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@ARTICLE{Malik2026-iq,
  title     = "Morphine disrupts antigen-presenting cell function through
               {TLR-4} and autophagy pathways",
  author    = "Malik, Jonaid Ahmad and Lamba, Taruna and Chhabra, Himanshi and
               Kashyap, Priyanshu and Gupta, Pawan and Sehrawat, Sharvan and
               Agrewala, Javed N",
  abstract  = "BACKGROUND: Morphine dependence is a major challenge worldwide.
               Besides, it has many adverse effects and suppresses its user's
               immune systems. Antigen-presenting cells (APCs) play a crucial
               role in activating T cells, thereby protecting us from various
               diseases. Therefore, understanding the influence of morphine on
               APC function may reveal its impact on immune modulation.
               METHODS: Macrophages and dendritic cells (DCs) were cultured
               with morphine and assessed for antigen uptake, processing, and
               presentation using flow cytometry, confocal microscopy, and
               colony-forming units (CFU). TLR-4 involvement was examined
               through gene silencing and pharmacological inhibition. Autophagy
               markers (LC3, Atg7, Atg12) were analyzed by RT-qPCR and
               immunofluorescence. RESULTS: We observed that morphine inhibited
               antigen uptake, as evidenced by reduced phagocytosis of
               Mycobacterium tuberculosis (Mtb), E. coli, and other antigens.
               Further, it inhibited the killing of Mtb and E. coli and the
               processing of their antigens, as evidenced by reduced
               colocalization of LC3/LAMP1 with Mtb and E. coli. It prevented
               LC3 colocalization with the lysosomal marker LAMP1. Furthermore,
               morphine impaired antigen presentation, as evidenced by
               downregulation of MHC I, MHC II, CD80, and CD86, and reduced
               activation of CD4 T cells. Additionally, we observed that
               morphine exerted its mechanistic effects for immunosuppression
               through the TLR-4/NF-ĸB and autophagy pathways. CONCLUSION: This
               study identifies a mechanism by which morphine suppresses immune
               function by impairing antigen uptake, processing, and
               presentation in antigen-presenting cells through TLR-4-dependent
               autophagy pathways. These findings provide important insights
               into opioid-induced immunosuppression and have direct clinical
               relevance for the use of morphine in immunocompromised
               individuals.",
  journal   = "Mol. Biol. Rep.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  53,
  number    =  1,
  month     =  jun,
  year      =  2026,
  keywords  = "Antigen presentation; Autophagy; Dendritic cells;
               Immunosuppression; Macrophages; Morphine; TLR-4",
  copyright = "https://www.springernature.com/gp/researchers/text-and-data-mining",
  language  = "en"
}