Exploring the full spectrum of macrophage activation

In the citing paper

“During cancer development, tumor cells and tumor‐associated stromal cells continuously change the composition and organization of ECM through deposition/degradation cycles and extensive crosslinking, shaping it more supportive for tumor growth.[ 33 ]”

In the citing paper

“A more recent model also hypothesizes the existence of a macrophage spectrum between M1 and M2, regulated through three major homeostatic processes involving the host defense, wound healing, and immune modulation.[ 40 ]”

In the citing paper

“Common examples of cytokines that polarize macrophages are IFN‐γ and LPS, which skew macrophages toward the M1 phenotype, whereas cytokines such as IL‐4 and IL‐13 promote a regenerative M2 phenotype (Figure 2 ).[ 40 ]”

In the citing paper

“This M1–M2 transition is critical for the resolution of inflammation and tipping the balance to tissue repair [49].”

In the citing paper

“Aβ deposition elicits a robust “M1” microglia-mediated inflammatory response contributing to disease pathogenesis (Gordon, 2003; Mosser and Edwards, 2008; Mandrekar-Colucci and Landreth, 2010).”

In the citing paper

“The biochemical composition of the microenvironment is especially important for the determination of macrophage phenotypes.”

In the citing paper

“Macrophages/microglia are capable of exhibiting a spectrum of phenotypic activation states which dictate their activities (Gordon, 2003; Mosser and Edwards, 2008; Mandrekar-Colucci and Landreth, 2010).”

In the citing paper

“the heterogeneity of cell morphologies observed (elongated and round cells) reflect the diverse plasticity of macrophage cells that define its myriad of phenotypes [56].”

In the citing paper

“It has been shown that macrophages, as part of their myeloid lineage, do not possess stress fibers,58 which may in large part be due to the fact that their interaction with their surrounding matrix, when not migrating, is not a key part of their innate function.29”

In the citing paper

“A pro-inflammatory macrophage phenotype correlates with elevated expression of Tumor Necrosis Factor α (TNF α), Interleukin 1 (IL1), and Interferon Regulatory Factor 5 (IRF5)44, 45, 46.”

In the citing paper

“There is a broad spectrum of macrophage activations which can be categorized into three states namely, classical activation (pro-inflammatory, MClassic), alternative activation (pro-healing, MWound), and regulatory activation (MReg)44.”

In the citing paper

“A pro-wound healing phenotype of macrophage correlates with up regulation in expression of Dendritic Cell Immune Receptor (Dcir), Stabilin 1 (Stab1), chemokine (C-C motif) ligand 22 (CCL22), Chitinase-like 3 (YM1), and Arginase 1 (Arg1)44, 45, 46.”

In the citing paper

“Meanwhile, a regulatory macrophage phenotype has been characterized to correlate with elevated expression of Interleukin 10 (IL10), TNF superfamily member 14 (Light), and Sphingosine Kinase 1 (Sphk1)44, 45, 46.”

In the citing paper

“Alternatively, the M2c subset is induced by IL-10 and plays a major role in tissue remodeling and suppression of inflammatory immune reactions by secreting transforming growth factor-b (TGF-b) and IL-10 [1,23].”

In the citing paper

“Rather, macrophage phenotype has been described as occurring along a continuum between the M1 and M2 extremes [12].”

In the citing paper

“While the term ‘M2’ encompasses all non-classically activated macrophages, M2 macrophages have been shown to include three well recognized sub-populations (M2a, M2b, and M2c), each with its own distinct inducers, markers, and functions.”

In the citing paper

“Macrophages, like the monocytes from which they derive, are a heterogeneous cell population each with different markers and functions [1,8–12].”

In the citing paper

“Indeed, macrophages serve three primary functions in the body: host defense, wound healing, and immune regulation.95”

In the citing paper

“Moreover, individual macrophages hold the potential for a dynamic phenotype switch, which affects the functional properties ofthe macrophage155,156.”

In the citing paper

“However, this nomenclature is now deemed inaccurate as accumulating evidence has revealed a broad diversity of macrophage activation statuses and shown that macrophages show remarkable plasticity to change phenotypes in response to environmental cues25,26.”

In the citing paper

“Transitioning from a pro-inflammatory macrophage-dominant wound to an anti-inflammatory macrophage-dominant milieu is essential in resolving inflammation and preparing the wound for effective repair [72].”

In the citing paper

“In the late stages of the inflammatory phase of wound healing, macrophages are found to switch from a proinflammatory to an alternatively activated phenotype, which has been assumed to be requisite for the switch from the inflammatory to the proliferative stages in wound healing as discussed below in more detail.46”

In the citing paper

“Thus, available evidence indicates that M1 and M2a/b/c are not discrete Mp differentiation states but instead represent convenient but limited and arbitrary in vitro-defined reference points on a time-dependent and multidimensional continuum of possible Mp phenotypes and functions [9].”

In the citing paper

“Finally and perhaps most importantly, rodent and human Mp do not exhibit entirely similar responses to in vitro activation [9,34,66,80], and it remains to be determined whether there are also species-dependent differences in Mp function during in vivo tissue repair.”