Abstract

To the Editor: We read with high interest the recent article titled ‘Age-matched reference values for B-cell subpopulation and CVID classifications in children’ by Schatorjé and colleagues [1]. The authors studied the expression of TACI and BAFF-R in both newborn and infant age groups starting from cord blood. In this sudy, they reported that while the percentage of BAFF-R+ B cells do not change during the first year of life, TACI+ B cell percentage showed an age-dependent increase. In accordance with these human studies by Schatorjé and colleagues, we found that murine newborn B cells also had low percentage of TACI+ B cells while BAFF-R and BCMA expressing B cell percentages were comparable to those of adult mice [2]. We have analyzed the expression and function of BAFF system molecules in newborn mice because newborns of mice and humans share several aspects of their hematopoietic development and function. For example both human and mice newborns do not respond to T cell-independent type 2 (TI-2) antigens such as bacterial polysaccharide vaccines [3]. In addition to low TACI expression in newborn mice [2], we also showed that low B cell TACI expression correlated with impaired immunoglobulin secretion, plasma cell generation and proliferation of B cells in response to either BAFF or APRIL stimulation in this age group. These results provided a rational explanation for the weak immunogenicity of TI-2 antigens in newborns because we could render the TI-2 antigen NP-Ficoll immunogenic in newborns by using the adjuvant CpG that increases TACI expression [4]. Finally as with CVID patients with TACI mutations, we found that BAFF levels were increased in newborn mice and in TACI knock-out mice, further supporting a role for TACI in modulating BAFF expression. Thus, the demonstration of low TACI expression in human infants reported by Schatorjé and colleagues signifies yet another similarity between mice and human immune system and underscores the relevance of studies on the BAFF system components conducted in mice as organismal models.

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