The mouse tumor cell lines EL4 and RMA display mosaic expression of NK-related and certain other surface molecules and appear to have a common origin

Citation
F. Gays et al., The mouse tumor cell lines EL4 and RMA display mosaic expression of NK-related and certain other surface molecules and appear to have a common origin, J IMMUNOL, 164(10), 2000, pp. 5094-5102
Citations number
81
Categorie Soggetti
Immunology
Journal title
JOURNAL OF IMMUNOLOGY
ISSN journal
00221767 → ACNP
Volume
164
Issue
10
Year of publication
2000
Pages
5094 - 5102
Database
ISI
SICI code
0022-1767(20000515)164:10<5094:TMTCLE>2.0.ZU;2-T
Abstract
As a potential means for facilitating studies of NK cell-related molecules, we examined the expression of these molecules on a range of mouse tumor ce ll lines. Of the lines we initially examined, only EL4 and RMA expressed su ch molecules, both lines expressing several members of the Ly49 and NKRP1 f amilies. Unexpectedly, several of the NK-related molecules, together with c ertain other molecules including CD2, CD3, CD4, CD32, and CD44, were often expressed in a mosaic manner, even on freshly derived clones, indicating fr equent switching in expression. In each case examined, switching was contro lled at the mRNA level, with expression of CD3 zeta determining expression of the entire CD3-TCR complex. Each of the variable molecules was expressed independently, with the exception that CD3 was restricted to cells that al so expressed CD2, Treatment with drugs that affect DNA methylation and hist one acetylation could augment the expression of at least some of the variab le molecules. The striking phenotypic similarity between EL4 and RMA led us to examine the state of their TCR beta genes. Both lines had identical rea rrangements on both chromosomes, indicating that RMA is in fact a subline o f EL4. Overall, these findings suggest that EL4 is an NK-T cell tumor that may have retained a genetic mechanism that permits the variable expression of a restricted group of molecules involved in recognition and signaling.