The study explains why treatments for many autoimmune and inflammatory diseases raise the risk of contracting TB—and also upends long-held assumptions about what kicks off an immune response.
New findings describe how the enzyme CST is recruited to the end of the telomere, where it maintains telomere length with the help of subtle chemical changes made to the protein POT1.
The end replication problem dictates that telomeres shrink unless telomerase intervenes. But the problem is actually twice as complicated, with telomerase providing only part of the solution.
The absence of a single immune cell receptor has been linked to both fewer defenses against mycobacterial infections, such as TB, and damaging buildup of sticky residue in the lungs.
