{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T00:06:15Z","timestamp":1788307575050,"version":"build-2803163510"},"reference-count":39,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,12,4]],"date-time":"2025-12-04T00:00:00Z","timestamp":1764806400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>\n                      Tuberculosis (TB) rema\\ins a major global health challenge. Mycobacterium avium (\n                      <jats:italic>M. avium<\/jats:italic>\n                      ), a non-tuberculosis mycobacterium, causes pulmonary infections and can evade host immune surveillance by persisting within macrophages. MicroRNAs (miRNAs) are key regulators of host immunity; however, their roles in mycobacterial pathogenesis are not fully understood. This study investigated the role of miR-17-5p in macrophage-mediated immune responses during M. avium infection, with a focus on MAP3K2-mediated MAPK signaling.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Differentially expressed miRNAs were identified through small RNA sequencing of exosomes from\n                      <jats:italic>M. avium<\/jats:italic>\n                      -infected THP-1 macrophages. Candidate miRNAs were validated by RT-qPCR in THP-1 derived exosomes and serum samples from TB patients. MAP3K2 was evaluated as a miR-17-5p target using bioinformatics prediction, dual-luciferase reporter assays, and expression analysis. Effects on immune responses and MAPK signaling were assessed using qPCR, ELISA, Western blotting, ROS measurement, and CFU assays.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      miR-17-5p expression was significantly elevated in\n                      <jats:italic>M. avium<\/jats:italic>\n                      \u2013infected macrophages, as well as in serum and peripheral blood mononuclear cells (PBMCs) from TB patients. Increased miR-17-5p suppressed MAP3K2 expression and attenuated MAPK signaling, reducing phosphorylation of ERK, JNK, and p38. This resulted in decreased production of inflammatory mediators (TNF-\u03b1, IL-6, IL-1\u03b2), reduced iNOS and ROS levels, and impaired bacterial clearance.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>\n                      miR-17-5p promotes\n                      <jats:italic>M. avium<\/jats:italic>\n                      survival by targeting MAP3K2 and suppressing MAPK-dependent immune functions in macrophages. These findings highlight miR-17-5p as a potential diagnostic biomarker and therapeutic target in TB and related mycobacterial infections.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2025.1676204","type":"journal-article","created":{"date-parts":[[2025,12,4]],"date-time":"2025-12-04T06:34:05Z","timestamp":1764830045000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":4,"title":["Elevated miR-17-5p facilitates mycobacterial immune evasion by targeting MAP3K2 in macrophages"],"prefix":"10.3389","volume":"16","author":[{"given":"Md 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