scholarly journals Toll-like receptor 2 (TLR2)-TLR9 crosstalk dictates IL-12 family cytokine production in microglia

Glia ◽  
2011 ◽  
Vol 60 (1) ◽  
pp. 29-42 ◽  
Author(s):  
Monica M. Holley ◽  
Yongqing Zhang ◽  
Elin Lehrmann ◽  
William H. Wood ◽  
Kevin G. Becker ◽  
...  
Keyword(s):  
Cytokine Production ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
Family Cytokine

Cytokine production by human odontoblast-like cells upon Toll-like receptor-2 engagement

Immunobiology ◽  
2011 ◽  
Vol 216 (4) ◽  
pp. 513-517 ◽  
Author(s):  
Jean-Christophe Farges ◽  
Florence Carrouel ◽  
Jean-François Keller ◽  
Caroline Baudouin ◽  
Philippe Msika ◽  
...  
Keyword(s):  
Cytokine Production ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

scholarly journals Non-LPS components ofChlamydia pneumoniae stimulate cytokine production through Toll-like receptor 2-dependent pathways

2002 ◽  
Vol 32 (4) ◽  
pp. 1188-1195 ◽  
Author(s):  
Mihai G. Netea ◽  
Bart Jan Kullberg ◽  
Jochem M. D. Galama ◽  
Anton F. H. Stalenhoef ◽  
Charles A. Dinarello ◽  
...  
Keyword(s):  
Cytokine Production ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

scholarly journals TLR2 Elicits IL-17-Mediated RANKL Expression, IL-17, and OPG Production in Neutrophils from Arthritic Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Viktoriya Milanova ◽  
Nina Ivanovska ◽  
Petya Dimitrova
Keyword(s):  
Nuclear Factor Kappa B ◽  
Cytokine Production ◽  
Receptor Expression ◽  
Toll Like Receptor ◽  
Rankl Expression ◽  
Zymosan A ◽  
Receptor Activator ◽  
Toll Like Receptor 2 ◽  
Neutrophil Depletion

We investigated the ability of neutrophils to express receptor activator of nuclear factor kappa-B ligand (RANKL), to secrete osteoprotegerin (OPG), and to produce IL-17. Arthritis was induced by intra-articular injection of zymosan, a ligand for Toll-like receptor 2 (TLR2). Frequencies of neutrophils in bone marrow (BM), blood and synovial fluid (SF), receptor expression, and cytokine production were evaluated by flow cytometry. 1A8 antibody (1A8 Ab) was used to deplete neutrophils in zymosan-injected SCID mice. IL-17, RANKL, and OPG amounts in SF, serum, or cell cultures were determined by ELISA. The development of arthritis was associated with increased secretion of IL-17, RANKL, and OPG in serum and SF, elevated frequencies of Ly6G+CD11b+cells in BM, blood, and SF and upregulated RANKL expression. Both IL-17 and OPG were absent in serum and SF after neutrophil depletion; therefore we assume that they were released by neutrophils. In vitro blood Ly6G+CD11b+cells from arthritic mice produced spontaneously IL-17, IFN-γ, and OPG and expressed RANKL. This phenotype was sustained by IL-17. TLR2 engagement increased IL-17 and IFN-γproduction, potentiated IL-17-mediated RANKL expression, and inhibited OPG secretion. We conclude that TLR2 regulates the destructive potential of neutrophils and its targeting might limit joint alterations in arthritis.

scholarly journals Difference in Strain Pathogenicity of Septicemic Yersinia pestis Infection in a TLR2−/− Mouse Model

2020 ◽  
Vol 88 (3) ◽  
Author(s):  
Kyle L. O’Donnell ◽  
Peter L. Knopick ◽  
Riley Larsen ◽  
Sanghita Sarkar ◽  
Matthew L. Nilles ◽  
...  
Keyword(s):  
Yersinia Pestis ◽  
Cytokine Production ◽  
Immune Cell ◽  
Neutrophil Infiltration ◽  
Cell Trafficking ◽  
Toll Like Receptor ◽  
Inflammatory Cytokine Production ◽  
Content Type ◽  
Immune Cell Trafficking ◽  
Toll Like Receptor 2

ABSTRACT Yersinia pestis is the causative agent of bubonic, pneumonic, and septicemic plague. We demonstrate that Toll-like receptor 2-deficient (TLR2−/−) mice are resistant to septicemic infection by the KIM5 strain of Y. pestis but not to infection by the CO92 Δpgm strain. This resistance is dependent on TLR2, the route of infection, and the isoform of YopJ. Elevated bacterial burdens were found in the spleens of CO92 Δpgm-infected animals by 24 h postinfection and in the livers by 4 days. The YopJ isoform present contributed directly to cytotoxicity and inflammatory cytokine production of bone marrow-derived macrophages from TLR2−/− mice. Immune cell trafficking is altered in CO92 Δpgm infections, with an increased neutrophil infiltration to the spleen 5 days postinfection. Immune cell infiltration to the liver was greater and earlier in KIM5-infected TLR2−/− mice. The functionality of the immune cells was assessed by the ability to develop reactive oxygen and nitrogen species. Our data suggest an inhibition of granulocytes in forming these species in CO92 Δpgm-infected TLR2−/− mice. These findings suggest that resistance to KIM5 in TLR2−/− mice is dependent on early immune cell trafficking and functionality.

The Toll-like receptor 2 R753Q mutation modifies cytokine production and Toll-like receptor expression in atopic dermatitis

2008 ◽  
Vol 121 (4) ◽  
pp. 1013-1019 ◽  
Author(s):  
Salima Mrabet-Dahbi ◽  
Alexander H. Dalpke ◽  
Margarete Niebuhr ◽  
Markus Frey ◽  
Christian Draing ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Cytokine Production ◽  
Receptor Expression ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

scholarly journals Cytadherence of Mycoplasma pneumoniae Induces Inflammatory Responses through Autophagy and Toll-Like Receptor 4

2014 ◽  
Vol 82 (7) ◽  
pp. 3076-3086 ◽  
Author(s):  
Takashi Shimizu ◽  
Yui Kimura ◽  
Yutaka Kida ◽  
Koichi Kuwano ◽  
Masato Tachibana ◽  
...  
Keyword(s):  
Immune Responses ◽  
Mycoplasma Pneumoniae ◽  
Cytokine Production ◽  
Inflammatory Responses ◽  
Hypothetical Protein ◽  
Toll Like Receptor ◽  
Wild Type ◽  
Toll Like Receptor 4 ◽  
Content Type ◽  
Toll Like Receptor 2

ABSTRACTMycoplasma pneumoniaecauses pneumonia, tracheobronchitis, pharyngitis, and asthma in humans. The pathogenesis ofM. pneumoniaeinfection is attributed to excessive immune responses. We previously demonstrated thatM. pneumoniaelipoproteins induced inflammatory responses through Toll-like receptor 2 (TLR2). In the present study, we demonstrated thatM. pneumoniaeinduced strong inflammatory responses in macrophages derived from TLR2 knockout (KO) mice. Cytokine production in TLR2 KO macrophages was increased compared with that in the macrophages of wild-type (WT) mice. Heat-killed, antibiotic-treated, and overgrownM. pneumoniaefailed to induce inflammatory responses in TLR2 KO macrophages. 3-Methyladenine and chloroquine, inhibitors of autophagy, decreased the induction of inflammatory responses in TLR2 KO macrophages. These inflammatory responses were also inhibited in macrophages treated with the TLR4 inhibitor VIPER and those obtained from TLR2 and TLR4 (TLR2/4) double-KO mice. Two mutants that lacked the ability to induce inflammatory responses in TLR2 KO macrophages were obtained by transposon mutagenesis. The transposons were inserted inatpCencoding an ATP synthase F0F1 ε subunit andF10_orf750encoding hypothetical protein MPN333. These mutants showed deficiencies in cytadherence. These results suggest that cytadherence ofM. pneumoniaeinduces inflammatory responses through TLR4 and autophagy.

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