{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThe polymeric immunoglobulin receptor (PIGR) is a central mediator of mucosal immunity that transports polymeric immunoglobulins—mostly dimeric IgA and pentameric IgM—from the basolateral surface of epithelial cells to the mucosal lumen. During this process, the extracellular portion (the secretory component, SC) is cleaved, stabilizing the antibodies and conferring innate antimicrobial properties. Structural and mutagenesis studies have delineated critical Ig‐binding domains as well as the conformational flexibility required for efficient Ig transcytosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nPIGR expression is dynamically regulated by both microbial products and host-derived cytokines. Stimulation through Toll-like receptors coupled with exposure to mediators such as interleukin‑4, tumor necrosis factor‑α, and interferon‑γ augments PIGR transcription via specific promoter and intronic enhancer elements regulated by transcription factors including NF‑κB and STAT6. In parallel, inflammatory responses—mediated for example by neutrophil-released serine proteases and modulators like secretory leukocyte protease inhibitor—can impact both the cleavage and up‑regulation of PIGR, underscoring its responsiveness to the local inflammatory milieu."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its canonical role in antibody transport, PIGR serves as a receptor exploited by pathogens during mucosal infections. Specific bacterial adhesins—such as those expressed by Streptococcus pneumoniae and pathogenic Escherichia coli—bind designated motifs within the Ig-like domains of PIGR, thereby mediating bacterial adherence, internalization, and even transcytosis. These interactions can trigger downstream signaling events, including calcium mobilization and the engagement of both clathrin-dependent and caveolar endocytic pathways, which collectively facilitate pathogen uptake."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAlterations in PIGR expression feature prominently in diverse disease contexts. In chronic inflammatory diseases—such as chronic obstructive pulmonary disease, inflammatory bowel disease, and IgA nephropathy—aberrant PIGR levels reflect and potentially contribute to dysregulated mucosal immunity. Similarly, in various cancers (including those of the lung, upper gastrointestinal tract, osteosarcoma, pancreatic, and breast origins) PIGR expression correlates with tumor aggressiveness and patient prognosis, serving both as a biomarker and as a potential conduit for targeted therapeutic delivery via its transcytotic properties. Such translational strategies are being explored, for instance, in polycystic kidney disease where dimeric IgA‐formatted agents can be ferried across epithelia using the PIGR pathway."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "25", "end_ref": "39"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "H Schjerven, P Brandtzaeg, F E Johansen "}, {"type": "b", "children": [{"type": "t", "text": "A novel NF-kappa B/Rel site in intron 1 cooperates with proximal promoter elements to mediate TNF-alpha-induced transcription of the human polymeric Ig receptor."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Immunol (2001)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.4049/jimmunol.167.11.6412"}], "href": "https://doi.org/10.4049/jimmunol.167.11.6412"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "11714807"}], "href": "https://pubmed.ncbi.nlm.nih.gov/11714807"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "R Sergio Solorzano-Vargas, Jiafang Wang, Lingling Jiang, et al. 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