The findings support the view that asymptomatic synovitis precedes clinically manifest arthritis in both early and established RA. This implies that the debut of RA already represents a chronic phase of the disease.

It is speculated that the autoimmune response to type II collagen (CII) is a driving force in the pathogenesis of human rheumatoid arthritis (RA). In this report, we describe the relationship between the induction of collagen arthritis and the CII‐specific humoral, as well as cellular, immune response in rhesus monkeys. Ten of 14 monkeys immunized with bovine type II collagen (B‐CII) developed polyarthritis. Susceptible animals showed a T cell response to B‐CII; resistant animals did not. After the primary immunization, the humoral response to B‐CII, as well as to rhesus monkey type II collagen, was dominated by antibodies of the IgM isotype in the susceptible animals and by antibodies of the IgG isotype in the resistant animals. Because of the close phylogenic relationship between the rhesus monkey and humans, these data contribute valuable information about the role of CII‐specific immunity in the pathogenesis of human RA.

No abstract

The ABO blood group system is known to act as a major transplantation barrier in primates. Different primate species share the presence of A and B antigens. The polymorphism of the macaque ABO blood group genes was analyzed by cloning and sequencing the exon 7 region. In the case of the rhesus macaque (Macaca mulatto) and cynomolgus monkey (Macaca fascicularis) we were able to identify ABO blood group gene segments which cluster into two lineages, namely: *A/*O1 and *B. In addition allelic variation was observed. The 2 amino acid replacements at positions 266 and 268, which are thought to be crucial for A or B transferase activity, could be confirmed for both macaque species. Comparison of primate sequences shows that A and B reactivity was generated independently from each other in the hominoids and Old World monkey lineages. Hence, the primate A and B blood group genes are subject to convergent evolution.

The availability of highly specific and homogeneous antibodies to human T cells by the hybridoma technique has elicited new interest in the clinical use of antibodies to lymphocytes as immunosuppressive agents. OKT3 is the murine monoclonal antibody that has been the most widely used in clinical transplantation to induce immunosuppression. This antibody recognizes a membrane molecular complex, exclusively present on mature human T lymphocytes, which is tightly linked to the T-cell antigen receptor. The long-term therapeutic use of murine monoclonal antibodies in vivo is hampered by the intense antibody response that occurs in most human patients. Thus, when administered alone, OKT3 manifests its immunosuppressive activity only during the 10 to 15 days that precede the onset of sensitization. The results presented here show, by use of isoelectrofocusing, that the antibody response to OKT3, already reported to be restricted in its specificity (only anti-isotypic and anti-idiotypic antibodies are produced), is in addition oligoclonal. This restriction of the anti-monoclonal response may suggest that an efficient way to circumvent the sensitization problem would be to administer consecutively different monoclonal antibodies presenting the same specificity but distinct idiotypes.