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| Content Provider | Springer Nature Link |
|---|---|
| Author | Matsuura, A. Takayama, Shinichi Kinebuchi, Miyuki Hashimoto, Yuji Kasai, Kiyoshi Kozutsumi, Daisuke Ichimiya, Shingo Honda, Ryoichi Natori, Takashi Kikuchi, Kokichi |
| Copyright Year | 1997 |
| Abstract | CD1 and TL were once thought to be genetic homologues because of their thymus-specific expression. We investigated their equivalents in the rat to clarify whether their structure and pattern of expression are conserved in rodents. Two rat class Ib genes, containing 3′ sequences very similar to mouse TL, were identified and designated RT1.P. Neither of them, however, can encode ordinary class I molecules due to the accumulation of harmful mutations in the 5′ regions that are unique to RT1.P, while the 3′TL-like regions still retain protein-coding capacity. Comparison of the structural organization of three types of TL family genes, which include mouse T3/T18-encoding TL antigens, mouse T1/T16, and rat RT1.P1/P2 pseudogenes, revealed the presence of a clear demarcation between the type-specific and TL-specific sequences at intron 3. This finding suggests that recombination plays an important role in creating the TL family genes in rodents. Characteristic features of TL, such as a low level of polymorphism and linkage to the major histocompatibility complex, were also observed in the rat. On the other hand, rat CD1 molecules were expressed at a high level on the surface of thymocytes. Absence of authentic TL antigens and thymic expression of CD1d molecules in the rat suggest the plasticity and conservation of class Ib genes in rodent evolution. Functions of TL may be substituted with CD1 or other class Ib molecules expressed by rat thymus. |
| Starting Page | 293 |
| Ending Page | 306 |
| Page Count | 14 |
| File Format | |
| ISSN | 00937711 |
| Journal | Immunogenetics |
| Volume Number | 46 |
| Issue Number | 4 |
| e-ISSN | 14321211 |
| Language | English |
| Publisher | Springer-Verlag |
| Publisher Date | 1997-07-22 |
| Publisher Place | Berlin, Heidelberg |
| Access Restriction | One Nation One Subscription (ONOS) |
| Content Type | Text |
| Resource Type | Article |
| Subject | Genetics Immunology |
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