SPECIAL REVIEW SERIES: New ultrastructural discoveries in the pathophysiology of liver diseases

Medical Molecular Morphology

, Volume 38, Issue 3, pp 136-141

First online:

Recruitment of dendritic cells to pathological niches in inflamed liver

  • Hiroyuki YoneyamaAffiliated withDepartment of Molecular Preventive Medicine, School of Medicine, The University of Tokyo Email author 
  • , Takafumi IchidaAffiliated withDepartment of Gastroenterology, Juntendo University School of Medicine, Shizuoka Hospital

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The liver is a specialized organ for host defense and immunity. Recruitment of dendritic cells (DCs) is crucial to host defense in a granulomatous liver disease in mice. In response to danger signals, DC precursors are mobilized de novo into the circulation. Myeloid DC (mDC) precursors are recruited to perisinusoidal spaces and activated to form granulomas. Recruited mDCs subsequently extravasate into Disse’s space and migrate to the portal area to induce portal tract-associated lymphoid tissue (PALT). Some mDCs are remobilized into draining hepatic lymph nodes (LNs) to prime antigen-specific CD4+ helper T cells. Kupffer cell-derived CCL3/MIP-1α attracts mDC precursors to the sinusoidal granulomas, whereas PALT composed cell-derived CCL21/SLC attracts activated mDCs to the T-cell zone of PALT. Inflammatory cytokines modulate this sinusoid-portal migration through IL-1R/TLR signaling. Recruited mDCs themselves also produce several chemokines and cytokines that modulate T-cell responses. A unique trafficking of circulating mDC precursors within the inflammation-associated, newly formed compartments (“pathological niches”) is strictly regulated by both homeostatic and inducible chemokines and determines the final efficiency of the immunity in this organ.

Key words

Dendritic cell Chemokine Granuloma Kupffer cell T cell