Study Clarifies Source of Lymph Node Swelling in Infections

Contrary to popular belief, lymph nodes swell due to recruitment of lymphocytes that are not specific for any given microbe, according to a report by Yale School of Medicine researchers in this week’s Proceedings of the National Academy of Sciences.

“It had been assumed that lymph nodes swell a few days following infection due to activation of lymphocytes specific for a given microbe, which multiply and make the lymph nodes expand in size,” said Akiko Iwasaki, assistant professor of the Section of Immunobiology. “The results from our study show this is not the case. The lymph nodes swell due to recruitment of non-specific naïve lymphocytes.”

She said the study by her and her colleagues show that a large number of naïve lymphocytes are targeted to migrate into the lymph nodes, draining the sites of infection, because of changes in the arteriole supplying blood to that lymph node. The arteriole, which is a small artery, remodels itself into a much larger tube. This remodeling of the arteriole is initiated by the innate immune signals associated with the infection.

The reason why the body accumulates non-specific naïve lymphocytes into the lymph node is because this process increases the efficiency for screening for the lymphocytes that recognize the microbe, Iwasaki said.

“The immune system is designed so that only one to 10 in a million lymphocytes react to a specific antigen of a virus or bacteria,” Iwasaki said. “If we relied on the lymphocytes that are normally circulating through a lymph node, it may take several days to find the lymphocytes with the correct specificity. By this time, the host animal, or human, will have succumbed to a full-fledged infection.”

She said by supplying a large number of lymphocytes, the lymph node effectively screens for the correct lymphocytes in order to initiate their activation and multiplication to combat the infection as quickly as possible.

Co-authors include Kelly Soderberg, Geoffrey Payne, Ayuko Sato, Ruslan Medzhitov, and Steven Segal.

PNAS: October 24, 2005