THIS ARTICLE HAS BEEN RETRACTED
Interleukin-13-induced type II polarization of inflammatory macrophages is mediated through suppression of nuclear factor-κB and preservation of IκBα in a T cell lymphoma

Abstract

R e t r a c t e d RetractionThe article from Clinical and Experimental Immunology, 'Interleukin-13-induced type II polarization of inflammatory macrophages is mediated through suppression of nuclear factor-kB and preservation of IkBa in a T cell lymphoma' , by P. Deepak, S. Kumar and A. Acharya (August 2007, 149(2) The retraction has been agreed due to lack of original data. R e t r a c t e dInterleukin-13-induced type II polarization of inflammatory macrophages is mediated through suppression of nuclear factor-kB and preservation of IkBa in a T cell lymphoma SummarySpontaneously arising transplantable T cell lymphoma, designated as Dalton's lymphoma (DL), is characterized by a highly invasive and deleterious nature almost completely paralysing the host immune system. The level of interleukin (IL)-13 is elevated in serum and ascitic fluid of the DL-bearing host. IL-13 is a potent immunosuppressive cytokine and is an alternative activator of macrophages that suppresses the production of nitric oxide (NO) and expression of inducible nitric oxide synthase (iNOS), and proinflammatory cytokines. The expression of iNOS and proinflammatory cytokines are dependent largely upon the activation of nuclear factor-kB (NF-kB). Activation of NF-kB involves the degradation of cytoplasmic inhibitor IkBa, allowing the nuclear translocation of NF-kB and thereby transcription of the iNOS gene. Therefore, in this study we sought to determine whether the alternative activation or type II polarization of macrophages induced by IL-13 is mediated by the suppression of NF-kB and cytoplasmic preservation of IkBa.Western blot analysis and electrophoretic mobility shift assay (EMSA) indicate that tumour-associated macrophages (TAM) or polarized type II macrophages are due to preserved protein expression of IkBa, and therefore suppressed NF-kB nuclear translocation. These findings suggest that IL-13 may operate through the suppression of NF-kB activation and preservation of IkBa.

Potent Phagocytic Activity with Impaired Antigen Presentation Identifying Lipopolysaccharide-Tolerant Human Monocytes: Demonstration in Isolated Monocytes from Cystic Fibrosis Patients

“…Tolerant monocytes seem to exhibit an M2 phenotype (24). Despite all of these works, a clear picture of the mechanism that governs ET in human monocytes and its (patho)physiological implications is still missing.…”

Lactic acid bacteria enhance autophagic ability of mononuclear phagocytes by increasing Th1 autophagy-promoting cytokine (IFN-γ) and nitric oxide (NO) levels and reducing Th2 autophagy-restraining cytokines (IL-4 and IL-13) in response to Mycobacterium tuberculosis antigen

“…The augmentation of IFN-γ production by LAB may also be mediated by TLR-TLR cross talk in human PBMC, resulting in synergistic regulation of IFN-γ [18], or combination of receptors which is required for induction of autophagy in response to Mtb [8]. In PBMCs, LAB induced IFN-γ and inhibited IL-4 and IL-13, whereas Mtb induced IL-4 and IL-13, which inhibit IFN-γ production, macrophage activity and autophagy by down-regulating TLR2 [2,6,22,23,48,51,60,61,63]. In addition, activation of TLR2 with Mtb and its components not only induces pro-inflammatory activation of immune cells, which has a protective role against mycobacterial infection, but also the TLR2-dependent activation of phagocyte cells skews adaptive immune responses toward the Th2-type responses, which favor intracellular survival of mycobacteria [26].…”

“…As TB progresses the subversive effect of the Th2-like response ultimately impairs bactericidal function. Potent immunosuppressive Th2 cytokines such as IL-4, IL-4delta2, IL-10, and IL-13 may be involved, since they inhibit macrophage activity by down-regulating the TLR2 pathway and inducible nitric oxide (iNOS) synthesis [2,6,48,51,61,63]. In agreement with this observation, live strains of Mtb and their products like lipid components also elicit production of the Th2 cytokines (IL-4, IL-5, IL-10, and IL-13) [22].…”

Wound Healing Is Impaired in MyD88-Deficient Mice

“…71 There has been considerable interest recently in alternatively activated macrophage phenotypes, with classically activated (M1) macrophages being implicated in the regulation of inflammation and alternatively activated M2 macrophages participating in the regulation of angiogenesis. [72][73][74][75][76][77][78] Acquisition of the M2 phenotype was originally proposed to require stimulation by glucocorticoids and cytokines such as IL-10 and IL-13. 73 We have proposed that the TLR/adenosine-mediated angiogenic switch provides a simple, physiologically relevant, mechanism for switching macrophages to an M2-like phenotype, in a manner that does not rely on the presence of particular cytokines, but only on the accumulation of extracellular adenosine, which occurs as a consequence of hypoxia and ischemia.…”