| First Author | Krug HE | Year | 1989 |
| Journal | Clin Exp Immunol | Volume | 78 |
| Issue | 1 | Pages | 97-101 |
| PubMed ID | 2805429 | Mgi Jnum | J:109935 |
| Mgi Id | MGI:3630111 | Citation | Krug HE, et al. (1989) Progressive ankylosis (ank/ank) in mice: an animal model of spondyloarthropathy. III. Proliferative spleen cell response to T cell mitogens. Clin Exp Immunol 78(1):97-101 |
| abstractText | Murine progressive ankylosis is a spontaneous disorder of mice resulting from a homozygous recessive genetic defect (ank/ank) which produces an inflammatory arthritis of peripheral and axial joints eventually resulting in ankylosis of these joints. This disorder resembles the human spondyloarthropathies clinically, radiographically and histologically. Various studies in humans with spondyloarthropathies have described defects of cellular immunity but these results are conflicting. We measured the spleen cell response to mitogen in ank/ank mice and in normal littermates. The spleen cell response to the T cell mitogens phytohaemagglutinin and concanavalin A was decreased in ank/ank mice compared with their normal littermates. The response to the B cell mitogen lypopolysaccharide was normal in both ank/ank mice and normal littermates. Serum from ank/ank mice did not inhibit spleen cell responses to mitogen. Ank/ank spleen cells were not inhibitory of normal spleen cell responses to mitogens. Addition of irradiated normal spleen cells to ank/ank spleen cells did not restore the mitogen responses to normal. It is possible that the ank/ank gene results in the phenotypic expression of an abnormal or decreased cell product involved in T cell proliferation. Several recently described cytokines could be potential candidates for this product. |
