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Association of autoimmune Addison's disease with alleles of STAT4 and GATA3 in European cohorts.

https://arctichealth.org/en/permalink/ahliterature271397
Source
PLoS One. 2014;9(3):e88991
Publication Type
Article
Date
2014
Author
Anna L Mitchell
Katie D R Macarthur
Earn H Gan
Lucy E Baggott
Anette S B Wolff
Beate Skinningsrud
Hazel Platt
Andrea Short
Anna Lobell
Olle Kämpe
Sophie Bensing
Corrado Betterle
Anna Kasperlik-Zaluska
Magdalena Zurawek
Marta Fichna
Ingrid Kockum
Gabriel Nordling Eriksson
Olov Ekwall
Jeanette Wahlberg
Per Dahlqvist
Anna-Lena Hulting
Marissa Penna-Martinez
Gesine Meyer
Heinrich Kahles
Klaus Badenhoop
Stephanie Hahner
Marcus Quinkler
Alberto Falorni
Amanda Phipps-Green
Tony R Merriman
William Ollier
Heather J Cordell
Dag Undlien
Barbara Czarnocka
Eystein Husebye
Simon H S Pearce
Source
PLoS One. 2014;9(3):e88991
Date
2014
Language
English
Publication Type
Article
Keywords
Addison Disease - genetics
Adolescent
Adult
Aged
Aged, 80 and over
Alleles
Autoimmune Diseases - genetics
Case-Control Studies
Child
Child, Preschool
Cohort Studies
European Continental Ancestry Group
Female
GATA3 Transcription Factor - genetics
Genetic Association Studies
Genetic Heterogeneity
Genetic Predisposition to Disease
Genotyping Techniques
Great Britain
Humans
Infant
Infant, Newborn
Male
Middle Aged
Norway
STAT4 Transcription Factor - genetics
Young Adult
Abstract
Gene variants known to contribute to Autoimmune Addison's disease (AAD) susceptibility include those at the MHC, MICA, CIITA, CTLA4, PTPN22, CYP27B1, NLRP-1 and CD274 loci. The majority of the genetic component to disease susceptibility has yet to be accounted for.
To investigate the role of 19 candidate genes in AAD susceptibility in six European case-control cohorts.
A sequential association study design was employed with genotyping using Sequenom iPlex technology. In phase one, 85 SNPs in 19 genes were genotyped in UK and Norwegian AAD cohorts (691 AAD, 715 controls). In phase two, 21 SNPs in 11 genes were genotyped in German, Swedish, Italian and Polish cohorts (1264 AAD, 1221 controls). In phase three, to explore association of GATA3 polymorphisms with AAD and to determine if this association extended to other autoimmune conditions, 15 SNPs in GATA3 were studied in UK and Norwegian AAD cohorts, 1195 type 1 diabetes patients from Norway, 650 rheumatoid arthritis patients from New Zealand and in 283 UK Graves' disease patients. Meta-analysis was used to compare genotype frequencies between the participating centres, allowing for heterogeneity.
We report significant association with alleles of two STAT4 markers in AAD cohorts (rs4274624: P?=?0.00016; rs10931481: P?=?0.0007). In addition, nominal association of AAD with alleles at GATA3 was found in 3 patient cohorts and supported by meta-analysis. Association of AAD with CYP27B1 alleles was also confirmed, which replicates previous published data. Finally, nominal association was found at SNPs in both the NF-?B1 and IL23A genes in the UK and Italian cohorts respectively.
Variants in the STAT4 gene, previously associated with other autoimmune conditions, confer susceptibility to AAD. Additionally, we report association of GATA3 variants with AAD: this adds to the recent report of association of GATA3 variants with rheumatoid arthritis.
Notes
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Erratum In: PLoS One. 2014;9(7):e102428
PubMed ID
24614117 View in PubMed
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Autoimmune disease in individuals and close family members and susceptibility to non-Hodgkin's lymphoma.

https://arctichealth.org/en/permalink/ahliterature87057
Source
Arthritis Rheum. 2008 Mar;58(3):657-66
Publication Type
Article
Date
Mar-2008
Author
Mellemkjaer Lene
Pfeiffer Ruth M
Engels Eric A
Gridley Gloria
Wheeler William
Hemminki Kari
Olsen Jørgen H
Dreyer Lene
Linet Martha S
Goldin Lynn R
Landgren Ola
Author Affiliation
Danish Cancer Society, Copenhagen, Denmark. lene@cancer.dk
Source
Arthritis Rheum. 2008 Mar;58(3):657-66
Date
Mar-2008
Language
English
Publication Type
Article
Keywords
Adult
Aged
Arthritis, Rheumatoid - genetics
Autoimmune Diseases - genetics
Case-Control Studies
Denmark
European Continental Ancestry Group - genetics
Family
Female
Genetic Predisposition to Disease - genetics
Humans
Logistic Models
Lupus Erythematosus, Systemic - genetics
Lymphoma, Non-Hodgkin - genetics
Male
Middle Aged
Risk factors
Sjogren's Syndrome - genetics
Sweden
Abstract
OBJECTIVE: Rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and Sj?gren's syndrome have been consistently associated with an increased risk of non-Hodgkin's lymphoma (NHL). This study was initiated to evaluate the risks of NHL associated with a personal or family history of a wide range of autoimmune diseases. METHODS: A population-based case-control study was conducted that included 24,728 NHL patients in Denmark (years 1977-1997) and Sweden (years 1964-1998) and 55,632 controls. Using univariate logistic and hierarchical regression models, we determined odds ratios (ORs) of NHL associated with a personal history of hospital-diagnosed autoimmune conditions. Risks of NHL associated with a family history of the same autoimmune conditions were assessed by similar regression analyses that included 25,941 NHL patients and 58,551 controls. RESULTS: A personal history of systemic autoimmune diseases (RA, SLE, Sj?gren's syndrome, systemic sclerosis) was clearly linked with NHL risk, both for individual conditions (hierarchical odds ratios [OR(h)] ranged from 1.6 to 5.4) and as a group (OR(h) 2.64 [95% confidence interval (95% CI) 1.72-4.07]). In contrast, a family history of systemic autoimmune diseases was modestly and nonsignificantly associated with NHL (OR(h) 1.31 [95% CI 0.85-2.03]). An increased risk of NHL was found for a personal history of 5 nonsystemic autoimmune conditions (autoimmune hemolytic anemia, Hashimoto thyroiditis, Crohn's disease, psoriasis, and sarcoidosis) (OR(h) ranged from 1.5 to 2.6) of 27 conditions examined. CONCLUSION: Overall, our results demonstrate a strong relationship of personal history of systemic autoimmune diseases with NHL risk and suggest that shared susceptibility may explain a very small fraction of this increase, at best. Positive associations were found for a personal history of some, though far from all, nonsystemic autoimmune conditions.
PubMed ID
18311836 View in PubMed
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[Autoimmune diseases in the family can modify the risk for type 1 diabetes in children].

https://arctichealth.org/en/permalink/ahliterature147019
Source
Kinderkrankenschwester. 2009 Nov;28(11):477
Publication Type
Article
Date
Nov-2009
Author
Christine Huber
Author Affiliation
Technischen Universität München. christine.huber@lrz.uni-muenchen.de
Source
Kinderkrankenschwester. 2009 Nov;28(11):477
Date
Nov-2009
Language
German
Publication Type
Article
Keywords
Adolescent
Autoimmune Diseases - genetics - nursing
Child
Diabetes Mellitus, Type 1 - genetics - nursing
Genetic Predisposition to Disease - genetics
Germany
Humans
Risk factors
Sweden
PubMed ID
19953856 View in PubMed
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Autoimmune interstitial nephritis induced in inbred mice. Analysis of mouse tubular basement membrane antigen and genetic control of immune response to it.

https://arctichealth.org/en/permalink/ahliterature57816
Source
Am J Pathol. 1988 Aug;132(2):304-18
Publication Type
Article
Date
Aug-1988
Author
S. Ueda
M. Wakashin
Y. Wakashin
H. Yoshida
R. Azemoto
K. Iesato
T. Mori
Y. Mori
M. Ogawa
K. Okuda
Author Affiliation
First Department of Internal Medicine, School of Medicine, Chiba University, Japan.
Source
Am J Pathol. 1988 Aug;132(2):304-18
Date
Aug-1988
Language
English
Publication Type
Article
Keywords
Animals
Antibodies - analysis
Antibody formation
Antigens - immunology
Autoimmune Diseases - genetics - immunology
Basement Membrane - immunology
Cell Division
Crosses, Genetic
Hybridization, Genetic
Immunization, Passive
Kidney - immunology
Kidney Tubules - immunology
Lymphocytes - immunology - pathology
Mice
Mice, Inbred Strains - genetics - immunology
Nephritis, Interstitial - genetics - immunology
Spleen - immunology - pathology
Abstract
Purified murine tubular basement membrane (TBM) antigen (molecular weight, 32,000) induced interstitial lesions in Brown Norway (BN) rats. TBM antigen prepared from mice of 3 inbred strains--BALB/c, C3H/He, and C57BL/6--and outbred ddY mice possessed both antigenicity and nephritogenecity. Using these TBM antigens, the roles of humoral and cellular immunity in the development of interstitial nephritis (IN) and the genetic control of the induction of IN in inbred mice were investigated. BALB/c mice were highly susceptible to IN and showed a high antibody response and a high lymphocyte proliferative response to syngeneic and allogeneic TBM antigen, whereas C57BL/6 mice did not. C3H/He mice, in which minimal interstitial lesions developed, showed a high antibody response but a low proliferative response of T cells to TBM antigen. TBM antigen sensitized T cells induced interstitial lesions, but anti-TBM antisera did not do so. Thus, the development of IN seemed to be related closely to cellular immunity. Further studies with their hybrids, backcrosses, congenic mice, and recombinant mice suggested that the induction of IN and the immune response to TBM antigen are controlled by 1 or a few dominant genes, whose loci are within, or closely linked to, the H-2 complex.
PubMed ID
3400774 View in PubMed
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Autoimmune polyendocrinopathy--candidosis--ectodermal dystrophy (APECED): autosomal recessive inheritance.

https://arctichealth.org/en/permalink/ahliterature238721
Source
Clin Genet. 1985 Jun;27(6):535-42
Publication Type
Article
Date
Jun-1985
Author
P. Ahonen
Source
Clin Genet. 1985 Jun;27(6):535-42
Date
Jun-1985
Language
English
Publication Type
Article
Keywords
Adrenal Insufficiency - genetics
Adult
Autoimmune Diseases - genetics
Candidiasis - genetics
Candidiasis, Chronic Mucocutaneous - genetics
Child
Consanguinity
Ectodermal Dysplasia - genetics
Female
Finland
Genes, Recessive
Heterozygote
Humans
Hypoparathyroidism - genetics
Male
Sex ratio
Syndrome
Abstract
A genetic analysis was made of 58 patients and their 42 families with APECED (autoimmune polyendocrinopathy--candidosis--ectodermal dystrophy). APECED is characterized by hypoparathyroidism, primary adrenocortical failure and chronic mucocutaneous candidosis, but none of its components is constant. Other endocrine deficiencies can occur as well and also dystrophy of dental enamel and nails. The proportion of affected siblings was 0.147 +/- 0.034 (S.D.) when corrected for truncate single ascertainment, 0.246 +/- 0.019 when corrected for a priori truncate complete ascertainment and 0.240 +/- 0.047 when corrected for a posteriori truncate complete ascertainment. The male/female ratio was 1.04. The results are compatible with autosomal recessive transmission. No heterozygous manifestations of the gene were found. The gene is enriched in isolated subpopulations in central and eastern Finland. APECED is part of the "Finnish heritage of disease".
PubMed ID
4017274 View in PubMed
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Autoimmunity and extranodal lymphocytic infiltrates in lymphoproliferative disorders.

https://arctichealth.org/en/permalink/ahliterature21092
Source
J Intern Med. 1999 Mar;245(3):277-86
Publication Type
Article
Date
Mar-1999
Author
V. Jønsson
A. Wiik
K. Hou-Jensen
M. Christiansen
L P Ryder
H O Madsen
C. Geisler
M M Hansen
K. Thomsen
S. Vorstrup
A. Svejgaard
Author Affiliation
Department of Haematology, Rigshospital, Denmark.
Source
J Intern Med. 1999 Mar;245(3):277-86
Date
Mar-1999
Language
English
Publication Type
Article
Keywords
Aged
Autoimmune Diseases - genetics - immunology
Autoimmunity
Denmark
Female
Gene Rearrangement
Hospitals, University
Humans
Immunoglobulin Heavy Chains - genetics
Immunoglobulins - blood
Leukemia, Lymphocytic - immunology
Lymphoma, Non-Hodgkin - immunology
Lymphoproliferative Disorders - genetics - immunology
Male
Middle Aged
Paraproteinemias - immunology
Receptors, Antigen, T-Cell - genetics
Sequence Analysis, DNA
Waldenstrom Macroglobulinemia - immunology
Abstract
OBJECTIVE: To examine the relationship between autoimmunity and extranodal lymphocytic infiltrates in different lymphoproliferative disorders with immunoglobulin alterations. SUBJECTS AND DESIGN: A clinical review combined with a retrospective cohort study of 380 patients, 28 with monoclonal gammopathy of undetermined significance, three with common variable immunodeficiency, 147 with chronic lymphocytic leukaemia, 57 with Waldenstr?m's macroglobulinaemia and 145 with non-Hodgkin's malignant lymphoma. SETTING: A university hospital and The State Serum Institute in Copenhagen. INTERVENTION: Clinical examination of each patient with special attention to chronic inflammatory and autoimmune manifestations. Biopsies were taken from non-infectious infiltrates, some of which were additionally tested with PCR analysis for gene rearrangements. Serological screening with a test battery for various autoantibodies was used in combination with techniques for the detection of M-components and monoclonal B-cell proliferation. MAIN OUTCOME MEASURES: Clinical and/or serological autoimmune manifestations, M-component and other immunoglobulin alterations, and inflammatory tissue changes were studied in patients with chronic inflammatory, polyclonal or oligoclonal pseudolymphomas and in monoclonal, malignant extranodal lymphomas. RESULTS: In 380 consecutive patients, 49 (12.9%) had extranodal manifestations, of whom 47 also had autoimmune manifestations. Nearly half of the 47 patients had more than one autoimmune manifestation. There was a strong correlation between clinical signs and corresponding autoantibodies such as anti-SSA and -SSB antibodies in Sj?gren's syndrome (10 cases), antithyroid peroxidase antibodies in thyroiditis and Graves' disease (10 cases), and parietal cell antibodies in gastric ulcers with maltoma (12 cases). Clinical and serological signs of autoimmunity correlated strongly with female sex (34, 72% women; and 13, 28% men) and with immunoglobulin alterations. CONCLUSIONS: To our knowledge this is the first systematic review of B-lymphoproliferative and autoimmune disorders indicating that pseudolymphoma and malignant lymphomas, including maltomas, may develop in the context of a permanent autoantigenic drive.
PubMed ID
10205590 View in PubMed
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Contact stomatitis to mercury associated with spontaneous mononuclear cell infiltrates in brown Norway (BN) rats with HgCl2-induced autoimmunity.

https://arctichealth.org/en/permalink/ahliterature57689
Source
J Oral Pathol Med. 1994 Nov;23(10):441-5
Publication Type
Article
Date
Nov-1994
Author
G. Warfvinge
A. Larsson
Author Affiliation
Department of Oral Pathology, Lund University, Malmö, Sweden.
Source
J Oral Pathol Med. 1994 Nov;23(10):441-5
Date
Nov-1994
Language
English
Publication Type
Article
Keywords
Administration, Topical
Animals
Autoimmune Diseases - genetics - immunology
Basement Membrane - immunology - pathology
Dendritic Cells - immunology - pathology
Epithelium - immunology - pathology
Immunization
Injections, Intradermal
Leukocytes, Mononuclear - immunology - pathology
Lichenoid Eruptions - chemically induced - immunology - pathology
Lymph Nodes - immunology - pathology
Macrophages - immunology - pathology
Male
Mercuric Chloride - administration & dosage - adverse effects - immunology
Mercury - adverse effects
Mouth Mucosa - immunology - pathology
Rats
Rats, Inbred BN
Rats, Inbred Lew
Research Support, Non-U.S. Gov't
Stomatitis - chemically induced - immunology - pathology
Abstract
Light microscopy and immunocytochemistry have been used to study the tissue reaction to non-irritant concentrations of mercury painted onto the oral mucosa of genetically mercury-sensitive BN rats. Low-dose skin injections of HgCl2 in BN rats result in an autoimmune syndrome, including also a spontaneous migration of T lymphocytes into the oral mucosa. Our results show that such infiltrates confer an increased degree of reactivity (contact stomatitis) to HgCl2 painted onto the BN (Hg) rat oral mucosa. In contrast, results were negative in the LEW rat strain, which is also resistant to development of autoimmunity to skin-injected mercury. The possible involvement of mucosal mercury-loaded macrophages is discussed. The results are also discussed with respect to possible etiologic and pathogenetic mechanisms involved in the development of dental material (amalgam)-associated lichenoid lesions of human oral mucosa.
PubMed ID
7861329 View in PubMed
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CTLA4 promoter and exon 1 dimorphisms in multiple sclerosis.

https://arctichealth.org/en/permalink/ahliterature202846
Source
Tissue Antigens. 1999 Jan;53(1):106-10
Publication Type
Article
Date
Jan-1999
Author
H F Harbo
E G Celius
F. Vartdal
A. Spurkland
Author Affiliation
Institute of Transplantation Immunology, The National Hospital, Oslo, Norway. h.f.harbo@labmed.uio.no
Source
Tissue Antigens. 1999 Jan;53(1):106-10
Date
Jan-1999
Language
English
Publication Type
Article
Keywords
Amino Acid Substitution
Antigens, CD
Antigens, Differentiation - genetics
Autoimmune Diseases - genetics
CTLA-4 Antigen
Disease Progression
Exons - genetics
Genetic Predisposition to Disease
Genotype
Humans
Immunoconjugates
Multiple Sclerosis - genetics
Norway
Point Mutation
Polymerase Chain Reaction
Polymorphism, Genetic
Polymorphism, Restriction Fragment Length
Promoter Regions, Genetic
Abstract
The human cytotoxic T-lymphocyte-associated protein 4 (CTLA4) gene may be a candidate susceptibility gene in multiple sclerosis (MS). In this study the distribution of the dimorphisms of exon 1 (+49 A/G) and promoter (-318 C/T) regions of the CTLA4 gene was analysed in 296 unrelated Norwegian MS patients and 271 matched controls by polymerase chain reaction and restriction fragment length polymorphism. The frequency of the exon 1 (+49) A-G genotype was increased in patients (57%) compared with controls (44%) (Pcorrected=0.01), and even more increased in patients with relapsing remitting MS (59%) (Pcorrected=0.006). No other significant differences were found between clinical subgroups of patients or between HLA-DRB1*1501, DQB1*0602-positive and negative patients and controls.
PubMed ID
10082437 View in PubMed
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Different HLA-DR-DQ and MHC class I chain-related gene A (MICA) genotypes in autoimmune and nonautoimmune gestational diabetes in a Swedish population.

https://arctichealth.org/en/permalink/ahliterature47142
Source
Hum Immunol. 2004 Dec;65(12):1443-50
Publication Type
Article
Date
Dec-2004
Author
Carina Törn
Manu Gupta
Carani B Sanjeevi
Anders Aberg
Anders Frid
Mona Landin-Olsson
Author Affiliation
Diabetes Laboratory, Institution of Medicine, Lund University, Lund University Hospital, Lund, Sweden. Carina.Torn@med.lu.se
Source
Hum Immunol. 2004 Dec;65(12):1443-50
Date
Dec-2004
Language
English
Publication Type
Article
Keywords
Adult
Autoimmune Diseases - genetics - immunology
Case-Control Studies
Diabetes, Gestational - genetics - immunology
Female
Gene Frequency
Genes, MHC Class I
Genotype
HLA-DQ Antigens - genetics
HLA-DR Antigens - genetics
Histocompatibility Antigens Class I
Humans
Middle Aged
Pregnancy
Proteins - genetics
Research Support, Non-U.S. Gov't
Risk factors
Sweden
Abstract
The genetic susceptibility for gestational diabetes (GDM) was estimated by comparisons of genotypes within human leukocyte antigen (HLA) and major histocompatibility complex class I chain-related gene A (MICA) in 199 women with GDM and 213 healthy women. At least one of ICA, glutamic acid decarboxylase antibodies, or islet cell antigen-2 antibodies/tyrosine phosphatase antibodies was found in 6.0% (12/199) of women with GDM and were considered as autoimmune GDM, whereas the remaining 187 were considered as nonautoimmune GDM. HLA genotyping was done with polymerase chain reaction and sequence-specific oligonucleotides. MICA polymorphism was determined with polymerase chain reaction and fragment size determination. HLA-DR3-DQ2/x or DR4-DQ8/x and MICA5.0/5.1 were more frequent in autoimmune GDM compared with controls; 92% versus 46% and 42% versus 13% and conferred increased risk (odds ratio [OR] = 13; 95% confidence interval [CI] 1.7-104) and (OR = 4.7; 95%CI 1.4-16). Four other genotypes were more frequent in nonautoimmune GDM compared with controls: HLA-DR7-DQ2/y, 24% versus 14%; DR9-DQ9/y, 9.6% versus 1.9%; DR14-DQ5/y, 7.5% versus 0.94%; and MICA5.0/z, 24% versus 13% and gave increased risk: OR = 2.0; 95%CI 1.2-3.4, OR = 5.6; 95%CI 1.8-17, OR = 8.5; 95%CI 1.9-38, and OR = 2.0; 95%CI 1.2-3.4, respectively. We concluded that autoimmune diabetes with onset during pregnancy is associated with the type 1 diabetes-associated genotypes and also with MICA5.0/5.1, whereas DR7-DQ2/y, DR9-DQ9/y, DR14-DQ5/y, and MICA5.0/z are risk factors for nonautoimmune GDM.
PubMed ID
15603871 View in PubMed
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Differential tumor necrosis factor expression by resident retinal cells from experimental uveitis-susceptible and -resistant rat strains.

https://arctichealth.org/en/permalink/ahliterature51139
Source
J Neuroimmunol. 1994 Nov;55(1):1-9
Publication Type
Article
Date
Nov-1994
Author
Y. de Kozak
M C Naud
J. Bellot
J P Faure
D. Hicks
Author Affiliation
Laboratoire d'Immunopathologie de l'Oeil, INSERM U 86, Université de Paris VI, France.
Source
J Neuroimmunol. 1994 Nov;55(1):1-9
Date
Nov-1994
Language
English
Publication Type
Article
Keywords
Animals
Autoimmune Diseases - genetics - immunology - pathology
Cells, Cultured
Disease Models, Animal
Disease Susceptibility
Interferon Type II - pharmacology
Lipopolysaccharides - pharmacology
Neuroglia - drug effects - immunology - secretion
Pigment Epithelium of Eye - drug effects - immunology - secretion
Rats
Rats, Inbred BN
Rats, Inbred Lew
Rats, Inbred Strains
Retinitis - genetics - immunology - pathology
Tumor Necrosis Factor-alpha - secretion
Uveitis - genetics - immunology - pathology
Abstract
Experimental autoimmune uveoretinitis (EAU) and endotoxin-induced uveitis (EIU), models for human ocular immunopathological syndromes, result in ocular inflammation in susceptible, but not in resistant rat strains. Moreover rapid photoreceptor degeneration occurs in susceptible rats developing EAU. In order to see whether differences in local ocular immune regulation may account for changes in resistance or susceptibility, we have examined the in vitro production of the cytotoxic cytokine tumor necrosis factor (TNF) by two resident ocular cell types, retinal Müller glia (RMG) and retinal pigmented epithelium (RPE). These cells were isolated and cultured in vitro from Lewis (Lew) (highly susceptible), Lew x Brown-Norway (BN) F1 hybrid (susceptible), BN and Long-Evans (LE) (resistant or poorly susceptible) rats. Constitutive production of the cytokine TNF, or its liberation in response to either interferon-gamma (IFN-gamma) or lipopolysaccharide (LPS) alone, was very low in RMG and RPE cells, irrespective of the strain. It was strongly induced by combined treatment with IFN-gamma and LPS in Lew RMG and RPE cells (mean values of 140 and 150 pg/10(5) cells, respectively) and in Lew x BN F1 RMG and RPE cells (mean values of 125 and 190 pg/10(5) cells, respectively), much less so from BN RMG and RPE cells (30 and 20 pg/10(5) cells, respectively) and remained undetectable in LE RMG and RPE cells. Hence susceptibility to EAU and EIU in vivo is correlated with the extent of TNF production by these two cell types under in vitro conditions, which may play a key role in initiating or perpetuating local immune responses.
PubMed ID
7962479 View in PubMed
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33 records – page 1 of 4.