The immune system in a sticky situation

     
   

Neutrophils, critical cells of the early immune response, travel quickly through the bloodstream to sites of infection to engulf and kill bacteria. If genetic defects slow down this neutrophil migration, more severe infections may result.

School of Medicine researchers have now identified a key gene that regulates neutrophil movement through the body, which may clarify why some individuals are more susceptible to infection and inflammation.

A team led by Richard A. Flavell, Ph.D., Sterling Professor and chair of Immunobiology and Howard Hughes investigator, reports in the October 6 issue of Science that mice lacking the gene Myo1f have neutrophils that adhere more readily to their surroundings and are therefore markedly slower in reaching sites of infection.

Myo1f, not previously known to play a role in immunity, limits the number of proteins known as integrins on the cell surface. In the gene’s absence, more integrins are released, making neutrophils more sluggish. “Without Myo1f, immune cells get too sticky and cannot move fast,” says first author Sang-won V. Kim, Ph.D., now at Memorial Sloan-Kettering Cancer Center. “So the host becomes vulnerable to acute infection.”


 

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