{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gustafson CE"],"funding":["NICHD NIH HHS","NCATS NIH HHS","NIAID NIH HHS"],"pagination":["467-77"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3959635"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(3)"],"pubmed_abstract":["The absence of immunoglobulin A (IgA) in the intestinal tract renders young infants highly susceptible to enteric infections. However, mediators of initial IgA induction in this population are undefined. We determined the temporal acquisition of plasma cells by isotype and expression of T cell-independent (TI) and -dependent (TD) IgA class switch factors in the human intestinal tract during early infancy. We found that IgA plasma cells were largely absent in the infant intestine until after 1 month of age, approaching adult densities later in infancy than both IgM and IgG. The restricted development of IgA plasma cells in the first month was accompanied by reduced expression of the TI factor a proliferation-inducing ligand (APRIL) and its receptors TACI (transmembrane activator and calcium-modulator and cyclophilin ligand interactor) and B cell maturation antigen (BCMA) within isolated lymphoid follicles (ILFs). Moreover, both APRIL and BCMA expression strongly correlated with increasing IgA plasma cell densities over time. Conversely, TD mediators (CD40 ligand (CD40L) and CD40) were expressed within ILFs before 1 month and were not associated with IgA plasma cell generation. In addition, preterm infants had lower densities of IgA plasma cells and reduced APRIL expression compared with full-term infants. Thus, blunted TI responses may contribute to the delayed induction of intestinal IgA during early human infancy."],"journal":["Mucosal immunology"],"pubmed_title":["Limited expression of APRIL and its receptors prior to intestinal IgA plasma cell development during human infancy."],"pmcid":["PMC3959635"],"funding_grant_id":["R01 HD059527","R21 AI083615","R21AI083615","R01 AI097265","T32 AI052066","TL1 TR000155","TL1 TR001081","UL1 TR001082","R01HD059527"],"pubmed_authors":["Gustafson CE","Jedlicka P","Wilson CC","De Zoeten EF","Higbee D","Yeckes AR","Janoff EN"],"additional_accession":[]},"is_claimable":false,"name":"Limited expression of APRIL and its receptors prior to intestinal IgA plasma cell development during human infancy.","description":"The absence of immunoglobulin A (IgA) in the intestinal tract renders young infants highly susceptible to enteric infections. However, mediators of initial IgA induction in this population are undefined. We determined the temporal acquisition of plasma cells by isotype and expression of T cell-independent (TI) and -dependent (TD) IgA class switch factors in the human intestinal tract during early infancy. We found that IgA plasma cells were largely absent in the infant intestine until after 1 month of age, approaching adult densities later in infancy than both IgM and IgG. The restricted development of IgA plasma cells in the first month was accompanied by reduced expression of the TI factor a proliferation-inducing ligand (APRIL) and its receptors TACI (transmembrane activator and calcium-modulator and cyclophilin ligand interactor) and B cell maturation antigen (BCMA) within isolated lymphoid follicles (ILFs). Moreover, both APRIL and BCMA expression strongly correlated with increasing IgA plasma cell densities over time. Conversely, TD mediators (CD40 ligand (CD40L) and CD40) were expressed within ILFs before 1 month and were not associated with IgA plasma cell generation. In addition, preterm infants had lower densities of IgA plasma cells and reduced APRIL expression compared with full-term infants. Thus, blunted TI responses may contribute to the delayed induction of intestinal IgA during early human infancy.","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 May","modification":"2025-04-04T19:32:34.637Z","creation":"2019-03-27T01:23:40Z"},"accession":"S-EPMC3959635","cross_references":{"pubmed":["24045575"],"doi":["10.1038/mi.2013.64"]}}