Genetic polymorphisms of CD14, Toll-like receptor-2 and Manan-binding lectin in ulcerative colitis

2007 ◽  
Vol 13 (supplement) ◽  
pp. 653-654
Author(s):  
T Tahara ◽  
T Arisawa ◽  
F Wang ◽  
T Shibata ◽  
M Nakamura ◽  
...  
2007 ◽  
Vol 13 ◽  
pp. 653-654
Author(s):  
T Tahara ◽  
T Arisawa ◽  
F Wang ◽  
T Shibata ◽  
M Nakamura ◽  
...  

2007 ◽  
Vol 22 (6) ◽  
pp. 925-929 ◽  
Author(s):  
Fangyu Wang ◽  
Tomomitsu Tahara ◽  
Tomiyasu Arisawa ◽  
Tomoyuki Shibata ◽  
Masakatsu Nakamura ◽  
...  

2014 ◽  
Vol 93 (11) ◽  
pp. 1859-1865 ◽  
Author(s):  
Hala Aly Abdel Rahman ◽  
Mervat Mamdooh Khorshied ◽  
Ola M. Reda Khorshid ◽  
Shirihan Mahmoud Mahgoub

2006 ◽  
Vol 12 (8) ◽  
pp. 659-663 ◽  
Author(s):  
Thor Ueland ◽  
Terje Espevik ◽  
John Kjekshus ◽  
Lars Gullestad ◽  
Torbjørn Omland ◽  
...  

2008 ◽  
Vol 205 (1) ◽  
pp. 169-181 ◽  
Author(s):  
W.K. Eddie Ip ◽  
Kazue Takahashi ◽  
Kathryn J. Moore ◽  
Lynda M. Stuart ◽  
R. Alan B. Ezekowitz

Innate immunity is the first-line defense against pathogens and relies on phagocytes, soluble components, and cell-surface and cytosolic pattern recognition receptors. Despite using hard-wired receptors and signaling pathways, the innate immune response demonstrates surprising specificity to different pathogens. We determined how combinatorial use of innate immune defense mechanisms defines the response. We describe a novel cooperation between a soluble component of the innate immune system, the mannose-binding lectin, and Toll-like receptor 2 that both specifies and amplifies the host response to Staphylococcus aureus. Furthermore, we demonstrate that this cooperation occurs within the phagosome, emphasizing the importance of engulfment in providing the appropriate cellular environment to facilitate the synergy between these defense pathways.


2007 ◽  
Vol 56 (3) ◽  
pp. 267-274 ◽  
Author(s):  
Lenka Frolova ◽  
Pavel Drastich ◽  
Pavel Rossmann ◽  
Klara Klimesova ◽  
Helena Tlaskalova-Hogenova

Dysregulation of innate and adaptive intestinal immune responses to bacterial microbiota is supposed to be involved in pathogenetic mechanisms of inflammatory bowel diseases (IBDs). We investigated expression of Toll-like receptor 2 (TLR2), TLR4, and their transmembrane coreceptor CD14 inbiopsy samples from patients with IBD and in non-inflamed gut mucosa from controls. Small intestine and colon samples were obtained by colonoscopy from patients with Crohn's disease (CD), ulcerative colitis (UC), and controls. Immunohistochemical analysis of cryostat sections using polyclonal and monoclonal antibodies specific for TLR2, TLR4, and CD14 showed a significant increase in TLR2 expression in the terminal ileum of patients with inactive and active UC against controls. Significant upregulation of TLR4 expression relative to controls was found in the terminal ileum and rectum of UC patients in remission and in the terminal ileum of CD patients with active disease. CD14 expression was upregulated in the terminal ileum of CD patients in remission and with active disease, in the cecum of UC patients in remission and with active disease, and in rectum of UC patients with active disease. Hence, dysregulation of TLR2, TLR4, and CD14 expression in different parts of the intestinal mucosa may be crucial in IBD pathogenesis.


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