The increased susceptibility to infections of neonates is caused by an immaturity of the immune system as a result of both qualitative and quantitative differences between neonatal and adult immune cells. With respect to B cells, neonatal antibody responses are known to be decreased. Accountable for this is an altered composition of the neonatal B cell compartment towards more immature B cells. However, it remains unclear whether the functionality of individual neonatal B cell subsets is altered as well. In the current study we therefore compared phenotypical and functional characteristics of corresponding neonatal and adult B cell subpopulations. No phenotypic differences could be identified with the exception of higher IgM expression in neonatal B cells. Functional analysis revealed differences in proliferation, survival, and B cell receptor signaling. Most importantly, neonatal B cells showed severely impaired class-switch recombination (CSR) to IgG and IgA. This was associated with increased expression of miR-181b in neonatal B cells. Deficiency of miR-181b resulted in increased CSR. With this, our results highlight intrinsic differences that contribute to weaker B cell antibody responses in newborns.
- Glaesener, S.
- Jaenke, C.
- Habener, A.
- Geffers, R.
- Hagendorff, P.
- Witzlau, K.
- Imelmann, E.
- Krueger, A.
- Meyer-Bahlburg, A.
Keywords
- Animals
- B-Lymphocytes/*immunology
- Enzyme-Linked Immunosorbent Assay
- Flow Cytometry
- Humans
- Immunoglobulin Class Switching/*immunology
- Infant, Newborn
- Mice
- Mice, Inbred C57BL
- MicroRNAs/*genetics