scholarly journals Interleukin-21 Receptor Deficiency Increases the Initial Toll-like Receptor 2 Response but Protects Against Joint Pathology by Reducing Th1 and Th17 Cells During Streptococcal Cell Wall Arthritis

2014 ◽  
Vol 66 (4) ◽  
pp. 886-895 ◽  
Author(s):  
Renoud J. Marijnissen ◽  
Debbie M. Roeleveld ◽  
Deborah Young ◽  
Cheryl Nickerson-Nutter ◽  
Shahla Abdollahi-Roodsaz ◽  
...  
Keyword(s):  
Cell Wall ◽  
Th17 Cells ◽  
Toll Like Receptor ◽  
Streptococcal Cell Wall ◽  
Joint Pathology ◽  
Toll Like Receptor 2 ◽  
Interleukin 21 ◽  
Streptococcal Cell Wall Arthritis

scholarly journals 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

2008 ◽  
Vol 58 (12) ◽  
pp. 3753-3764 ◽  
Author(s):  
Shahla Abdollahi-Roodsaz ◽  
Leo A. B. Joosten ◽  
Monique M. Helsen ◽  
Birgitte Walgreen ◽  
Peter L. van Lent ◽  
...  
Keyword(s):  
Cell Wall ◽  
Interleukin 17 ◽  
Toll Like Receptor ◽  
Streptococcal Cell Wall ◽  
Toll Like Receptor 2 ◽  
Streptococcal Cell Wall Arthritis

scholarly journals Toll-Like Receptor 2 Pathway Drives Streptococcal Cell Wall-Induced Joint Inflammation: Critical Role of Myeloid Differentiation Factor 88

2003 ◽  
Vol 171 (11) ◽  
pp. 6145-6153 ◽  
Author(s):  
Leo A. B. Joosten ◽  
Marije I. Koenders ◽  
Ruben L. Smeets ◽  
Marleen Heuvelmans-Jacobs ◽  
Monique M. A. Helsen ◽  
...  
Keyword(s):  
Cell Wall ◽  
Critical Role ◽  
Joint Inflammation ◽  
Myeloid Differentiation ◽  
Toll Like Receptor ◽  
Streptococcal Cell Wall ◽  
Differentiation Factor ◽  
Toll Like Receptor 2 ◽  
Myeloid Differentiation Factor

scholarly journals Membrane-Associated Proteins of a Lipopolysaccharide-Deficient Mutant of Neisseria meningitidis Activate the Inflammatory Response through Toll-Like Receptor 2

2001 ◽  
Vol 69 (4) ◽  
pp. 2230-2236 ◽  
Author(s):  
Robin R. Ingalls ◽  
Egil Lien ◽  
Douglas T. Golenbock
Keyword(s):  
Cell Wall ◽  
Inflammatory Response ◽  
Neisseria Meningitidis ◽  
Parental Strain ◽  
Host Responses ◽  
Deficient Mutant ◽  
Toll Like Receptor ◽  
Gram Negative ◽  
Negative Cell ◽  
Toll Like Receptor 2

ABSTRACT The recent isolation of a lipopolysaccharide (LPS)-deficient mutant of Neisseria meningitidis has allowed us to explore the roles of other gram-negative cell wall components in the host response to infection. The experiments in this study were designed to examine the ability of this mutant strain to activate cells. Although it was clearly less potent than the parental strain, we found the LPS-deficient mutant to be a capable inducer of the inflammatory response in monocytic cells, inducing a response similar to that seen with Staphylococcus aureus. Cellular activation by the LPS mutant was related to expression of CD14, a high-affinity receptor for LPS and other microbial products, as well as Toll-like receptor 2, a member of the Toll family of receptors recently implicated in host responses to gram-positive bacteria. In contrast to the parental strain, the synthetic LPS antagonist E5564 did not inhibit the LPS-deficient mutant. We conclude that even in the absence of LPS, the gram-negative cell wall remains a potent inflammatory stimulant, utilizing signaling pathways independent of those involved in LPS signaling.

scholarly journals GM-CSF neutralisation suppresses inflammation and protects cartilage in acute streptococcal cell wall arthritis of mice

2006 ◽  
Vol 66 (4) ◽  
pp. 452-457 ◽  
Author(s):  
C Plater-Zyberk ◽  
L A B Joosten ◽  
M M A Helsen ◽  
J Hepp ◽  
P A Baeuerle ◽  
...  
Keyword(s):  
Cell Wall ◽  
Streptococcal Cell Wall ◽  
Gm Csf ◽  
Streptococcal Cell Wall Arthritis

DIFFERENT ROLES OF TUMOUR NECROSIS FACTOR α AND INTERLEUKIN 1 IN MURINE STREPTOCOCCAL CELL WALL ARTHRITIS

Cytokine ◽  
1998 ◽  
Vol 10 (9) ◽  
pp. 690-702 ◽  
Author(s):  
Sandra Kuiper ◽  
Leo A.B. Joosten ◽  
Alison M. Bendele ◽  
Carl K. Edwards III ◽  
Onno J. Arntz ◽  
...  
Keyword(s):  
Cell Wall ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Interleukin 1 ◽  
Tumour Necrosis Factor Α ◽  
Streptococcal Cell Wall ◽  
Factor Α ◽  
Streptococcal Cell Wall Arthritis ◽  
Necrosis Factor

scholarly journals Interleukin-1 Receptor but Not Toll-Like Receptor 2 Is Essential for MyD88-Dependent Th17 Immunity to Coccidioides Infection

2014 ◽  
Vol 82 (5) ◽  
pp. 2106-2114 ◽  
Author(s):  
Chiung-Yu Hung ◽  
María del Pilar Jiménez-Alzate ◽  
Angel Gonzalez ◽  
Marcel Wüthrich ◽  
Bruce S. Klein ◽  
...  
Keyword(s):  
Respiratory Disease ◽  
Th17 Cell ◽  
Th17 Cells ◽  
Cell Activation ◽  
Pulmonary Infection ◽  
Interleukin 1 ◽  
Signal Pathways ◽  
Toll Like Receptor ◽  
Content Type ◽  
Toll Like Receptor 2

ABSTRACTInterleukin-17A (IL-17A)-producing CD4+T helper (Th17) cells have been shown to be essential for defense against pulmonary infection withCoccidioidesspecies. However, we have just begun to identify the required pattern recognition receptors and understand the signal pathways that lead to Th17 cell activation after fungal infection. We previously reported thatCard9−/−mice vaccinated with formalin-killed spherules failed to acquire resistance toCoccidioidesinfection. Here, we report that bothMyD88−/−andCard9−/−mice immunized with a live, attenuated vaccine also fail to acquire protective immunity to this respiratory disease. LikeCard9−/−mice, vaccinatedMyD88−/−mice revealed a significant reduction in numbers of both Th17 and Th1 cells in their lungs afterCoccidioidesinfection. Both Toll-like receptor 2 (TLR2) and IL-1 receptor type 1 (IL-1r1) upstream of MyD88 have been implicated in Th17 cell differentiation. Surprisingly, vaccinatedTLR2−/−and wild-type (WT) mice showed similar outcomes after pulmonary infection withCoccidioides, while vaccinatedIL-1r1−/−mice revealed a significant reduction in the number of Th17 cells in their infected lungs compared to WT mice. Thus, activation of both IL-1r1/MyD88- and Card9-mediated Th17 immunity is essential for protection againstCoccidioidesinfection. Our data also reveal that the numbers of Th17 cells were reduced inIL-1r1−/−mice to a lesser extent than inMyD88−/−mice, raising the possibility that other TLRs are involved in MyD88-dependent Th17 immunity to coccidioidomycosis. An antimicrobial action of Th17 cells is to promote early recruitment of neutrophils to infection sites. Our data revealed that neutrophils are required for vaccine immunity to this respiratory disease.

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