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IL-13R?1 is a surface marker for M2 macrophages influencing their differentiation and function.

ABSTRACT: In this study, we examined the role IL-13 receptor alpha 1 (IL-13R?1) plays in macrophage differentiation and function. The findings indicate that IL-13R?1 is expressed on the M2 but not on the M1 subset of macrophages and specifically heterodimerizes with the IL-4R? chain to form a type II receptor, which controls the differentiation and function of these cells. Indeed, BM cells from IL-13R?1(+/+) and IL-13R?1(-/-) mice yield equivalent numbers of macrophages when cultured under M2 polarizing conditions. However, IL-13R?1(-/-) BM cells yield a much higher number of macrophages than IL-13R?1(+/+) BM cells when the differentiation is carried out under M1-polarizing conditions. Further analyses indicated that macrophages that express IL-13R?1 also display surface markers associated with an M2 phenotype. In addition, the IL-13R?1(+) macrophages were highly efficient in phagocytizing zymosan bioparticles both in vitro and in vivo, and supported differentiation of naïve T cells to a Th2 phenotype. Finally, when stimulated by IL-13, a cytokine that uses the heteroreceptor, the cells were able to phosphorylate STAT6 efficiently. These previously unrecognized findings indicate that IL-13R?1 serves as a marker for M2 macrophages and the resulting heteroreceptor influences both their differentiation and function.

SUBMITTER: Dhakal M

PROVIDER: S-EPMC3959573 | biostudies-other | 2014 Mar

REPOSITORIES: biostudies-other

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IL-13Rα1 is a surface marker for M2 macrophages influencing their differentiation and function.

Dhakal Mermagya M Hardaway John C JC Guloglu Fatma Betul FB Miller Mindy M MM Hoeman Christine M CM Zaghouani Adam A AA Wan Xiaoxiao X Rowland Linda M LM Cascio Jason A JA Sherman Michael P MP Zaghouani Habib H

European journal of immunology 20140113 3

In this study, we examined the role IL-13 receptor alpha 1 (IL-13Rα1) plays in macrophage differentiation and function. The findings indicate that IL-13Rα1 is expressed on the M2 but not on the M1 subset of macrophages and specifically heterodimerizes with the IL-4Rα chain to form a type II receptor, which controls the differentiation and function of these cells. Indeed, BM cells from IL-13Rα1(+/+) and IL-13Rα1(-/-) mice yield equivalent numbers of macrophages when cultured under M2 polarizing c ...[more]

PMID: 24281978

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Project description:Background:Tumor-associated macrophage (TAM) is emerging as one of the important complications in cancer promotion. Interleukin-17 (IL-17), a potent pro-inflammatory cytokine, plays an active role in promoting M2 macrophage differentiation (TAMs are M2-like phenotypes). In this study, we aimed to evaluate that IL-17 stimulates key phenotypic and functional signatures of M2 macrophages associated with cancer progression in non-small-cell lung cancer (NSCLC) patients. Patients and methods:The markers and cytokines of M2 macrophages were detected in THP-1-derived macrophages and mouse peritoneal macrophages treated with IL-17. The activation of nuclear factor kappa B (NF-?B) and nuclear localization of p65 in IL-17-treated cells were investigated. The BAY11-7082 inhibitor and the siRNA of p65 were used to block the NF-?B activation. A total of 85 patients who underwent surgery for histologically verified NSCLC were enrolled in this study. The expression of IL-17 and M2 macrophage markers were assessed by immunostaining. Survivals were estimated using the Kaplan-Meier method. Results:The CD163 and CD206 cell surface markers and transforming growth factor beta (TGF-?), vascular endothelial growth factor (VEGF) and IL-10 of M2 macrophages were significantly increased in IL-17-treated THP-1-derived macrophages in a dose-dependent manner. IL-17 increased the mRNA levels of Arginase I and Fizz1, the phosphorylation of IkB? and nuclear localization of p65 (a subunit of NF-?B). The BAY11-7082 abrogated IL-17-induced CD206 and CD163 expression, TGF-?, VEGF, IL-10, Arginase I and Fizz1 expression and p65 nuclear translocation. Further experiments showed that IL-17 induced the expression of CD206, CD163, Arginase I, Fizz1 and Ym1 in mouse peritoneal macrophages that were inhibited by siRNA of p65. The immunostaining experiments on human NSCLC tissues indicated that high IL-17 expression was significantly correlated with CD163 and c-Maf. The intratumoral IL-17+ CD163+ c-Maf+ cells were associated with NSCLC progression. Conclusion:IL-17 stimulated macrophages to M2-like phenotypes via NF-?B activation. IL-17 may be a potential therapeutic target for NSCLC.

Dataset Information

IL-13R?1 is a surface marker for M2 macrophages influencing their differentiation and function.

Publications

IL-13Rα1 is a surface marker for M2 macrophages influencing their differentiation and function.

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