Toll-like Receptor 2 (TLR2) and TLR4 Differentially Activate Human Dendritic Cells

Human dendritic cells respond to Porphyromonas gingivalis LPS by promoting a Th2 effector response in vitro

“…2 and Table 1). Thus these data are consistent with the concept that MDDC can become polarized [3,8,28] when exposed to different bacterial pathogenassociated molecular patterns and that these MDDC can than induce a T helper cell subset response that is consistent with the cytokine profiles (and maturation status) of MDDC [28].…”

“…P. gingivalis LPS is active in C3H/HeJ mice that possess a point mutation in tlr4 [9,10,31] and thus do not respond to enteric LPS moieties. TLR4 is the principal TLR species involved in LPS signaling, whereas TLR2 is the paradigmatic receptor for bacterial components other than LPS, including lipoteichoic acid, peptidoglycan and lipoproteins [8]. Recent studies suggest that TLR2 might be the primary signal-transducing molecule for LPS from certain nonenterobacterial Gramnegative organisms, including P. gingivalis [9,11,12] and Leptospira interrogans [32].…”

“…DC can become cytokine-polarized by these microenvironmental signals, and can pass this information on to naive T cells in the lymph nodes, thereby promoting a Th1 or Th2 response (reviewed in [3]). Although many factors have been implicated in cytokine polarization [3][4][5][6][7][8][9], our group is particularly interested in the ability of different pathogen-associated molecular patterns to modulate the immune response [9]. Understanding this process may facilitate the improvement of vaccines to treat human diseases with an immunopathogenic etiology, such as autoimmune diseases, atopic dermatitis, asthma and periodontitis.…”

Pathophysiology of psoriasis: Recent advances on IL-23 and Th17 cytokines

“…Interestingly, dendritic cells produce IL-23 when stimulated by infection with Candida albicans, and this event is mediated by dectin-1, a C-type lectin receptor [16••,17••]. In addition, activation through other innate receptors can trigger IL-23 production by dendritic cells, including Toll-like receptor (TLR) 4 signaling induced by lipopolysaccharide from Bordetella pertussis and other sources [18,19]. It is unknown whether C. albicans and TLR ligands stimulate keratinocytes to make IL-23, but this is an intriguing possibility, because microorganisms have long been postulated to trigger some types of psoriasis.…”

Shift from toll‐like receptor 2 (TLR‐2) toward TLR‐4 dependency in the erosive stage of chronic streptococcal cell wall arthritis coincident with TLR‐4–mediated interleukin‐17 production

“…TLR ligands are potent inducers of a variety of proinflammatory cytokines, including TNF␣, IL-1, and IL-6, as well as the matrix metalloproteinases (MMPs). In addition, they promote the interaction between antigen-presenting cells and T cells through upregulation of costimulatory molecules in the immunologic synapse (3,4). It is known that direct TLR activation occurs in certain self-limiting types of arthritis, such as Lyme disease and Chlamydia-induced arthritis, and contributes to bacterial clearance (5,6).…”