Vol.44, No.2, 2020, pp.237-246, doi:10.32604/biocell.2020.08887
Age-related modifications of macrophages influenced by “inflammageing” in graft vs. host disease
1 Fujian Institute of Hematology, Fujian Provincial Key Laboratory on Hematology, Department of Hematology, Fujian Medical University Union Hospital, Fuzhou, 350000, China
2 Union Clinical Medical Colleges, Fujian Medical University, Fuzhou, 350000, China
3 Faculty of Life Sciences and Medicine, King’s College London, London, UK
4 INSERM U1160, Hopital Saint Louis, Université Paris Diderot, Sorbonne Paris Cité, Paris, France
* Address correspondence to: Xiaofan Li, morningshiplee@sina.com
Received 21 October 2019; Accepted 03 February 2020; Issue published 27 May 2020
Most studies focus on the adaptive immune cells in the GVHD pathogenesis, while little is known about innate immune cells in GVHD occurrence and development, especially macrophages. Meanwhile, a higher incidence of graft versus host disease (GVHD) is also found in the elderly patients. Though advances have been made in the modification of macrophages influenced by the inflamm-ageing, there is still no review on the role of macrophages in GVHD and the association between GVHD and the altered macrophages by inflamm-ageing. In this review, we focus on the potential age-related modifications of macrophage in GVHD, which contributes to the change of morbidity and mortality of GVHD. Via literature review, we found that the infiltration of macrophages is associated with GVHD and macrophages are modified in inflamm-ageing state, including the proliferation, migration, phagocytosis, antigen presentation, interaction with other immune cells, and pro-fibrosis. We suppose that altered macrophage functions in inflamm-ageing state contribute to GVHD in elderly patients.
Macrophages, Inflamm-ageing, Graft vs. host disease, Hematopoietic stem cell transplantation, Age, Innate immune cells
Cite This Article
HONG, Y., WAN, B., LI, X. (2020). Age-related modifications of macrophages influenced by “inflammageing” in graft vs. host disease. BIOCELL, 44(2), 237–246.
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