A New Paradigm in Immune Surveillance

Courtesy of Adelheid Cerwenka and Lewis Lanier © 2003 Blackwell Publishing  DIFFERENT MAMMALS, SAME ESCAPE ACT: Human and murine cytomegalovirus have developed strategies to escape from NK-cell attack. HMCV (a) produces UL16, which can sequester some, but not all, NKG2D-ligands inside the infected cell. MCMV (b) produces the protein gp40, capable of sequestering RAE-1 molecules, but not H60. In mice, NKG2D exists in two alternatively spliced isoforms capable of binding different adapt

Linda Schultz
Sep 21, 2003
Courtesy of Adelheid Cerwenka and Lewis Lanier © 2003 Blackwell Publishing
 DIFFERENT MAMMALS, SAME ESCAPE ACT: Human and murine cytomegalovirus have developed strategies to escape from NK-cell attack. HMCV (a) produces UL16, which can sequester some, but not all, NKG2D-ligands inside the infected cell. MCMV (b) produces the protein gp40, capable of sequestering RAE-1 molecules, but not H60. In mice, NKG2D exists in two alternatively spliced isoforms capable of binding different adapters: DAP12 and DAP10. No evidence has yet suggested alternate forms of human NKG2D.

Researchers have long tried to understand how natural killer (NK) cells, the body's first line of defense against infection, recognize sick cells, such as those virally infected or transformed. In 1999, investigators found the ligands for an activating NK receptor, NKG2D. These ligands, called MICA and MICB, are expressed endogenously when cells are under stress, infected, or turning into tumors. In a form of assisted...

Interested in reading more?

Magaizne Cover

Become a Member of

Receive full access to digital editions of The Scientist, as well as TS Digest, feature stories, more than 35 years of archives, and much more!
Already a member?