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Regulation of immunopathology in hepatitis B virus infection

Nature Medicine volume 21, pages 548–549 (2015)Cite this article

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In the liver there is a fine balance between immune surveillance of blood-borne infections and regulation of immunopathology. A new study identifies a role for granulocytic myeloid-derived suppressor cells in limiting T cell–mediated immunopathology in hepatitis B virus infection.

The liver contains several types of resident immune cell populations, including macrophages (Kupffer cells (KCs)), natural killer (NK) cells, invariant (i)NKT cells, endothelial cells (liver sinusoidal endothelial cells (LSECs)), platelets, and dendritic cells (DCs)1. Under normal conditions, these cells cooperate to regulate immune responses by multiple, not mutually exclusive mechanisms in order to guarantee organ survival1. In the presence of infections or inflammatory cytokines, some of these immune sentinels can be induced to stimulate resident iNKT cells that patrol the liver sinusoids, to activate pathogen-specific T cells, and to recruit a plethora of non-antigen-specific immune cells that amplify liver inflammation by bystander mechanisms2. HBV is one such infection that may challenge the liver, and it is a non-cytopathic DNA virus causing an immune-mediated liver disease. The virus is cleared in the majority of acutely infected individuals, but it results in a state of chronic liver immunopathology in about 10% of affected individuals via a complex interaction between genetic, immunologic, and environmental factors.

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Figure 1: Dynamics of gMDSCs in chronic HBV infection.

Kim Caesar/Nature Publishing Group

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Authors and Affiliations

  1. Silvia Piconese and Vincenzo Barnaba are in the Dipartimento di Medicina Interna e Specialità Mediche, Sapienza Università di Roma, and at the Istituto Pasteur-Fondazione Cenci Bolognetti, Rome, Italy.,

    Silvia Piconese & Vincenzo Barnaba

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  1. Silvia Piconese
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  2. Vincenzo Barnaba
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Correspondence to Vincenzo Barnaba.

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Piconese, S., Barnaba, V. Regulation of immunopathology in hepatitis B virus infection. Nat Med 21, 548–549 (2015). https://doi.org/10.1038/nm.3873

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