Gut-associated lymphoid tissue contains the molecular machinery to support T-cell-dependent and T-cell-independent class switch recombination
Author(s) -
Francesca Barone,
P Patel,
J Sanderson,
Jo Spencer
Publication year - 2009
Publication title -
mucosal immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.596
H-Index - 101
eISSN - 1935-3456
pISSN - 1933-0219
DOI - 10.1038/mi.2009.106
Subject(s) - lamina propria , cytidine deaminase , biology , immunoglobulin class switching , gut associated lymphoid tissue , immunohistochemistry , activation induced (cytidine) deaminase , receptor , antibody , microbiology and biotechnology , immunology , b cell , lymphatic system , epithelium , genetics
A PRoliferation-Inducing Ligand (APRIL) is a secreted cytokine member of the tumor necrosis factor family. It is a B-cell survival factor that also induces class switch recombination (CSR) toward immunoglobulin A (IgA), independent of T cells. It is therefore an important contributor to the maintenance of the mucosal immunological barrier, which has been linked to a putative extrafollicular inductive phase of the IgA response in lamina propria. By immunohistochemistry (IHC) and quantitative real-time PCR (qRT-PCR) on microdissected tissue from normal human gut, we observed APRIL expression, together with TACI (transmembrane activator and CAML interactor) and BCMA (B-cell maturation antigen), in gut-associated lymphoid tissue (GALT), lamina propria, and in the epithelium of stomach, small and large intestine, and rectum. However, no activation-induced cytidine deaminase (AID) expression (an absolute requirement for class switching) was detected in lamina propria by IHC or qRT-PCR. APRIL and its receptors were only observed alongside AID in GALT, showing that GALT contains the apparatus to support both T-independent and T-dependent routes to IgA CSR.
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