The genetic control of sialadenitis versus arthritis in a NOD.QxB10.Q F2 cross.
(2002) In European Journal of Immunology 32(1). p.243-250- Abstract
- The non-obese diabetic (NOD) mouse spontaneously develops diabetes and sialadenitis. The sialadenitis is characterized by histopathological changes in salivary glands and functional deficit similar to Sjögren's syndrome. In humans, Sjögren's syndrome could be associated with other connective tissue disorders, such as rheumatoid arthritis. In the present study the genetic control of sialadenitis in mice was compared to that of arthritis. We have previously reported a NOD locus, identified in an F2 cross with the H2(q) congenic NOD (NOD.Q) and C57BL/10.Q (B10.Q) strains, that promoted susceptibility to collagen-induced arthritis. The sialadenitis in NOD.Q showed a similar histological phenotype as in NOD, whereas no submandibular gland... (More)
- The non-obese diabetic (NOD) mouse spontaneously develops diabetes and sialadenitis. The sialadenitis is characterized by histopathological changes in salivary glands and functional deficit similar to Sjögren's syndrome. In humans, Sjögren's syndrome could be associated with other connective tissue disorders, such as rheumatoid arthritis. In the present study the genetic control of sialadenitis in mice was compared to that of arthritis. We have previously reported a NOD locus, identified in an F2 cross with the H2(q) congenic NOD (NOD.Q) and C57BL/10.Q (B10.Q) strains, that promoted susceptibility to collagen-induced arthritis. The sialadenitis in NOD.Q showed a similar histological phenotype as in NOD, whereas no submandibular gland infiltration was found in B10.Q. The development of sialadenitis was independent of immunization with type II collagen and established arthritis. To identify the genetic control of sialadenitis, a gene segregation experiment was performed on an (NOD.QxB10.Q)F2 cross and genetic mapping of 353 F2 mice revealed one significant locus associated with sialadenitis on chromosome 4, LOD score 4.7. The NOD.Q allele-mediated susceptibility under a recessive inheritance pattern. The genetic control of sialadenitis seemed to be unique in comparison to diabetes and arthritis, as no loci associated with these diseases have been identified at the same location. (Less)
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https://lup.lub.lu.se/record/106771
- author
- organization
- publishing date
- 2002
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Chromosomes, Female, Haplotypes, Histocompatibility Antigens Class II : immunology, Male, Mice, Mice Inbred C3H, Mice Inbred C57BL, Mice Inbred NOD, Phenotype, Sialadenitis : genetics : pathology : physiopathology, Support Non-U.S. Gov't, Submandibular Gland : pathology, Crosses Genetic, Chromosome Mapping, Arthritis Rheumatoid : chemically induced : genetics, Arthritis Experimental : chemically induced : genetics, Animal
- in
- European Journal of Immunology
- volume
- 32
- issue
- 1
- pages
- 243 - 250
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- wos:000173527400027
- pmid:11782015
- scopus:0036146469
- ISSN
- 1521-4141
- DOI
- 10.1002/1521-4141(200201)32:1<243::AID-IMMU243>3.0.CO;2-X
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Medical Inflammation Research (013212019)
- id
- 86e4cde0-6292-4688-9e77-de197beb281a (old id 106771)
- alternative location
- http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11782015&dopt=Abstract
- date added to LUP
- 2016-04-01 11:40:21
- date last changed
- 2022-03-12 23:01:13
@article{86e4cde0-6292-4688-9e77-de197beb281a,
abstract = {{The non-obese diabetic (NOD) mouse spontaneously develops diabetes and sialadenitis. The sialadenitis is characterized by histopathological changes in salivary glands and functional deficit similar to Sjögren's syndrome. In humans, Sjögren's syndrome could be associated with other connective tissue disorders, such as rheumatoid arthritis. In the present study the genetic control of sialadenitis in mice was compared to that of arthritis. We have previously reported a NOD locus, identified in an F2 cross with the H2(q) congenic NOD (NOD.Q) and C57BL/10.Q (B10.Q) strains, that promoted susceptibility to collagen-induced arthritis. The sialadenitis in NOD.Q showed a similar histological phenotype as in NOD, whereas no submandibular gland infiltration was found in B10.Q. The development of sialadenitis was independent of immunization with type II collagen and established arthritis. To identify the genetic control of sialadenitis, a gene segregation experiment was performed on an (NOD.QxB10.Q)F2 cross and genetic mapping of 353 F2 mice revealed one significant locus associated with sialadenitis on chromosome 4, LOD score 4.7. The NOD.Q allele-mediated susceptibility under a recessive inheritance pattern. The genetic control of sialadenitis seemed to be unique in comparison to diabetes and arthritis, as no loci associated with these diseases have been identified at the same location.}},
author = {{Johansson, Åsa and Nakken, Britt and Sundler, Martin and Lindqvist, Anna-Karin and Johannesson, Martina and Alarcón-Riquelme, Marta and Bolstad, Anne Isine and Humphreys-Beher, Michael G and Jonsson, Roland and Skarstein, Kathrine and Holmdahl, Rikard}},
issn = {{1521-4141}},
keywords = {{Chromosomes; Female; Haplotypes; Histocompatibility Antigens Class II : immunology; Male; Mice; Mice Inbred C3H; Mice Inbred C57BL; Mice Inbred NOD; Phenotype; Sialadenitis : genetics : pathology : physiopathology; Support Non-U.S. Gov't; Submandibular Gland : pathology; Crosses Genetic; Chromosome Mapping; Arthritis Rheumatoid : chemically induced : genetics; Arthritis Experimental : chemically induced : genetics; Animal}},
language = {{eng}},
number = {{1}},
pages = {{243--250}},
publisher = {{John Wiley & Sons Inc.}},
series = {{European Journal of Immunology}},
title = {{The genetic control of sialadenitis versus arthritis in a NOD.QxB10.Q F2 cross.}},
url = {{http://dx.doi.org/10.1002/1521-4141(200201)32:1<243::AID-IMMU243>3.0.CO;2-X}},
doi = {{10.1002/1521-4141(200201)32:1<243::AID-IMMU243>3.0.CO;2-X}},
volume = {{32}},
year = {{2002}},
}