SFA-1 PETA3 (CD151), A MEMBER OF THE TRANSMEMBRANE-4-SUPERFAMILY, ASSOCIATES PREFERENTIALLY WITH ALPHA(5)BETA(1) INTEGRIN AND REGULATES ADHESION OF HUMAN T-CELL LEUKEMIA-VIRUS TYPE-1-INFECTED T-CELLS TO FIBRONECTIN/

Citation
H. Hasegawa et al., SFA-1 PETA3 (CD151), A MEMBER OF THE TRANSMEMBRANE-4-SUPERFAMILY, ASSOCIATES PREFERENTIALLY WITH ALPHA(5)BETA(1) INTEGRIN AND REGULATES ADHESION OF HUMAN T-CELL LEUKEMIA-VIRUS TYPE-1-INFECTED T-CELLS TO FIBRONECTIN/, The Journal of immunology (1950), 161(6), 1998, pp. 3087-3095
Citations number
66
Categorie Soggetti
Immunology
ISSN journal
00221767
Volume
161
Issue
6
Year of publication
1998
Pages
3087 - 3095
Database
ISI
SICI code
0022-1767(1998)161:6<3087:SP(AMO>2.0.ZU;2-V
Abstract
In this study we have analyzed the adhesion molecules associated with and the biologic function of SFA-1/PETA-3 (CD151) in human T cell leuk emia virus type 1 (HTLV-1)-infected T cells and in freshly isolated ad ult T cell leukemia (ATL) cells using an anti-CD151 mAb. The anti-CD15 1 mAb coprecipitated alpha(5)beta(1) integrin from HTLV-1-infected T c ells. Conversely, an anti-alpha(5) integrin mAb coprecipitated CD151. The anti-CD151 mAb inhibited the adhesion of HTLV-1-infected T cells t o fibronectin but did not have any effect on their adhesion to laminin , collagen type I, or collagen type IV. Moreover, antisense CD151 olig onucleotide-treated HTLV-1-infected T cells showed significant inhibit ion of adhesion to fibronectin, These findings showed that the CD151 m olecule was associated with the alpha(5)beta(1) integrin molecule and that it enhanced alpha(5)beta(1) integrin-mediated adhesion to fibrone ctin. In addition, the expression levels of CD151, alpha(4)beta(1) int egrin, and alpha(5)beta(1) integrin on ATL cells from lymph nodes of l ymphoma-type ATL patients were significantly higher than those on circ ulating ATL cells from leukemia-type ATL patients. This suggests that the increased expression of these integrins may contribute to lymphoma formation through the adhesion of ATL cells to the extracellular matr ix and dendritic cells, rather than contributing to transmigration.