Follicular Th (T FH) cells have emerged as a new Th subset providing help to B cells and supporting their differentiation into long-lived plasma cells or memory B cells. Their differentiation had not yet been investigated following neonatal immunization, which elicits delayed and limited germinal center (GC) responses. We demonstrate that neonatal immunization induces CXCR5 high PD-1 high CD4+ T FH cells that exhibit T FH features (including Batf, Bcl6, c-Maf, ICOS, and IL-21 expression) and are able to migrate into the GCs. However, neonatal T FH cells fail to expand and to acquire a full-blown GC T FH phenotype, as reflected by a higher ratio of GC T FH/non-GC CD4+ T cells in immunized adults than neonates (3.8× 10− 3 versus 2.2× 10− 3, p= 0.01). Following the adoptive transfer of naive adult OT-II CD4+ T cells, OT-II T FH cells expand in the vaccine-draining lymph nodes of immunized adult but not infant recipients, whereas naive 2-wk-old CD4+ OT-II cells failed to expand in adult hosts, reflecting the influence of both environmental and T cell–intrinsic factors. Postponing immunization to later in life increases the number of T FH cells in a stepwise manner, in direct correlation with the numbers of GC B cells and plasma cells elicited. Remarkably, adjuvantation with CpG oligonucleotides markedly increased GC T FH and GC B cell neonatal responses, up to adult levels. To our knowledge, this is the first demonstration that the T FH cell development limits early life GC responses and that adjuvants/delivery systems supporting T FH differentiation may restore adultlike early life GC B cell responses.