2) and interferon-gamma are known as Th1 cells and mediate classical cell-mediated immune responses such as delayed-type hypersensitivity. Cells secreting interleukin-4 (IL-4) are known as Th2 cells and promote humoral immune responses, in particular the production of IgE and IgG4 (human) or IgG1 (rodents). Over-activity of either cell type can result in tissue-damaging autoimmune disease. A number of human diseases including asthma and some kidney diseases are thought to be caused by a Th-2 type autoimmune response. Study of an animal model of Th2-driven autoimmunity (mercuric chloride-induced autoimmunity in Brown Norway rats) has yielded insights into a possible role for oxidant stress in the generation of Th-2 driven autoimmune responses. Mercuric chloride probably causes oxidant stress by the generation of free-radicals, activating NK-kappaB, a transcription factor for the IL-4 gene. Treatment with the antioxidants N-acetlcysteine and desferrioxamine has been shown to suppress vasculitis and IgE production in this model. These findings suggest a possible clinical role for antioxidants in the therapy of human autoimmune disease.
PubMed ID
15032693 View in PubMed
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Role of genetically determined production of immunoregulatory cytokines in immunopathogenesis of chronic viral hepatitides.

https://arctichealth.org/en/permalink/ahliterature87783
Source
Bull Exp Biol Med. 2007 Jun;143(6):706-12
Publication Type
Article
Date
Jun-2007
Author
Naslednikova I OI
Konenkov V
Ryazantseva N V
Novitskii V V
Tkachenko S B
Zima A P
Avdoshina V V
Beloborodova E I
Beloborodova E V
Dortman V V
Author Affiliation
Department of Pathophysiology, Siberian State Medical University, Federal Agency of Health Care and Social Development, Tomsk. ira_naslednikova@mail.ru
Source
Bull Exp Biol Med. 2007 Jun;143(6):706-12
Date
Jun-2007
Language
English
Russian
Publication Type
Article
Keywords
Adolescent
Adult
Blood Donors
Female
Hepatitis B, Chronic - immunology
Hepatitis C, Chronic - immunology
Humans
Interleukin-10 - biosynthesis - genetics
Interleukin-2 - biosynthesis - genetics
Interleukin-4 - biosynthesis - genetics
Male
Middle Aged
Abstract
Immunopathogenesis of chronic viral hepatitides was studied by modern immunological, molecular, genetic methods. We revealed an imbalance in the production of immunoregulatory cytokines by mononuclear leukocytes (primarily of the Th2 type). The risk of progression and chronic course of viral hepatitides in Caucasian population was associated with alleles of promoter regions -330G and -592A in the IL-2 and IL-10 genes, respectively, as well as with the T/T genotype of the polymorphic region C590T in the IL-4 gene. The C/C genotype of the IL-10 gene promoter region C592A was shown to be a factor determining resistance to long-term persistence of hepatitis B and C viruses.
PubMed ID
18239807 View in PubMed
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10 records – page 1 of 1.