Classical and alternative activation of macrophages: different pathways of macrophage-mediated tumor promotion

Ginderachter, Jo Van; Liu, Yuanqing; Devoogdt, Nick; Noël, W.; Brys, Lea; Gh., Gholamreza Hassanzadeh; Raes, Geert; Geldhof, Anja; Beschin, Alain; Revets, Hilde; Baetseĺier, Patrick De

doi:10.1007/978-1-4020-6729-7_9

Cited by 1 publication

(1 citation statement)

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“…Conversely, M2 cells seem to depend on an IL-4 or IL-13 environment and on other transcription factors, such as STAT-6 and peroxisome proliferator-activated receptor-␥ [15]. Moreover, they show high expression of arginase 1, mannose receptor 1, or CD206 [15], anti-inflammatory cytokine IL-1R antagonist, and IL-10 [16]. It has also been suggested that PI3K activation and SHIP, a PI3K-negative regulator, are requirements for M2 skewing [13].…”

Section: Macrophages and Their Polarizationmentioning

confidence: 99%

Alveolar macrophages in diabetes: friends or foes?

Sunahara

Martins

2012

Journal of Leukocyte Biology

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AMs constitute an important bridge between innate and adaptive immunity. AMs patrol the lungs against pathogens, remove senescent cells, and help repair tissue. AM function is altered in many diseases, including DM, where AM abnormal immune responses may worsen infections or lead to exacerbation of inflammatory reactions. In vivo experimental models have greatly contributed to our knowledge of AM function. Studies have shown that during hyperglycemic states, the phagocytic function of AMs and the expression of adhesion molecules may be altered, interfering with the recruitment of immune cells to the inflammatory site. Insulin treatment seems to recover the normal function of impaired AMs. However, much research is still needed to characterize AMs and to better understand their role in inflammation and infection, particularly in diabetic patients. In this review, we attempt to explore recently accumulated knowledge about AM function and how this function is deficient in DM. Additionally, AM polarization is compared briefly with that of T cells, and this may interfere with how immune response is driven. This review discusses how impaired AMs lead to an aberrant immune response that contributes to worsening infection and autoimmunity, opening up discussion for future work in the field.

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