Macrophage Polarization Comes of Age

Mantovani, Alberto; Sica, Antonio; Locati, Massimo

doi:10.1016/j.immuni.2005.10.001

Cited by 1,025 publications

(835 citation statements)

References 13 publications

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“…[19][20][21][22] In our study, most of the macrophages were positively stained with the M2 marker CD163. This finding was compatible with that in another study, 29 which only included advanced NSCLC. Taken together, these data indicate that host immunosurveillance is intact to some extent in the early stages, whereas immunosubversion deteriorates in the advanced stages.…”

Section: Tumor Immunologysupporting

confidence: 92%

“…In some conditions, alternatively activated macrophages polarize to the M2 phenotype, which secrete matrix-degrading enzymes, angiogenic factors and immunosuppressive cytokines/chemokines that promote tumor growth and metastasis. 29 Recent reports on early-stage NSCLC demonstrate that macrophages in the tumor islet are predominantly of M1 phenotype in patients with long survival. The number of islet M1 macrophages is dramatically decreased in those patients with short survival.…”

Section: Tumor Immunologymentioning

confidence: 99%

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Tumor‐associated macrophages correlate with response to epidermal growth factor receptor‐tyrosine kinase inhibitors in advanced non‐small cell lung cancer

Chung

Lee

Wang

et al. 2012

Intl Journal of Cancer

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Our study investigated whether tumor-associated macrophages (TAMs) in advanced non-small cell lung cancer (NSCLC) are related to treatment response to epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) and may be a predictor of survival. Of 206 advanced NSCLC patients treated (first-line) with an EGFR-TKI at the study hospital from 2006 to 2009, 107 with adequate specimens for assessing CD68 immunohistochemistry as a marker of TAMs were assessed. After EGFR-TKI treatment, response was observed in 55 (51%) patients, and the median follow-up period was 13.5 months. Most TAMs were located in the tumor stroma (>95%) and positively costained with the M2 marker CD163. TAM counts were significantly higher in patients with progressive disease than in those without (p < 0.0001), a trend that remained in patients with known EGFR mutation status (n 5 59) and those with wild-type EGFR (n 5 20). High TAM counts, among other factors (e.g., wild-type EGFR), were significantly related to poor progression-free survival (PFS) and overall survival (OS) (all p < 0.0001 for TAMs). Multivariate Cox analyses showed that high TAM counts and EGFR mutations were both independent factors associated with PFS [odds ratio (OR), 8.0; 95% confidence interval (CI), 2.87-22.4; p 5 0.0001 and OR, 0.03; 95% CI, 0.003-0.31; p 5 0.003, respectively] and OS (OR, 2.641; 95% CI, 1.08-6.5; p 5 0.03 and OR, 0.14; 95% CI, 0.03-0.56; p 5 0.006, respectively). TAMs are related to treatment response irrespective of EGFR mutation and can independently predict survival in advanced NSCLC treated with an EGFR-TKI.

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Section: Tumor Immunologysupporting

confidence: 92%

Section: Tumor Immunologymentioning

confidence: 99%

Tumor‐associated macrophages correlate with response to epidermal growth factor receptor‐tyrosine kinase inhibitors in advanced non‐small cell lung cancer

Chung

Lee

Wang

et al. 2012

Intl Journal of Cancer

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“…During C. burnetii infection, a main target of Vanin-1 action is the MU skewed toward an M2 phenotype. The plasticity of MU polarization has already been shown to be influenced by tissue imprinting [32]. Interestingly, we have previously shown that Vanin -/-mice exhibited reduced inflammatory damage during S. mansoni infection [17].…”

Section: Discussionmentioning

confidence: 83%

“…2007. 37: [24][25][26][27][28][29][30][31][32] to L929 cells, and cultures were maintained in antibiotic-free Eagle MEM supplemented with 4% FBS and 2 mM L-glutamine (Invitrogen). The number of passages did not exceed five passages.…”

Section: Methodsmentioning

confidence: 99%

Vanin‐1 controls granuloma formation and macrophage polarization in Coxiella burnetii infection

Meghari¹,

Berruyer-Pouyet²,

Lépidi³

et al. 2006

Eur J Immunol

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Q fever is caused by Coxiella burnetii, a bacterium that survives in MU. Vanin-1 is a membrane-anchored pantetheinase that controls tissue inflammation. Consequently, Vanin-1-deficient mice represent a unique mouse model in which stress-induced inflammation is limited by the reaction of resident tissue cells. To investigate the contribution of host tissues in the control of a bacterial infection, we infected Vanin-1-deficient mice with C. burnetii. Mortality and morbidity of mice were not affected. The lack of Vanin-1 had no effect on C. burnetii clearance but decreased the formation of granulomas in spleen and liver. Granuloma formation depends upon MU recruitment and activation in these tissues. Whereas the former was slightly impaired in mutant mice, the lack of Vanin-1 significantly affected the activation pattern of BM-derived MU stimulated by C. burnetii. While their microbicidal activity against C. burnetii was moderately impaired, they exhibited decreased inducible nitric oxide synthase (iNOS) and MCP-1 gene expression, and increased IL-10 and arginase expression. In liver from mutant mice, increased arginase expression and decreased expression of MCP-1 and iNOS were reminiscent of MU data. These results suggest a role of Vanin-1 in granuloma formation in response to C. burnetii by skewing MU activation toward an M2 program. See accompanying commentary http://dx

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“…Of interest, this profile appeared to be more pronounced in patients with peripheral arthritis than in those with pure axial SpA (26). Based on the fact that IFN␥ is an important determinant of M1 polarization (2,3,(20)(21)(22) and on the association of synovial CD163ϩ M2 macrophages, but not T lymphocytes, with disease activity in peripheral SpA (9), the present study examined in more detail whether the presence of distinct macrophage subsets in both diseases is associated with different local inflammatory milieus.…”

Section: Discussionmentioning

confidence: 87%

Absence of a classically activated macrophage cytokine signature in peripheral spondylarthritis, including psoriatic arthritis

Vandooren¹,

Noordenbos²,

Ambarus³

et al. 2009

Arthritis & Rheumatism

147

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Objective. Peripheral spondylarthritis (SpA) is characterized by macrophages that express CD163, a marker of alternative activation (M2). The purpose of this study was to assess whether this differential infiltration with macrophage subsets was associated with a different local inflammatory milieu in SpA as compared with rheumatoid arthritis (RA).Methods Conclusion. The local inflammatory milieu is clearly different in SpA as compared with RA peripheral arthritis. Synovitis in SpA, including that in PsA, is characterized by a selective decrease in M1-derived proinflammatory mediators, such as TNF␣ and IL-1␤.

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Macrophage Polarization Comes of Age

Cited by 1,025 publications

References 13 publications

Tumor‐associated macrophages correlate with response to epidermal growth factor receptor‐tyrosine kinase inhibitors in advanced non‐small cell lung cancer

Tumor‐associated macrophages correlate with response to epidermal growth factor receptor‐tyrosine kinase inhibitors in advanced non‐small cell lung cancer

Vanin‐1 controls granuloma formation and macrophage polarization in Coxiella burnetii infection

Absence of a classically activated macrophage cytokine signature in peripheral spondylarthritis, including psoriatic arthritis

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