Home Other Sections Medical News How B Lymphocytes Prevents Preterm Birth?

How B Lymphocytes Prevents Preterm Birth?

217

How B Lymphocytes Prevents Preterm Birth?A recent study uncovers the important role of a type of mother’s immune cells called B lymphocytes   in resisting preterm birth triggered by inflammation. The study was conducted under the leadership of Kang Chen, Ph.D., assistant professor at Wayne State University.

Preterm birth can be defined as child birth before normal 37 weeks of pregnancy which affects up to one in every six births in the United States and many other countries. It is the primary cause of infant death and long-term illnesses and enforces heavy social and economic burdens. Even though preterm birth is a difficult condition, infection of the mother and resulting inflammation in pregnancy are very familiar causes.

Role of B lymphocytes

As per Chen, B lymphocytes produce antibodies to protect the body against infections, but scientists and clinicians have always considered that these cells are uncommon or absent in the uterine lining and not significant for pregnancy.

Chen’s lab found that in late pregnancy, mothers’ B lymphocytes not only exist in the uterine lining in both humans and mice, but also sense inflammation and uterine stress, which are main causes of preterm birth, and consecutively, make molecules such as PIBF1, inhibit uterine inflammation and premature birth.

“This research not only describes the long-neglected role of B lymphocytes in supporting healthy pregnancy, but also promotes therapeutic approaches of utilizing B lymphocyte-derived molecules like PIBF1 to avoid or treat preterm birth,” explained Chen.

Chen’s team has conducted proof-of-concept and efficiency studies in animal models, and with the support of the Wayne State University’s Technology Commercialization Office, applied for a patent for this potential therapeutic approach.

For more fascinating research news, visit our website frequently. Subscribe to our newsletter; we bring the latest news to your inbox.