SWR/J mice are resistant to collagen-induced arthritis (CIA) despite having a susceptible H-2(q) haplotype. We have earlier demonstrated the possible role of the V(β) TCR mutation of SWR in the resistance to CIA. To investigate the influence of the C5 deficiency of SWR in this resistance, crosses were made between SWR and A/J (C5 deficient, TCR(wild), H-2a), and between SWR and C3H.A (C5 sufficient, TCR(wild), H-2a). Upon immunization with bovine type II collagen in adjuvant, there was a similar incidence and severity of arthritis in H-2(q)-bearing mice in the backcrosses A x (SWR x A) and C3H.A x (SWR x C3H.A). The absence of hemolytic complement was confirmed in the arthritic A x (SWR x A) back-cross mice by standard SRBC hemolytic assays. In addition C57L (H-2b) mice, which were C5 sufficient but had a V(β) TCR deletion mutation similar to SWR, could not complement for CIA susceptibility in H-2(q)-bearing C57L x (SWR x C57L) back-crosses and in (C57L x SWR)F2 hybrids. These studies show that complement C5 does not play a significant role in CIA susceptibility, and further implicate the V(β) TCR mutation in the resistance to CIA in SWR mice.
|Original language||English (US)|
|Number of pages||7|
|Journal||Journal of Immunology|
|State||Published - Jan 1 1989|
ASJC Scopus subject areas
- Immunology and Allergy