6533b821fe1ef96bd127b7ad
RESEARCH PRODUCT
Autoreactivity to mouse C1q in a murine model of SLE.
Markus MaeurerP. K. E. TrinderMichael LoosH. U. Schorlemmersubject
Systemic diseaseImmunologyArthritischemical and pharmacologic phenomenaEnzyme-Linked Immunosorbent Assayurologic and male genital diseasesmedicine.disease_causeAutoimmunityMiceRheumatologyimmune system diseasesImmunology and AllergyMedicineAnimalsLupus Erythematosus Systemicskin and connective tissue diseasesAutoantibodiesLupus erythematosusbusiness.industryComplement C1qAutoantibodyGlomerulonephritismedicine.diseaseConnective tissue diseaseLupus NephritisDisease Models AnimalImmunologybusinessAnti-SSA/Ro autoantibodiesdescription
A large proportion of systemic lupus erythematosus (SLE) patients develop glomerulonephritis, coincident with the appearance of autoantibodies to C1q, the Fc-recognizing collagen-like subcomponent of the first component of complement, C1. The MRL/lpr/lpr mouse is an established model for SLE, developing both antinuclear and anti-type II collagen autoantibodies, and rheumatoid factors(s), exhibiting reduced complement levels and later on developing glomerulonephritis and often arthritis. We report here an age-dependent decrease in serum C1q levels coincident with the development of IgG2b autoantibodies reactive with mouse C1q in MRL/lpr/lpr mice. Unlike IgG2b, although high levels of IgM, IgG1 and IgG2a are present in these mice, few, if any, antibodies of these subclasses reactive with mouse C1q were observed in this study. This is the first report of autoantibodies against autologous C1q in an animal model, and the results should facilitate in clarification of the roles of C1q and autoantibodies reactive with C1q in SLE, as well as their potential connection with glomerulonephritis.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 1995-09-01 | Rheumatology international |