TY - JOUR
T1 - Cutting edge: Loss of TLR2, TLR4, and TLR5 on Langerhans cells abolishes bacterial recognition
AU - van der Aar, Angelic M. G.
AU - Sylva-Steenland, Regien M. R.
AU - Bos, Jan D.
AU - Kapsenberg, Martien L.
AU - de Jong, Esther C.
AU - Teunissen, Marcel B. M.
PY - 2007
Y1 - 2007
N2 - It is unknown whether closely related epidermal dendritic cells, Langerhans cells (M), and dermal dendritic cells (DDCs) have unique functions. In this study, we show that human DDCs have a broad TLR expression profile, whereas human LCs have a selective impaired expression of cell surface TLR2, TLR4, and TLR5, all involved in bacterial recognition. This distinct TLR expression profile is acquired during the TGF-beta 1-driven development of LCs in vitro. Consequently, and in contrast to DDCs, LCs weakly respond to bacterial TLR2, TLR4, and TLR5 ligands in terms of cytokine production and maturation, as well as to whole Gram-positive and Gram-negative bacteria, whereas their responsiveness to viral TLR ligands and viruses is fully active and comparable to DDCs. Unresponsiveness of M to bacteria may be a mechanism that contributes to tolerance to bacterial commensals that colonize the skin. The Journal of Immunology, 2007, 178: 1986-1990
AB - It is unknown whether closely related epidermal dendritic cells, Langerhans cells (M), and dermal dendritic cells (DDCs) have unique functions. In this study, we show that human DDCs have a broad TLR expression profile, whereas human LCs have a selective impaired expression of cell surface TLR2, TLR4, and TLR5, all involved in bacterial recognition. This distinct TLR expression profile is acquired during the TGF-beta 1-driven development of LCs in vitro. Consequently, and in contrast to DDCs, LCs weakly respond to bacterial TLR2, TLR4, and TLR5 ligands in terms of cytokine production and maturation, as well as to whole Gram-positive and Gram-negative bacteria, whereas their responsiveness to viral TLR ligands and viruses is fully active and comparable to DDCs. Unresponsiveness of M to bacteria may be a mechanism that contributes to tolerance to bacterial commensals that colonize the skin. The Journal of Immunology, 2007, 178: 1986-1990
U2 - https://doi.org/10.4049/jimmunol.178.4.1986
DO - https://doi.org/10.4049/jimmunol.178.4.1986
M3 - Article
C2 - 17277101
SN - 0022-1767
VL - 178
SP - 1986
EP - 1990
JO - Journal of immunology (Baltimore, Md.
JF - Journal of immunology (Baltimore, Md.
IS - 4
ER -