Macrophage reprogramming for therapy
Summary Dysfunction of the immune system underlies a plethora of human diseases, requiring the development of immunomodulatory therapeutic intervention. To date, most strategies employed have been focusing on the modification of T lymphocytes, and although remarkable improvement has been obtained, r...
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Published in: | Immunology Vol. 163; no. 2; pp. 128 - 144 |
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Main Authors: | , , , |
Format: | Journal Article |
Language: | English |
Published: |
England
Wiley Subscription Services, Inc
01-06-2021
John Wiley and Sons Inc |
Subjects: | |
Online Access: | Get full text |
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Summary: | Summary
Dysfunction of the immune system underlies a plethora of human diseases, requiring the development of immunomodulatory therapeutic intervention. To date, most strategies employed have been focusing on the modification of T lymphocytes, and although remarkable improvement has been obtained, results often fall short of the intended outcome. Recent cutting‐edge technologies have highlighted macrophages as potential targets for disease control. Macrophages play central roles in development, homeostasis and host defence, and their dysfunction and dysregulation have been implicated in the onset and pathogenesis of multiple disorders including cancer, neurodegeneration, autoimmunity and metabolic diseases. Recent advancements have led to a greater understanding of macrophage origin, diversity and function, in both health and disease. Over the last few years, a variety of strategies targeting macrophages have been developed and these open new therapeutic opportunities. Here, we review the progress in macrophage reprogramming in various disorders and discuss the potential implications and challenges for macrophage‐targeted approaches in human disease.
Macrophages play roles at the heart of normal tissue physiology and in many diseases and show impressive capacity to adapt to their environment. Strategies to reprogramme macrophages represent new treatment options to be explored and exploited. |
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Bibliography: | PRT and NI contributed equally as co‐last author. VMTB and RJP contributed equally as co‐first author. ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 0019-2805 1365-2567 |
DOI: | 10.1111/imm.13300 |