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Porin-incorporated liposome induces Toll-like receptors 2- and 6-dependent maturation and type 1 response of dendritic cell.
Int Immunol. 2008 Dec; 20(12):1551-63.II

Abstract

Porin of Shigella dysenteriae was incorporated in liposome (PIL) and presented to mouse splenic dendritic cells (DC). PIL up-regulated Toll-like receptor (TLR) 2 and TLR6 on DC, showing that co-expression of the two TLRs is involved in recognition of porin. Detection of myeloid differentiating factor 88 (MyD88)-TLR2 complex confirmed interaction between the two for triggering the downstream signaling, which ultimately led to TLR2-dependent nuclear translocation of nuclear factor-kappa B. PIL-induced expression of MHC class II (I-Ab), CD40 and CD80 showed maturation of DC, whereas up-regulation of intercellular adhesion molecule-1 and CCR7 implicated the capacity of splenic DC to migrate. Induction of messenger ribonucleic acid for the chemokines, macrophage-inflammatory protein (MIP)-1alpha, MIP-1beta and regulated upon activation, normal T cell expressed and secreted indicated a strong bias of PIL for type 1 polarization that was supported by the intracellular expression and release of tumor necrosis factor (TNF)-alpha and IL-12. Along with CD40 and CD80 expression, release of the cytokines of CD11c+ JAWS II cells was inhibited by TLR2 or simultaneous TLR2 and 6 knockdown showing that recognition of PIL by the two TLRs is essential for DC activation and type 1 polarization. The signaling pathway initiated upon recognition of PIL by the TLRs was MyD88 dependent as confirmed by inhibition of IL-6, TNF-alpha and IL-12 release of MyD88-knockdown JAWS II cells. The maturation and polarization of DC induced T(h)1 phenotype, as evident from proliferation, activation and IFN-gamma release of allogeneic CD4+ T cells in response to PIL-stimulated DC, thereby suggesting that the adjuvant activity of PIL can successfully bridge the innate and adaptive immunity.

Authors+Show Affiliations

Division of Immunology, National Institute of Cholera and Enteric Diseases, P-33, C.I.T. Road, Scheme XM, Kolkata 700 010, West Bengal, India.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18931363

Citation

Banerjee, Pallavi, et al. "Porin-incorporated Liposome Induces Toll-like Receptors 2- and 6-dependent Maturation and Type 1 Response of Dendritic Cell." International Immunology, vol. 20, no. 12, 2008, pp. 1551-63.
Banerjee P, Biswas A, Biswas T. Porin-incorporated liposome induces Toll-like receptors 2- and 6-dependent maturation and type 1 response of dendritic cell. Int Immunol. 2008;20(12):1551-63.
Banerjee, P., Biswas, A., & Biswas, T. (2008). Porin-incorporated liposome induces Toll-like receptors 2- and 6-dependent maturation and type 1 response of dendritic cell. International Immunology, 20(12), 1551-63. https://doi.org/10.1093/intimm/dxn114
Banerjee P, Biswas A, Biswas T. Porin-incorporated Liposome Induces Toll-like Receptors 2- and 6-dependent Maturation and Type 1 Response of Dendritic Cell. Int Immunol. 2008;20(12):1551-63. PubMed PMID: 18931363.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Porin-incorporated liposome induces Toll-like receptors 2- and 6-dependent maturation and type 1 response of dendritic cell. AU - Banerjee,Pallavi, AU - Biswas,Amlan, AU - Biswas,Tapas, Y1 - 2008/10/17/ PY - 2008/10/22/pubmed PY - 2009/7/31/medline PY - 2008/10/22/entrez SP - 1551 EP - 63 JF - International immunology JO - Int Immunol VL - 20 IS - 12 N2 - Porin of Shigella dysenteriae was incorporated in liposome (PIL) and presented to mouse splenic dendritic cells (DC). PIL up-regulated Toll-like receptor (TLR) 2 and TLR6 on DC, showing that co-expression of the two TLRs is involved in recognition of porin. Detection of myeloid differentiating factor 88 (MyD88)-TLR2 complex confirmed interaction between the two for triggering the downstream signaling, which ultimately led to TLR2-dependent nuclear translocation of nuclear factor-kappa B. PIL-induced expression of MHC class II (I-Ab), CD40 and CD80 showed maturation of DC, whereas up-regulation of intercellular adhesion molecule-1 and CCR7 implicated the capacity of splenic DC to migrate. Induction of messenger ribonucleic acid for the chemokines, macrophage-inflammatory protein (MIP)-1alpha, MIP-1beta and regulated upon activation, normal T cell expressed and secreted indicated a strong bias of PIL for type 1 polarization that was supported by the intracellular expression and release of tumor necrosis factor (TNF)-alpha and IL-12. Along with CD40 and CD80 expression, release of the cytokines of CD11c+ JAWS II cells was inhibited by TLR2 or simultaneous TLR2 and 6 knockdown showing that recognition of PIL by the two TLRs is essential for DC activation and type 1 polarization. The signaling pathway initiated upon recognition of PIL by the TLRs was MyD88 dependent as confirmed by inhibition of IL-6, TNF-alpha and IL-12 release of MyD88-knockdown JAWS II cells. The maturation and polarization of DC induced T(h)1 phenotype, as evident from proliferation, activation and IFN-gamma release of allogeneic CD4+ T cells in response to PIL-stimulated DC, thereby suggesting that the adjuvant activity of PIL can successfully bridge the innate and adaptive immunity. SN - 1460-2377 UR - https://www.unboundmedicine.com/medline/citation/18931363/Porin_incorporated_liposome_induces_Toll_like_receptors_2__and_6_dependent_maturation_and_type_1_response_of_dendritic_cell_ L2 - https://academic.oup.com/intimm/article-lookup/doi/10.1093/intimm/dxn114 DB - PRIME DP - Unbound Medicine ER -