Author/Authors :
Koike، نويسنده , , Ryuji and Watanabe، نويسنده , , Toshiki and Satoh، نويسنده , , Hitoshi and Hee، نويسنده , , Choi Soon and Kitada، نويسنده , , Kazuhiro and Kuramoto، نويسنده , , Takashi and Serikawa، نويسنده , , Tadao and Miyawaki، نويسنده , , Shigeki and Miyasaka، نويسنده , , Masayuki، نويسنده ,
Abstract :
Thealy,alymphoplasia, is an autosomal recessive mutation in mice of an unknown etiology, which induces total aplasia of lymph nodes and Peyerʹs patches. We hypothesized that the lack of lymphoid tissue may be due to abnormalities of lymphocyte traffic into these tissues. Therefore, we analyzed the expression of various adhesion molecules associated with lymphocyte homing. Among the adhesion molecules examined, all were normally expressed except the mucosal addressin MAdCAM-1. Inaly/alymice MAdCAM-1 was absent in the spleen at mRNA and protein levels, but was normally expressed in the intestinal venules. The FISH analysis and linkage analysis using microsatellite markers demonstrated that the MAdCAM-1 gene is located on chromosome 10, indicating that MAdCAM-1 is not encoded by thealygene, which is located on chromosome 11. Our results indicate that the aberrant expression of MAdCAM-1 is not the direct cause ofalymutation but rather a secondary defect.