Mouse strains B10, B10.RIII, RIIIS/J and the F1 and backcross progeny arising from them were tested for susceptibility to porcine type II collagen-induced arthritis (PII-CIA). The clinically severe arthritis of rapid onset that is characteristic of PII-immunized B10.RIII mice developed predominantly in hybrid offspring that had inherited at least one copy of wild type T cell receptor (TCR) genes (V beta b genotype) from the B10 or B10.RIII parent. The results indicate that, in the development of PII-CIA, mice expressing the H-2r/r haplotype preferentially utilize TCR V beta genes that are normally encoded within the TCR V beta genomic deletion region of RIIIS mice (V beta c). After aggressive immunization with PII, the use of alternative TCR V beta genes, encoded outside of the RIIIS deletion region, produced a high IgG antibody response that was cross-reactive with mouse type II collagen (MII) and equivalent to that of B10.RIII mice, but only a very mild, late onset arthritis of 56% (27/48) incidence in RIIIS male mice and 28% (10/35) incidence in RIIIS female mice. In comparison, B10.RIII mice routinely developed early onset of PII-CIA of significantly higher incidence (100%; p < 0.005) and four-fold greater severity, even after milder immunization protocols. The data are compatible with the proposal that the clinically weak CIA response of RIIIs mice may be primarily antibody driven while the severe CIA of B10.RIII mice reflects the added inflammatory effects of collagen-reactive effector-T cells in the joint.(ABSTRACT TRUNCATED AT 250 WORDS)

A total of 29 rheumatoid patients and 19 nonrheumatoid patients were tested for evidence of present or past infection b y M pneumoniae, M hominis, M fermentam, M arthritidis, M pulmonis, and M hyorhinis. T h e techniques of lymphocyte transformation, metabolic-inhibiting antibody test, and mycoplasmacidal antibody test indicated no significant difference in the response of rheumatoid as opposed to nonrheumatoid patients.Although a wide variety of immunologic processes are apparent within the joints of patients exhibiting rheumatoid arthritis (RA), the nature of the initiating agent or event appears elusive. An infectious etiology for human rheumatoid arthritis remains an attractive hypothesis despite numerous conflicting and inconclusive results on the isolation of an agent.