Acquired resistance to type II collagen‐induced arthritis in rhesus monkeys is reflected by a T cell low‐responsiveness to the antigen

• Published in: Clinical and experimental immunology 1991-11, Vol.86 (2), p.219-223
• Main Authors: BAKKER, N. P. M., ERCK, M. G. M., HART, L. A. T, JONKER, M.
• Format: Article
• Language: English
• Subjects: AIDS/HIV; Animals; Arthritis, Experimental - immunology; Biological and medical sciences; CD4-CD8 Ratio; Collagen - immunology; collagen‐induced arthritis; Diseases of the osteoarticular system; IL‐2; Inflammatory joint diseases; Interleukin-2 - pharmacology; Lymphocyte Activation; Macaca mulatta; Medical sciences; Receptors, Interleukin-2 - analysis; Recombinant Proteins; rhesus monkey; T cell low‐responsiveness; T-Lymphocyte Subsets - immunology; T-Lymphocytes - immunology
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1111/j.1365-2249.1991.tb05799.x

SUMMARY Ten out of 14 rhesus monkeys developed arthritis after a single immunization with bovine type II collagen (B‐CII). In contrast to primary resistant monkeys, arthritic animals showed a B‐CII specific T cell proliferation during the induction phase of the disease. All surviving animals showed a full remission of the disease. Two monkeys acquired resistance to collagen‐induced arthritis (CIA) after one period of disease, but in three animals a booster immunization with B‐CII induced a slight flare‐up. It is demonstrated that B‐CII immunized rhesus monkeys have the capacity to restore resistance to CIA. The development of resistance to CIA is reflected by a decreased T cell responsiveness to B‐CII, It is shown that the lack of IL‐2 plays a role in B‐CII‐induced T cell low‐responsiveness. A potential role of CD8+ T cells in the down regulation of the T cell response to B‐CIl is discussed.