The role of bone cells in immune regulation during the course of infection

Semin Immunopathol. 2019 Sep;41(5):619-626. doi: 10.1007/s00281-019-00755-2. Epub 2019 Sep 24.

Abstract

Bone homeostasis depends on a balance between osteoclastic bone resorption and osteoblastic bone formation. Bone cells are regulated by a variety of biochemical factors, such as hormones and cytokines, as well as various types of physical stress. The immune system affects bone, since such factors are dysregulated under pathologic conditions, including infection. The bone marrow, one of the primary lymphoid organs, provides a special microenvironment that supports the function and differentiation of immune cells and hematopoietic stem cells (HSCs). Thus, bone cells contribute to immune regulation by modulating immune cell differentiation and/or function through the maintenance of the bone marrow microenvironment. Although osteoblasts were first reported as the population that supports HSCs, the role of osteoblast-lineage cells in hematopoiesis has been shown to be more limited than previously expected. Osteoblasts are specifically involved in the differentiation of lymphoid cells under physiological and pathological conditions. It is of critical importance how bone cells are modified during inflammation and/or infection and how such modification affects the immune system.

Keywords: Bone marrow microenvironment; Infection; Lymphopoiesis; Osteoblast; Sepsis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Bone and Bones / cytology*
  • Bone and Bones / metabolism*
  • Cell Differentiation
  • Disease Susceptibility
  • Hematopoiesis
  • Hematopoietic Stem Cells / cytology
  • Hematopoietic Stem Cells / metabolism
  • Humans
  • Immune System / immunology
  • Immune System / metabolism
  • Immunomodulation*
  • Osteitis / diagnosis
  • Osteitis / etiology*
  • Osteitis / metabolism*
  • Osteoblasts / immunology
  • Osteoblasts / metabolism*
  • Osteoclasts / immunology
  • Osteoclasts / metabolism*