"This study helped explain why patients who have mutations in STAT3 can't generate an effective secondary response to infection," said Associate Professor Tangye.
"STAT 3 directly affects the creation of memory cells, and so while these patients have a few, they are reduced tenfold."
"When people mount a normal primary or secondary immune response, various messenger molecules known as 'cytokines' bind to receptors on the cell surface and activate STAT3."
"Many structurally different cytokines, with complementary roles in antibody production, converge at STAT3 it's literally like a roundabout, showing cytokines which route to take next within the cell."
"This study has shown us that memory cells are much more sensitive to the cytokine signals they receive. They are more robust and efficient, and the magnitude of their response is much greater than that of nave cells."
"B cells fundamentally change their biology between the nave state and the memory state. STAT3 appears to be the key to this molecular rewiring because without it, memory cells cannot form properly."
"These findings explain a lot to me about how immunological memory works, and also throw more light on Hyper IgE Syndrome. They also tell us that if you want to improve antibody responses, there are certain pathways and cell types that can be targeted."
"We can see the future potential to amplify the potency of vaccines, as well as help Hyper IgE patients."
|Contact: Alison Heather|
Garvan Institute of Medical Research