Human Keratinocytes Express Functional CD14 and Toll-Like Receptor 4

Song, Peter I.; Neparidze, Natalia; Armstrong, Cheryl A.; Ansel, John C.; Park, Young-Min; Abraham, Tonya; Harten, Brad; Zivony, Adam

doi:10.1046/j.1523-1747.2002.01847.x

Cited by 184 publications

(185 citation statements)

References 57 publications

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“…4c). In keratinocytes, the TLR2 and TLR4 receptors are important for activation of the innate immunity by recognizing various microbial components, such as LPS [21]. The reason for the unchanged expression levels of MAIL and IκBα following LPS stimulation is unclear.…”

Section: Discussionmentioning

confidence: 99%

Role of NF-.KAPPA.B in Constitutive Expression of MAIL in Epidermal Keratinocytes

Oonuma

Morimatsu

Ochiai

et al. 2007

The Journal of Veterinary Medical Science

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ABSTRACT. Molecule possessing ankyrin-repeats induced by lipopolysaccharide (MAIL) is a nuclear IκB protein that is also known as interleukin-1-inducible nuclear ankyrin repeat protein and inhibitor of nuclear factor κBζ (IκBζ). We previously observed that MAILdeficient mice were affected by atopic dermatitis-like skin lesions and demonstrated the importance of MAIL in the skin. In this study, we investigated MAIL expression in mouse keratinocytes. MAIL mRNA was constitutively expressed in the skin epidermis. MAIL expression was also confirmed in primary keratinocytes and the PAM212 keratinocyte cell line. The inhibitors of nuclear factor κB (NF-κB)-Bay11-7082 and the IκBαM supersuppressor-considerably downregulated MAIL expression in the keratinocytes. Immunoreactivity for NF-κB components was localized in the cytoplasm and nucleus of normal unstimulated keratinocytes. The expression level of MAIL in the skin did not change following lipopolysaccharide (LPS) administration to mice. Interestingly, in accordance with the in vivo findings, the MAIL expression level did not change following LPS stimulation even in primary keratinocytes; however, MAIL expression was strongly increased by interleukin-1 stimulation. These results collectively suggest that the constitutive expression of MAIL in keratinocytes is controlled, at least in part, by NF-κB and that there may be LPS-specific repressive mechanisms that inhibit MAIL induction.

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Section: Discussionmentioning

confidence: 99%

Role of NF-.KAPPA.B in Constitutive Expression of MAIL in Epidermal Keratinocytes

Oonuma

Morimatsu

Ochiai

et al. 2007

The Journal of Veterinary Medical Science

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“…Similar to TLR1, 2 and 3, TLR4 was found to be expressed by monocytes, but also by polymorphonuclear (PMN) cells and DCs, at low levels in B cells, on fibroblasts, astrocytes, keratinocytes, myocytes, endothelial cells and epithelial cells (47,(84)(85)(86). A number of endogenous ligands for TLR4 have been described.…”

Section: Tlr4: Tlr4 Was the First Of The Human Tlrs To Be Identifiedmentioning

confidence: 91%

TLRs and chronic inflammation

Ospelt

Gay

2010

The International Journal of Biochemistry & Cell Biology

162

127

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After the discovery of Toll-like receptors (TLRs), innate immune mechanisms came back in the focus of scientific research. With more and more mechanisms of TLR biology known, it has become clear that these and also other innate immune receptors are not only of crucial importance in the immune response to invading pathogens, but also play a role in the homeostasis of commensal flora and in the response to stress and danger signals. In this respect, increasing evidence is found that inappropriate quantity or quality of TLR ligands or aberrant response to TLR activation plays a role in a variety of chronic inflammatory diseases. In this review, an overview of the currently known TLRs and their signaling pathways is given and reports about their expression and activation in chronic inflammatory diseases are recapitulated. TLRs and chronic inflammation Abstract:After the discovery of Toll-like receptors (TLRs), innate immune mechanisms came back in the focus of scientific research. With more and more mechanisms of TLR biology known, it has become clear that these and also other innate immune receptors are not only of crucial importance in the immune response to invading pathogens, but also play a role in the homeostasis of commensal flora and in the response to stress and danger signals. In this respect, increasing evidence is found that inappropriate quantity or quality of TLR ligands or aberrant response to TLR activation plays a role in a variety of chronic inflammatory diseases.In this review, an overview of the currently known TLRs and their signaling pathways isgiven and reports about their expression and activation in chronic inflammatory diseases are recapitulated.2

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“…Cytokines, chemokines, and antimicrobial peptides produced by epithelial cells enable them to participate in innate and acquired immune responses (1)(2)(3)(4)(5)(6). In addition, epithelia express certain TLRs, which may contribute to their ability to sense and respond to invading pathogens (3,(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21).…”

mentioning

confidence: 99%

TGF-α Regulates TLR Expression and Function on Epidermal Keratinocytes

Miller¹,

Sørensen

Liu³

et al. 2005

The Journal of Immunology

148

117

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The expression of TLRs on epithelial cells provides a first line of defense against invading pathogens. We investigated the regulated expression and function of TLR5 and TLR9 on human keratinocytes, because we found by immunohistochemistry that these TLRs are expressed in distinct layers of the epidermis. We found that TGF-α, a growth and differentiation factor that is present during wound healing and in psoriasis, increased the expression of both TLR5 and TLR9 on keratinocytes. In addition, TGF-α regulated the function of TLR5 and TLR9, because activation with their respective ligands enhanced the production of IL-8 and human β-defensins. These findings provide evidence that TGF-α up-regulates TLR expression and function, augmenting host defense mechanisms at epithelial surfaces.

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Human Keratinocytes Express Functional CD14 and Toll-Like Receptor 4

Cited by 184 publications

References 57 publications

Role of NF-.KAPPA.B in Constitutive Expression of MAIL in Epidermal Keratinocytes

Role of NF-.KAPPA.B in Constitutive Expression of MAIL in Epidermal Keratinocytes

TLRs and chronic inflammation

TGF-α Regulates TLR Expression and Function on Epidermal Keratinocytes

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