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Maya Chrabieh - One of the best experts on this subject based on the ideXlab platform.
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inherited human irak 1 deficiency selectively impairs tlr signaling in fibroblasts
Proceedings of the National Academy of Sciences of the United States of America, 2017Co-Authors: Laura Israel, Erika Della Mina, Salim Bougarn, Ilaria Meloni, Alessandro Borghesi, Sabri Boughorbel, Hao Zhou, Maya ChrabiehAbstract:Most members of the Toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) families transduce signals via a canonical pathway involving the MyD88 adapter and the interleukin-1 receptor-associated kinase (IRAK) complex. This complex contains four molecules, including at least two (IRAK-1 and IRAK-4) active kinases. In mice and humans, deficiencies of IRAK-4 or MyD88 abolish most TLR (except for TLR3 and some TLR4) and IL-1R signaling in both leukocytes and fibroblasts. TLR and IL-1R responses are weak but not abolished in mice lacking IRAK-1, whereas the role of IRAK-1 in humans remains unclear. We describe here a boy with X-linked MECP2 deficiency-related syndrome due to a large de novo Xq28 chromosomal deletion encompassing both MECP2 and IRAK1. Like many boys with MECP2 null mutations, this child died very early, at the age of 7 mo. Unlike most IRAK-4– or MyD88-deficient patients, he did not suffer from invasive bacterial diseases during his short life. The IRAK-1 protein was completely absent from the patient’s fibroblasts, which responded very poorly to all TLR2/6 (PAM2CSK4, LTA, FSL-1), TLR1/2 (PAM3CSK4), and TLR4 (LPS, MPLA) agonists tested but had almost unimpaired responses to IL-1β. By contrast, the patient’s peripheral blood mononuclear cells responded normally to all TLR1/2, TLR2/6, TLR4, TLR7, and TLR8 (R848) agonists tested, and to IL-1β. The death of this child precluded long-term evaluations of the clinical consequences of inherited IRAK-1 deficiency. However, these findings suggest that human IRAK-1 is essential downstream from TLRs but not IL-1Rs in fibroblasts, whereas it plays a redundant role downstream from both TLRs and IL-1Rs in leukocytes.
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igm igd cd27 b cells are markedly reduced in irak 4 myd88 and tirap but not unc 93b deficient patients
Blood, 2012Co-Authors: Sandra K. Weller, Mélanie Bonnet, Héloïse Delagreverie, Laura Israel, Maya Chrabieh, Chaim Roifman, Ben-zion Garty, Laszlo Marodi, Carlos Rodriguezgallego, Andrew C. IssekutzAbstract:We studied the distribution of peripheral B-cell subsets in patients deficient for key factors of the TLR-signaling pathways (MyD88, TIRAP/MAL, IL-1 receptor–associated kinase 4 [IRAK-4], TLR3, UNC-93B, TRIF). All TLRs, except TLR3, which signals through the TRIF adaptor, require MyD88 and IRAK-4 to mediate their function. TLR4 and the TLR2 heterodimers (with TLR1, TLR6, and possibly TLR10) require in addition the adaptor TIRAP, whereas UNC-93B is needed for the proper localization of intracellular TLR3, TLR7, TLR8, and TLR9. We found that IgM+IgD+CD27+ but not switched B cells were strongly reduced in MyD88-, IRAK-4-, and TIRAP-deficient patients. This defect did not appear to be compensated with age. However, somatic hypermutation of Ig genes and heavy-chain CDR3 size distribution of IgM+IgD+CD27+ B cells were not affected in these patients. In contrast, the numbers of IgM+IgD+CD27+ B cells were normal in the absence of TLR3, TRIF, and UNC-93B, suggesting that UNC-93B–dependent TLRs, and notably TLR9, are dispensable for the presence of this subset in peripheral blood. Interestingly, TLR10 was found to be expressed at greater levels in IgM+IgD+CD27+ compared with switched B cells in healthy patients. Hence, we propose a role for TIRAP-dependent TLRs, possibly TLR10 in particular, in the development and/or maintenance of IgM+IgD+CD27+ B cells in humans.
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IgM+IgD+CD27+ B cells are markedly reduced in IRAK-4-, MyD88- and TIRAP- but not UNC-93B-deficient patients
Blood, 2012Co-Authors: Sandra K. Weller, Mélanie Bonnet, Héloïse Delagreverie, Laura Israel, Maya Chrabieh, Chaim Roifman, Ben-zion Garty, Carlos Rodríguez-gallego, Laszlo Marodi, Andrew C. IssekutzAbstract:We studied the distribution of peripheral B-cell subsets in patients deficient for key factors of the TLR-signaling pathways (MyD88, TIRAP/MAL, IL-1 receptor–associated kinase 4 [IRAK-4], TLR3, UNC-93B, TRIF). All TLRs, except TLR3, which signals through the TRIF adaptor, require MyD88 and IRAK-4 to mediate their function. TLR4 and the TLR2 heterodimers (with TLR1, TLR6, and possibly TLR10) require in addition the adaptor TIRAP, whereas UNC-93B is needed for the proper localization of intracellular TLR3, TLR7, TLR8, and TLR9. We found that IgM+IgD+CD27+ but not switched B cells were strongly reduced in MyD88-, IRAK-4-, and TIRAP-deficient patients. This defect did not appear to be compensated with age. However, somatic hypermutation of Ig genes and heavy-chain CDR3 size distribution of IgM+IgD+CD27+ B cells were not affected in these patients. In contrast, the numbers of IgM+IgD+CD27+ B cells were normal in the absence of TLR3, TRIF, and UNC-93B, suggesting that UNC-93B–dependent TLRs, and notably TLR9, are dispensable for the presence of this subset in peripheral blood. Interestingly, TLR10 was found to be expressed at greater levels in IgM+IgD+CD27+ compared with switched B cells in healthy patients. Hence, we propose a role for TIRAP-dependent TLRs, possibly TLR10 in particular, in the development and/or maintenance of IgM+IgD+CD27+ B cells in humans.
Laura Israel - One of the best experts on this subject based on the ideXlab platform.
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inherited human irak 1 deficiency selectively impairs tlr signaling in fibroblasts
Proceedings of the National Academy of Sciences of the United States of America, 2017Co-Authors: Laura Israel, Erika Della Mina, Salim Bougarn, Ilaria Meloni, Alessandro Borghesi, Sabri Boughorbel, Hao Zhou, Maya ChrabiehAbstract:Most members of the Toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) families transduce signals via a canonical pathway involving the MyD88 adapter and the interleukin-1 receptor-associated kinase (IRAK) complex. This complex contains four molecules, including at least two (IRAK-1 and IRAK-4) active kinases. In mice and humans, deficiencies of IRAK-4 or MyD88 abolish most TLR (except for TLR3 and some TLR4) and IL-1R signaling in both leukocytes and fibroblasts. TLR and IL-1R responses are weak but not abolished in mice lacking IRAK-1, whereas the role of IRAK-1 in humans remains unclear. We describe here a boy with X-linked MECP2 deficiency-related syndrome due to a large de novo Xq28 chromosomal deletion encompassing both MECP2 and IRAK1. Like many boys with MECP2 null mutations, this child died very early, at the age of 7 mo. Unlike most IRAK-4– or MyD88-deficient patients, he did not suffer from invasive bacterial diseases during his short life. The IRAK-1 protein was completely absent from the patient’s fibroblasts, which responded very poorly to all TLR2/6 (PAM2CSK4, LTA, FSL-1), TLR1/2 (PAM3CSK4), and TLR4 (LPS, MPLA) agonists tested but had almost unimpaired responses to IL-1β. By contrast, the patient’s peripheral blood mononuclear cells responded normally to all TLR1/2, TLR2/6, TLR4, TLR7, and TLR8 (R848) agonists tested, and to IL-1β. The death of this child precluded long-term evaluations of the clinical consequences of inherited IRAK-1 deficiency. However, these findings suggest that human IRAK-1 is essential downstream from TLRs but not IL-1Rs in fibroblasts, whereas it plays a redundant role downstream from both TLRs and IL-1Rs in leukocytes.
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igm igd cd27 b cells are markedly reduced in irak 4 myd88 and tirap but not unc 93b deficient patients
Blood, 2012Co-Authors: Sandra K. Weller, Mélanie Bonnet, Héloïse Delagreverie, Laura Israel, Maya Chrabieh, Chaim Roifman, Ben-zion Garty, Laszlo Marodi, Carlos Rodriguezgallego, Andrew C. IssekutzAbstract:We studied the distribution of peripheral B-cell subsets in patients deficient for key factors of the TLR-signaling pathways (MyD88, TIRAP/MAL, IL-1 receptor–associated kinase 4 [IRAK-4], TLR3, UNC-93B, TRIF). All TLRs, except TLR3, which signals through the TRIF adaptor, require MyD88 and IRAK-4 to mediate their function. TLR4 and the TLR2 heterodimers (with TLR1, TLR6, and possibly TLR10) require in addition the adaptor TIRAP, whereas UNC-93B is needed for the proper localization of intracellular TLR3, TLR7, TLR8, and TLR9. We found that IgM+IgD+CD27+ but not switched B cells were strongly reduced in MyD88-, IRAK-4-, and TIRAP-deficient patients. This defect did not appear to be compensated with age. However, somatic hypermutation of Ig genes and heavy-chain CDR3 size distribution of IgM+IgD+CD27+ B cells were not affected in these patients. In contrast, the numbers of IgM+IgD+CD27+ B cells were normal in the absence of TLR3, TRIF, and UNC-93B, suggesting that UNC-93B–dependent TLRs, and notably TLR9, are dispensable for the presence of this subset in peripheral blood. Interestingly, TLR10 was found to be expressed at greater levels in IgM+IgD+CD27+ compared with switched B cells in healthy patients. Hence, we propose a role for TIRAP-dependent TLRs, possibly TLR10 in particular, in the development and/or maintenance of IgM+IgD+CD27+ B cells in humans.
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IgM+IgD+CD27+ B cells are markedly reduced in IRAK-4-, MyD88- and TIRAP- but not UNC-93B-deficient patients
Blood, 2012Co-Authors: Sandra K. Weller, Mélanie Bonnet, Héloïse Delagreverie, Laura Israel, Maya Chrabieh, Chaim Roifman, Ben-zion Garty, Carlos Rodríguez-gallego, Laszlo Marodi, Andrew C. IssekutzAbstract:We studied the distribution of peripheral B-cell subsets in patients deficient for key factors of the TLR-signaling pathways (MyD88, TIRAP/MAL, IL-1 receptor–associated kinase 4 [IRAK-4], TLR3, UNC-93B, TRIF). All TLRs, except TLR3, which signals through the TRIF adaptor, require MyD88 and IRAK-4 to mediate their function. TLR4 and the TLR2 heterodimers (with TLR1, TLR6, and possibly TLR10) require in addition the adaptor TIRAP, whereas UNC-93B is needed for the proper localization of intracellular TLR3, TLR7, TLR8, and TLR9. We found that IgM+IgD+CD27+ but not switched B cells were strongly reduced in MyD88-, IRAK-4-, and TIRAP-deficient patients. This defect did not appear to be compensated with age. However, somatic hypermutation of Ig genes and heavy-chain CDR3 size distribution of IgM+IgD+CD27+ B cells were not affected in these patients. In contrast, the numbers of IgM+IgD+CD27+ B cells were normal in the absence of TLR3, TRIF, and UNC-93B, suggesting that UNC-93B–dependent TLRs, and notably TLR9, are dispensable for the presence of this subset in peripheral blood. Interestingly, TLR10 was found to be expressed at greater levels in IgM+IgD+CD27+ compared with switched B cells in healthy patients. Hence, we propose a role for TIRAP-dependent TLRs, possibly TLR10 in particular, in the development and/or maintenance of IgM+IgD+CD27+ B cells in humans.
Christian Fehrmann - One of the best experts on this subject based on the ideXlab platform.
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toll like receptor expression profile of human stem progenitor cells form the apical papilla
Journal of Endodontics, 2020Co-Authors: Christian Fehrmann, Christof E. Dörfer, Karim Fawzy M ElsayedAbstract:Abstract Introduction Stem/progenitor cells from the apical papilla (SCAPs) demonstrate remarkable regenerative and immunomodulatory properties. During their regenerative events, SCAPs, similar to other stem/progenitor cells, could interact with their local inflammatory microenvironment via their expressed toll-like receptors (TLRs). The present study aimed to describe for the first time the unique TLR expression profile of SCAPs. Methods Cells were isolated from the apical papilla of extracted wisdom teeth (n = 8), STRO-1 immunomagnetically sorted, and cultured to obtain single colony-forming units. The expression of CD14, 34, 45, 73, 90, and 105 were characterized on the SCAPs, and their multilineage differentiation potential was examined to prove their multipotent aptitude. After their incubation in basic or inflammatory medium (25 ng/mL interleukin 1 beta, 103 U/mL interferon gamma, 50 ng/mL tumor necrosis factor alpha, and 3 × 103 U/mL interferon alpha), a TLR expression profile for SCAPs under uninflamed as well as inflamed conditions was respectively generated. Results SCAPs demonstrated all predefined stem/progenitor cell characteristics. In basic medium, SCAPs expressed TLRs 1–10. The inflammatory microenvironment up-regulated the expression of TLR1, TLR2, TLR4, TLR5, TLR6, and TLR9 and down-regulated the expression of TLR3, TLR7, TLR8, and TLR10 in SCAPs under the inflamed condition. Conclusions The present study defines for the first time a distinctive TLR expression profile for SCAPs under uninflamed and inflamed conditions. This profile could greatly impact SCAP responsiveness to their inflammatory microenvironmental agents under regenerative conditions in vivo.
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Toll-like Receptor Expression Profile of Human Stem/Progenitor Cells Form the Apical Papilla.
Journal of Endodontics, 2020Co-Authors: Christian Fehrmann, Christof E. Dörfer, Karim M. Fawzy El-sayedAbstract:Abstract Introduction Stem/progenitor cells from the apical papilla (SCAPs) demonstrate remarkable regenerative and immunomodulatory properties. During their regenerative events, SCAPs, similar to other stem/progenitor cells, could interact with their local inflammatory microenvironment via their expressed toll-like receptors (TLRs). The present study aimed to describe for the first time the unique TLR expression profile of SCAPs. Methods Cells were isolated from the apical papilla of extracted wisdom teeth (n = 8), STRO-1 immunomagnetically sorted, and cultured to obtain single colony-forming units. The expression of CD14, 34, 45, 73, 90, and 105 were characterized on the SCAPs, and their multilineage differentiation potential was examined to prove their multipotent aptitude. After their incubation in basic or inflammatory medium (25 ng/mL interleukin 1 beta, 103 U/mL interferon gamma, 50 ng/mL tumor necrosis factor alpha, and 3 × 103 U/mL interferon alpha), a TLR expression profile for SCAPs under uninflamed as well as inflamed conditions was respectively generated. Results SCAPs demonstrated all predefined stem/progenitor cell characteristics. In basic medium, SCAPs expressed TLRs 1–10. The inflammatory microenvironment up-regulated the expression of TLR1, TLR2, TLR4, TLR5, TLR6, and TLR9 and down-regulated the expression of TLR3, TLR7, TLR8, and TLR10 in SCAPs under the inflamed condition. Conclusions The present study defines for the first time a distinctive TLR expression profile for SCAPs under uninflamed and inflamed conditions. This profile could greatly impact SCAP responsiveness to their inflammatory microenvironmental agents under regenerative conditions in vivo.
Andrew C. Issekutz - One of the best experts on this subject based on the ideXlab platform.
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igm igd cd27 b cells are markedly reduced in irak 4 myd88 and tirap but not unc 93b deficient patients
Blood, 2012Co-Authors: Sandra K. Weller, Mélanie Bonnet, Héloïse Delagreverie, Laura Israel, Maya Chrabieh, Chaim Roifman, Ben-zion Garty, Laszlo Marodi, Carlos Rodriguezgallego, Andrew C. IssekutzAbstract:We studied the distribution of peripheral B-cell subsets in patients deficient for key factors of the TLR-signaling pathways (MyD88, TIRAP/MAL, IL-1 receptor–associated kinase 4 [IRAK-4], TLR3, UNC-93B, TRIF). All TLRs, except TLR3, which signals through the TRIF adaptor, require MyD88 and IRAK-4 to mediate their function. TLR4 and the TLR2 heterodimers (with TLR1, TLR6, and possibly TLR10) require in addition the adaptor TIRAP, whereas UNC-93B is needed for the proper localization of intracellular TLR3, TLR7, TLR8, and TLR9. We found that IgM+IgD+CD27+ but not switched B cells were strongly reduced in MyD88-, IRAK-4-, and TIRAP-deficient patients. This defect did not appear to be compensated with age. However, somatic hypermutation of Ig genes and heavy-chain CDR3 size distribution of IgM+IgD+CD27+ B cells were not affected in these patients. In contrast, the numbers of IgM+IgD+CD27+ B cells were normal in the absence of TLR3, TRIF, and UNC-93B, suggesting that UNC-93B–dependent TLRs, and notably TLR9, are dispensable for the presence of this subset in peripheral blood. Interestingly, TLR10 was found to be expressed at greater levels in IgM+IgD+CD27+ compared with switched B cells in healthy patients. Hence, we propose a role for TIRAP-dependent TLRs, possibly TLR10 in particular, in the development and/or maintenance of IgM+IgD+CD27+ B cells in humans.
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IgM+IgD+CD27+ B cells are markedly reduced in IRAK-4-, MyD88- and TIRAP- but not UNC-93B-deficient patients
Blood, 2012Co-Authors: Sandra K. Weller, Mélanie Bonnet, Héloïse Delagreverie, Laura Israel, Maya Chrabieh, Chaim Roifman, Ben-zion Garty, Carlos Rodríguez-gallego, Laszlo Marodi, Andrew C. IssekutzAbstract:We studied the distribution of peripheral B-cell subsets in patients deficient for key factors of the TLR-signaling pathways (MyD88, TIRAP/MAL, IL-1 receptor–associated kinase 4 [IRAK-4], TLR3, UNC-93B, TRIF). All TLRs, except TLR3, which signals through the TRIF adaptor, require MyD88 and IRAK-4 to mediate their function. TLR4 and the TLR2 heterodimers (with TLR1, TLR6, and possibly TLR10) require in addition the adaptor TIRAP, whereas UNC-93B is needed for the proper localization of intracellular TLR3, TLR7, TLR8, and TLR9. We found that IgM+IgD+CD27+ but not switched B cells were strongly reduced in MyD88-, IRAK-4-, and TIRAP-deficient patients. This defect did not appear to be compensated with age. However, somatic hypermutation of Ig genes and heavy-chain CDR3 size distribution of IgM+IgD+CD27+ B cells were not affected in these patients. In contrast, the numbers of IgM+IgD+CD27+ B cells were normal in the absence of TLR3, TRIF, and UNC-93B, suggesting that UNC-93B–dependent TLRs, and notably TLR9, are dispensable for the presence of this subset in peripheral blood. Interestingly, TLR10 was found to be expressed at greater levels in IgM+IgD+CD27+ compared with switched B cells in healthy patients. Hence, we propose a role for TIRAP-dependent TLRs, possibly TLR10 in particular, in the development and/or maintenance of IgM+IgD+CD27+ B cells in humans.
Sefik S. Alkan - One of the best experts on this subject based on the ideXlab platform.
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tlr tlr cross talk in human pbmc resulting in synergistic and antagonistic regulation of type 1 and 2 interferons il 12 and tnf α
International Immunopharmacology, 2007Co-Authors: Tarun K Ghosh, Dan J Mickelson, Jonathan Solberg, Kenneth E Lipson, Jon R Inglefield, Sefik S. AlkanAbstract:Abstract Currently, single TLR agonists are being utilized for vaccination and tumor immunotherapy. Here we investigated the effects of tandem combinations of TLR agonists on the production of cytokines with major focus on IFN-α, -β, -γ, TNF-α, and IL-12. Using a primary human PBMC culture system, we found that tandem combinations of TLR2–9 agonists can be inert, additive, synergistic or antagonistic. The most interesting combination was TLR2 or TLR4 agonists in combination with TLR7/8 or TLR8 agonists. TLR4–TLR7/8 combinations synergistically up-regulated IFN-γ and IL-12, enhanced IFN-α and also moderately induced TNF-α. TLR2–TLR7/8 like TLR4–TLR7/8 synergistically up-regulated IFN-γ but not IL-12. TLR9 agonist CpG2216 produced high IFN-α but failed to up regulate IFN-γ singly or in tandem. Furthermore, TLR9-induced type-1 IFN was down regulated in combination with TLR7, or TLR8 agonists. TLR3 induced significant IFN-α/-β responses when used in a complex with membrane permeability enhancer DOTAP, and additively enhanced response with agonists to TLR2, 5, 7/8, and 8. To our knowledge, this study is the first to compare cytokine responses of all the possible tandem combinations of TLR agonists in human PBMC. We identified certain combinations of TLR agonists that may or may not have advantages over single agonists, for generating an “optimal cytokine combination” preferred in combating diseases.
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oligodeoxynucleotides differentially modulate activation of tlr7 and TLR8 by imidazoquinolines
Journal of Immunology, 2006Co-Authors: Keith B Gorden, John J L Battiste, Paul D Wightman, John P Vasilakos, Sefik S. AlkanAbstract:Among the 11 human TLRs, a subfamily TLR7, TLR8, and TLR9 display similarities in structure and endosomal localization. Natural agonists consisting of nucleic acids, such as ssRNA or DNA with CpG motifs, activate the innate immune cells through these TLRs. Immune response modifiers (IRMs) of imidazoquinoline class compounds 3M-001, 3M-002, and 3M-003 have been shown to activate the innate immune system via TLR7, TLR8, and TLR7/8, respectively. In looking at the effect of the agonists of the TLR7, TLR8, and TLR9 on the activation of NF-κB of transfected HEK cells, we discovered that some oligodeoxynucleotides (ODNs) could modulate imidazoquinoline effects in a negative or positive manner. In this study we demonstrate that poly(T) ODNs can inhibit TLR7 and enhance TLR8 signaling events involving NF-κB activation in HEK cells and cytokine production (IFN-α, TNF, and IL-12) by human primary PBMC. In contrast, TLR3 agonist poly(I:C) does not affect imidazoquinoline-induced responses. The modulation of TLR7 and TLR8 responses is independent of CpG motifs or the nature of the ODN backbone structure. Furthermore, we show that to be an effective modulator, the ODNs need to be in the cell at the same time with either of the TLR7 or TLR8 agonist. We have also demonstrated that there is a physical interaction between IRMs and ODNs. The cross-talk between ODNs, IRMs, and TLR7 and TLR8 uncovered by this study may have practical implications in the field of microbial infections, vaccination, and tumor therapy.
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toll like receptor tlr 2 9 agonists induced cytokines and chemokines i comparison with t cell receptor induced responses
Cellular Immunology, 2006Co-Authors: Tarun K Ghosh, Dan J Mickelson, Jonathan Solberg, Jon R Inglefield, Jason R Fink, Derek J Hook, Shalley K Gupta, Sheila J Gibson, Sefik S. AlkanAbstract:Abstract The cells of innate and adaptive immunity, although activated by different ligands, engage in cross talk to ensure a successful immune outcome. To better understand this interaction, we examined the demographic picture of individual TLR (TLRs 2–9) -driven profiles of eleven cytokines (IFN-α/β, IFN-γ, IL-12p40/IL-12p70, IL-4, 1L-13, TNF-α, IL-1β, IL-2, IL-10) and four chemokines (MCP-1, MIP1β, IL-8, and RANTES), and compared them with direct T-cell receptor triggered responses in an assay platform using human PBMCs. We find that T-cell activation by a combination of anti-CD3/anti-CD28/PHA induced a dominant IL-2, IL-13, and Type-II interferon (IFN-γ) response without major IL-12 and little Type-I interferon (IFN-αβ) release. In contrast, TLR7 and TLR9 agonists induced high levels of Type-I interferons. The highest IFN-γ levels were displayed by TLR8 and TLR7/8 agonists, which also induced the highest levels of pro-inflammatory cytokines IL-12, TNF-α, and IL-1β. Amongst endosomal TLRs, TLR7 displayed a unique profile producing weak IL-12, IFN-γ, TNF-α, IL-1β, and IL-8. TLR7 and TLR9 resembled each other in their cytokine profile but differed in MIP-1β and MCP1 chemokine profiles. Gram positive (TLR2, TLR2/6) and gram negative (TLR4) pathogen-derived TLR agonists displayed significant similarities in profile, but not in potency. TLR5 and TLR2/6 agonists paralleled TLR2 and TLR4 in generating pro-inflammatory chemokines MCP-1, MIP-1β, RANTES, and IL-8 but yielded weak TNF-α and IL-1 responses. Taken together, the data show that diverse TLR agonists, despite their operation through common pathways induce distinct cytokine/chemokine profiles that in turn have little or no overlap with TCR-mediated response.
