Abstract

As a subset of myeloid progenitors and immature myeloid cells, previous studies revealed that MDSCs could be generated in the presence of various cytokines and growth factors, including G-CSF, GM-CSF, PGE2, VEGF, IL-6, IL-1β and TNF-α [4]. To be noted, through binding to the murine receptor paired immunoglobulin like receptor-B (PIR-B) expressed on MDSCs, human leukocyte antigen-G (HLA-G) has been found with the capability to contribute the expansion and suppressive functions of MDSCs [5].

Highlights

  • Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of granulocytic or monocytic cells that could inhibit both innate and adaptive immune response [1]

  • Suppressive factors expressed by MDSCs, such as arginase-1, reactive oxygen species, inducible nitric oxide synthase and program death ligand 1, play critical roles in inhibition of T cell, B cell and NK cell mediated immune responses, and in induction of tolerogenic Tregs and regulatory DCs [2]

  • In the context of virus infection, significance of human leukocyte antigen-G (HLA-G) expression was addressed in amounts of previous studies, where HLA-G was markedly increased during various virus infection such as such as human immunodeficiency virus (HIV) [7], Human papillomavirus (HPV) [8], human cytomegalovirus virus (HCMV) [9], influenza A virus [10], hepatitis B and C virus [11,12], herpes simplex virus and rabies virus [13], etc

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Summary

Introduction

Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of granulocytic or monocytic cells that could inhibit both innate and adaptive immune response [1]. Aifen Lin and Wei-Hua Yan* Medical Research Centre, Taizhou Hospital of Zhejiang Province, Wenzhou Medical University, Zhejiang, China Suppressive factors expressed by MDSCs, such as arginase-1, reactive oxygen species, inducible nitric oxide synthase and program death ligand 1, play critical roles in inhibition of T cell, B cell and NK cell mediated immune responses, and in induction of tolerogenic Tregs and regulatory DCs [2].

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Conclusion

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