While humans and other vertebrates do not produce chitin, the human body is equipped to recognize and eliminate it. A new study by researchers at University of California indicates that a less active form of AMCase might allow our adaptive, or learned, immune system to recruit too many cells in its attempt to rid the body of chitin, eventually inflaming airways and setting off asthma. A team led by Locksley, an immunologist at the University of California San Francisco, observed an important difference from the standard process for eliminating a foreign particle, however, when they observed activation of AMCase. The lungs produce AMCase in response to the presence of IL-4 and IL-13 following exposure to chitin. The researchers found that when mice have more AMCase than normal, the immune response to chitin is greatly reduced. They also observed a dampened immune response when they exposed chitin to AMCase before the animals inhaled it. Locksley believes his study points to the importance of chitin exposure and a plausible explanation for the role of AMCase in the development of asthma.