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Macrophage polarization is a process by which macrophages adopt different functional programs in response to the signals from their microenvironment. This ability is connected to their multiple roles in the organism: they are powerful effector cells of the innate immune system, but also important in removal of cellular debris, embryonic development and tissue repair.
M1 macrophages are seen to have a pro-inflammatory and cytotoxic (anti-tumoral) function; M2 macrophages are anti-inflammatory (pro-tumoral) and promote wound healing. However, use of the M1/M2 polarization paradigm has led to confusing terminology since M1/M2 are used to describe mature macrophages, but the activation process is complex and ...
Regulatory macrophages (Mregs) represent a subset of anti-inflammatory macrophages. In general, macrophages are a very dynamic and plastic cell type and can be divided into two main groups: classically activated macrophages (M1) and alternatively activated macrophages (M2). [1] M2 group can further be divided into sub-groups M2a, M2b, M2c, and ...
Macrophages have been classified as M1 or M2 depending on the adaptive immune response that elicited the phenotype: Th1 or Th2 respectively. [2] [4] [5] The phrase 'alternatively activated macrophage' is used to refer to M2 macrophages. [2] Regulatory macrophages do not fit into the M1/M2 classification system, and they display different ...
U-937-derived macrophages preferentially respond to M2-inducing stimuli, subsequently leading them to acquire the phenotype of alternatively activated macrophages. Whereas, in the case of THP-1 cells, the polarization is reversed in favor of classical M1 macrophages. Both cell lines can be artificially polarized in either direction though.
A macrophage can be polarized into the classic M1 or M2 phenotype, and this phenomenon can be seen in cigarette consumption. [2] In this polarization scheme, lower M1 markers and higher M2 markers have been observed. [4] The reprogram of macrophage implies a dysregulated inflammation that can damage healthy lung cells.
Key ligands expressed by macrophages Wnt5a and Wnt11 enhance the expression of the VEGF inhibitory receptor Flt1 so that blocking this pathway supports vascularization. [11] Other study focuses on heart injury. They found that during the late phase of scar formation M2 macrophages are needed for vascularization together with fibrosis to form a ...
[2] [3] Dermal macrophages' ability to acquire pro-inflammatory properties also potentiates them in cancer defence. M1 macrophages can suppress tumour growth in the skin by their pro-inflammatory properties. However, M2 macrophages support tumour growth and invasion by the production of Th2 cytokines such as TGFβ and IL-10. [4]