Chronic Arthritis in Rats; Pathogenesis and genetic factors

Research output: ThesisDoctoral Thesis (compilation)

Standard

Chronic Arthritis in Rats; Pathogenesis and genetic factors. / Vingsbo Lundberg, Carina.

Center for Molecular Biomedicine, Lund University, 1997. 142 p.

Research output: ThesisDoctoral Thesis (compilation)

Harvard

Vingsbo Lundberg, C 1997, 'Chronic Arthritis in Rats; Pathogenesis and genetic factors', Doctor, Immunology.

APA

Vingsbo Lundberg, C. (1997). Chronic Arthritis in Rats; Pathogenesis and genetic factors. Center for Molecular Biomedicine, Lund University.

CBE

Vingsbo Lundberg C. 1997. Chronic Arthritis in Rats; Pathogenesis and genetic factors. Center for Molecular Biomedicine, Lund University. 142 p.

MLA

Vingsbo Lundberg, Carina Chronic Arthritis in Rats; Pathogenesis and genetic factors Center for Molecular Biomedicine, Lund University. 1997.

Vancouver

Vingsbo Lundberg C. Chronic Arthritis in Rats; Pathogenesis and genetic factors. Center for Molecular Biomedicine, Lund University, 1997. 142 p.

Author

Vingsbo Lundberg, Carina. / Chronic Arthritis in Rats; Pathogenesis and genetic factors. Center for Molecular Biomedicine, Lund University, 1997. 142 p.

RIS

TY - THES

T1 - Chronic Arthritis in Rats; Pathogenesis and genetic factors

AU - Vingsbo Lundberg, Carina

N1 - Defence details Date: 1997-11-08 Time: 10:15 Place: Hörsal A, Kemicentum, Lund External reviewer(s) Name: Emmrich, Frank Title: [unknown] Affiliation: [unknown] --- 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)

PY - 1997

Y1 - 1997

N2 - The immune pathology and MHC association of chronic arthritis was studied in three rat models for reumatoid arthritis (RA). Susceptible rat strains develop a T cell dependent chronic disease after immunization with rat collagen type II (CII). The LEW rat does not develop arthritis after immunization with rat CII, but a heterologous immune response to pepsin can break the tolerance to CII and render it susceptible to collagen induced arthritis (CIA). DA rats are protected against CIA if pre-treated with denatured CII or native CII in a non arthritogenic fashion. This was associated with a poor B cell response but a normal T cell response compared to that of CIA, suggesting that B cells specific for conformational epitopes on the CII molecule are essential for the development of chronic CIA. The non-immunogenic adjuvants, avridine and pristane induced chronic T cell dependent arthritis in rats. CIA, AvIA and PIA had a similar MHC association, with RT1a and RT1f being the most susceptible haplotypes. In AvIA and PIA, the MHC mainly influenced the chronicity of arthritis. The genetic control of the PIA model, apart from the MHC association (pia1), was further analyzed in a cross between E3 and DA. A total genome scan of the F2 progeny revealed an additional loci; pia2 on chromosome 12 and two suggestive loci pia3 on chromosome 6 and pia4 on chromosome 11. Pia2 and pia4 were also associated with an a1-acid glycoprotein production and an IgG2b and rheumatoid factor response, whereas pia3 was associated with a fibronectin and IL-6 response.

AB - The immune pathology and MHC association of chronic arthritis was studied in three rat models for reumatoid arthritis (RA). Susceptible rat strains develop a T cell dependent chronic disease after immunization with rat collagen type II (CII). The LEW rat does not develop arthritis after immunization with rat CII, but a heterologous immune response to pepsin can break the tolerance to CII and render it susceptible to collagen induced arthritis (CIA). DA rats are protected against CIA if pre-treated with denatured CII or native CII in a non arthritogenic fashion. This was associated with a poor B cell response but a normal T cell response compared to that of CIA, suggesting that B cells specific for conformational epitopes on the CII molecule are essential for the development of chronic CIA. The non-immunogenic adjuvants, avridine and pristane induced chronic T cell dependent arthritis in rats. CIA, AvIA and PIA had a similar MHC association, with RT1a and RT1f being the most susceptible haplotypes. In AvIA and PIA, the MHC mainly influenced the chronicity of arthritis. The genetic control of the PIA model, apart from the MHC association (pia1), was further analyzed in a cross between E3 and DA. A total genome scan of the F2 progeny revealed an additional loci; pia2 on chromosome 12 and two suggestive loci pia3 on chromosome 6 and pia4 on chromosome 11. Pia2 and pia4 were also associated with an a1-acid glycoprotein production and an IgG2b and rheumatoid factor response, whereas pia3 was associated with a fibronectin and IL-6 response.

KW - rheumatology locomotion

KW - muscle system

KW - Skeleton

KW - autoimmunity/inflammation/adjuvans/MHC association

KW - Skelett

KW - muskelsystem

KW - reumatologi

M3 - Doctoral Thesis (compilation)

SN - 91-628-2715-4

PB - Center for Molecular Biomedicine, Lund University

ER -