For years, researchers and physicians have known that infants' immune systems do not respond well to certain vaccines, thus the need for additional boosters as children develop. Now, in a new study from the
Habib Zaghouani, a professor of molecular microbiology and immunology and child health at the MU
Zaghouani found that while the antigen would prompt a response of the immune system, it was not the expected response. In the adult immune system, two major types of cells, known as T-helper 1 (Th-1) and T-helper 2 (Th-2) cells, are instrumental in the development of an effective immune response. Typically, Th-1 cells respond when dangerous microbes enter the body. The Th-1 cells then work to help destroy the foreign microbes. When an antigen from a vaccine enters a body with a mature immune system, Th-1 cells respond and, after destroying the invader, the Th-1 cells "remember" how to fight the antigen for future battles. Th-2 cells typically develop when the body is exposed to allergens. The responses of Th-2 cells are usually strong and manifest in the form of allergic reactions.
When Zaghouani gave the newborn mice an antigen shortly after birth, he noticed the presence of both Th-1 and Th-2 cells. However, when he gave the antigen a second time, he noticed an abundance of Th-2 cells that responded to the antigen instead of Th-1 cells. Zaghouani was surprised to notice that the Th-2 cells worked to destroy the small contingent of Th-1 cells that had responded to the antigen given at birth.
"Perhaps we should test vaccines at a very early age in animals to establish a regimen with the most effectiveness," Zaghouani said.
When a baby first gets an infection, the immature immune system responds with both types of T cells. Unfortunately, Th-1 cells have an unusual receptor that binds to a specific hormone, which is deadly to the Th-1 cells. Ironically, this particular hormone is produced by the Th-2 cells. This results in an overabundance of Th-2 cells during the first few days of life.
"We found that after six days, the immune systems in the mice matured enough to stop the death of the Th-1 cells," Zaghouani said. "After those initial days, the immune system is producing Th-1 cells with diminished hormonal receptors, thus surviving the effect of the compound that the Th-2 cells make."
Zaghouani's paper, "Delayed maturation of an IL-12-producing dendritic cell subset explains the early Th2 bias in neonatal immunity," was published in the Journal of Experimental Medicine.