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The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
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Myeloid-derived suppressor cells modulate B-cell responses.

Felipe J N Lelis1, Jennifer Jaufmann2, Anurag Singh3

  • 1Children's Hospital and Interdisciplinary Center for Infectious Diseases, University of Tuebingen, Tuebingen, Germany; Department of Pediatrics, Department of Infectious Diseades, Boston Children's Hospital, Harvard Medical School,300 Longwood Avenue, Boston, MA 02115, USA.

Immunology Letters
|July 9, 2017
PubMed
Summary

Human myeloid-derived suppressor cells (MDSCs) suppress B-cell proliferation and antibody production. This cell contact-dependent interaction involves arginase-1, nitric oxide, and reactive oxygen species, impacting B-cell function.

Keywords:
B cellsMDSCsMyeloid-derived suppressor cells

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Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Myeloid-derived suppressor cells (MDSCs) are critical regulators of adaptive immunity, primarily known for suppressing T-cell functions.
  • The precise mechanisms by which MDSCs influence B cells, a key component of the humoral immune system, have remained largely unclear.

Purpose of the Study:

  • To investigate the functional effects of human polymorphonuclear MDSCs on B-cell activity.
  • To elucidate the mechanisms underlying MDSC-mediated modulation of B cells.

Main Methods:

  • Co-culture experiments involving human polymorphonuclear MDSCs and B cells.
  • Assessment of B-cell proliferation, antibody production, and cell viability.
  • Analysis of key mediators including arginase-1, nitric oxide (NO), and reactive oxygen species (ROS).

Main Results:

  • Human polymorphonuclear MDSCs significantly suppress B-cell proliferation and reduce antibody production.
  • The suppressive effects are dependent on direct cell-to-cell contact between MDSCs and B cells.
  • MDSC-mediated B-cell suppression involves the action of arginase-1, NO, and ROS, leading to increased B-cell death.

Conclusions:

  • Human MDSCs actively modulate B-cell function, extending their regulatory role beyond T cells.
  • These findings reveal novel mechanisms of immune suppression impacting humoral immunity.
  • Understanding MDSC-B cell interactions may offer new avenues for developing immunotherapies.