M2b macrophage polarization and its roles in diseases

Wang, Lexun; Zhang, Shengxi; Wu, Huijuan; Rong, Xianglu; Guo, Jiao

doi:10.1002/jlb.3ru1018-378rr

Cited by 587 publications

(520 citation statements)

References 177 publications

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“…Activated macrophages are often classified as proinflammatory M1 macrophages or anti-inflammatory M2 macrophages. The M1-like phenotype is induced by toll-like receptor ligands (bacterial lipopolysaccharide) or Th1 cytokines, such as tumor necrosis factor alpha (TNF-α), interferon gamma (IFNγ ) and colony stimulating factor 2 (CSF2) (3,4). M1-like macrophages exert high antigen presenting capacity (5).…”

Section: Introductionmentioning

confidence: 99%

Evaluating the Polarization of Tumor-Associated Macrophages Into M1 and M2 Phenotypes in Human Cancer Tissue: Technicalities and Challenges in Routine Clinical Practice

et al. 2020

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Tumor-associated macrophages (TAMs) as immune cells within the tumor microenvironment have gained much interests as basic science regarding their roles in tumor progression unfolds. Better understanding of their polarization into pro-tumoral phenotype to promote tumor growth, tumor angiogenesis, immune evasion, and tumor metastasis has prompted various studies to investigate their clinical significance as a biomarker of predictive and prognostic value across different cancer types. Yet, the methodologies to investigate the polarization phenomena in solid tumor tissue vary. Nonetheless, quantifying the ratio of M1 to M2 TAMs has emerged to be a prevailing parameter to evaluate this polarization phenomena for clinical application. This mini-review focuses on recent studies exploring clinical significance of M1/M2 TAM ratio in human cancer tissue and critically evaluates the technicalities and challenges in quantifying this parameter for routine clinical practice. Immunohistochemistry appears to be the preferred methodology for M1/M2 TAM evaluation as it is readily available in clinical laboratories, albeit with certain limitations. Recommendations are made to standardize the quantification of TAMs for better transition into clinical practice and for better comparison among studies in various populations of patients and cancer types.

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Section: Introductionmentioning

confidence: 99%

Evaluating the Polarization of Tumor-Associated Macrophages Into M1 and M2 Phenotypes in Human Cancer Tissue: Technicalities and Challenges in Routine Clinical Practice

et al. 2020

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“…M2c macrophages present high levels of CD206, CD163, MMP-8, TIMP1, and MARCO, which are associated with angiogenesis and matrix remodeling (32). Especially, CD163 is considered as a M2c specific marker expressed predominantly on the cells (39,40). Human M2c macrophages also express CD163 and high levels of CD206 (41).…”

Section: Discussionmentioning

confidence: 99%

Magnolol Attenuates Cisplatin-Induced Muscle Wasting by M2c Macrophage Activation

et al. 2020

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Cancer chemotherapy induces sarcopenia, which is a rapid loss of muscle mass that directly restricts daily activities and leads to poor quality of life and increased mortality. Although hormone-related therapies have been used to improve appetite and nutritional status, current treatments are considered palliative. Thus, the protection of skeletal muscle loss without adverse effects is essential to allow the maintenance of chemotherapy in cancer patients. Magnolol from Magnolia officinalis has several pharmacological effects including anti-cancer and anti-inflammatory activities, but the protection from muscle atrophy is not well-understood. In the present study, we investigated the effects of magnolol on muscle wasting and macrophage subtypes in a cisplatin-induced sarcopenia mouse model. We showed that magnolol significantly attenuated the body weight and the muscle loss induced by cisplatin injection. The diameter of the tibialis anterior muscle was markedly increased after magnolol treatment in cisplatin-treated mice. Importantly, magnolol increased macrophage infiltration into skeletal muscle while not affecting proliferation of macrophages. Magnolol attenuated the imbalance of M1/M2c macrophages by increasing CD206 + CD163 + M2c tissue reparative macrophages. Further, magnolol increased insulin-like growth factor (IGF)-1 expression. This effect was also observed in bone marrow-derived macrophages upon magnolol treatment. Taken together, magnolol may be a promising chemoprotective agent for the prevention of muscle atrophy through the upregulating M2c macrophages, which are a major source of IGF-1.

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“…Several studies were used for Cd86 as an M1 marker . However, Cd86 is also known as an M2b marker . The expression of the M2b‐specific marker Ccl1 did not differ between the control and IVD injury groups, and CD86 was used therefore as an M1 marker.…”

Section: Methodsmentioning

confidence: 99%

Sequential CCL2 Expression Profile After Disc Injury in Mice

Nakawaki

Uchida

Miyagi

et al. 2019

Journal Orthopaedic Research

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Macrophages produce proinflammatory cytokines in injured intervertebral discs (IVDs). We recently showed that macrophage‐derived inflammatory cytokines contribute to the production of pain‐related factors. However, the mechanism by which macrophages are recruited to injured IVDs has not been fully clarified. Here, we examined the expression dynamics of the chemokine CCL2 in a mouse IVD injury model and the mechanisms of its regulation. The percentage of macrophages increased from day 1 after injury and persisted up until day 28. At 1 and 3 days after injury, the expression of both Ccl2 messenger RNA (mRNA) and CCL2 protein was elevated in the IVD injury group, after which expression decreased to basal levels. Consistent with the increase in CCL2 expression, Ccr2 and Tnfa expression and various types of macrophages were also immediately elevated following disc injury. Further, tumor necrosis factor‐α (TNF‐α) stimulated Ccl2 mRNA and CCL2 protein expression in IVD cells in vitro. The expressions of M1 (Cd86 and Nos2) and M2a (Ym1) macrophage markers were all significantly elevated from day 1 following injury in injured compared with control mice. Meanwhile, the expression of Cd206 (M2a and M2c marker) was significantly elevated on days 3, 7, 14, and 28 following injury. These results suggest that in IVD injury, TNF‐α stimulates CCL2, which, in turn, mediates the recruitment of macrophages with the recruited macrophages subsequently differentiating into M1 and M2 subtypes. CCL2 signaling may, therefore, play an important role in IVD pathology via macrophage recruitment. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 38:895‐901, 2020

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M2b macrophage polarization and its roles in diseases

Cited by 587 publications

References 177 publications

Evaluating the Polarization of Tumor-Associated Macrophages Into M1 and M2 Phenotypes in Human Cancer Tissue: Technicalities and Challenges in Routine Clinical Practice

Evaluating the Polarization of Tumor-Associated Macrophages Into M1 and M2 Phenotypes in Human Cancer Tissue: Technicalities and Challenges in Routine Clinical Practice

Magnolol Attenuates Cisplatin-Induced Muscle Wasting by M2c Macrophage Activation

Sequential CCL2 Expression Profile After Disc Injury in Mice

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