scholarly journals DNA Vaccines: MHC II-Targeted Vaccine Protein Produced by Transfected Muscle Fibres Induces a Local Inflammatory Cell Infiltrate in Mice

PLoS ONE ◽  
2014 ◽  
Vol 9 (10) ◽  
pp. e108069 ◽  
Author(s):  
Tom-Ole Løvås ◽  
Jo C. Bruusgaard ◽  
Inger Øynebråten ◽  
Kristian Gundersen ◽  
Bjarne Bogen
Keyword(s):  
Inflammatory Cell ◽  
Dna Vaccines ◽  
Inflammatory Cell Infiltrate ◽  
Muscle Fibres ◽  
Cell Infiltrate ◽  
Mhc Ii

scholarly journals Higher Number of EBI3 Cells in Mucosal Chronic Hyperplastic Candidiasis May Serve to Regulate IL-17-Producing Cells

2021 ◽  
Vol 7 (7) ◽  
pp. 533
Author(s):  
Ailish Williams ◽  
Helen Rogers ◽  
David Williams ◽  
Xiao-Qing Wei ◽  
Damian Farnell ◽  
...  
Keyword(s):  
Oral Mucosa ◽  
Oral Lichen Planus ◽  
Inflammatory Cell ◽  
Candida Infection ◽  
Inflammatory Cell Infiltrate ◽  
T Helper ◽  
Cell Infiltrate ◽  
High Prevalence ◽  
Squamous Cell Papilloma ◽  
Oral Lichen

Previous research into the inflammatory cell infiltrate of chronic hyperplastic candidosis (CHC) determined that the immune response is primarily composed of T cells, the majority of which are T helper (CD4+) cells. This present investigation used immunohistochemistry to further delineate the inflammatory cell infiltrate in CHC. Cells profiled were those expressing IL-17A cytokine, EBI3 and IL-12A subunits of the IL-35 cytokine, and FoxP3+ cells. Squamous cell papilloma (with Candida infection) and oral lichen planus tissues served as comparative controls to understand the local immune responses to Candida infection. The results demonstrated that Candida-induced inflammation and immune regulation co-exist in the oral mucosa of CHC and that high prevalence of cells expressing the EBI3 cytokine subunit may play an important role in this regulation. This balance between inflammation and immune tolerance toward invading Candida in the oral mucosa may be critical in determining progress of infection.

Immunohistochemical characterization of seminoma and its inflammatory cell infiltrate

1987 ◽  
Vol 18 (5) ◽  
pp. 511-520 ◽  
Author(s):  
Debra A. Bell ◽  
Thomas J. Flotie ◽  
Atul K. Bhan
Keyword(s):  
Inflammatory Cell ◽  
Inflammatory Cell Infiltrate ◽  
Cell Infiltrate

Characterisation of the inflammatory cell infiltrate in chronic hyperplastic candidosis of the oral mucosa

1997 ◽  
Vol 26 (2) ◽  
pp. 83-89 ◽  
Author(s):  
D. W. Williams ◽  
A. J. C. Potts ◽  
M. J. Wilson ◽  
J. B. Matthews ◽  
M. A. O. Lewis
Keyword(s):  
Oral Mucosa ◽  
Inflammatory Cell ◽  
Inflammatory Cell Infiltrate ◽  
Cell Infiltrate

The relationship between tumour necrosis, circulating IL-6 concentrations, and inflammatory responses in patients undergoing curative resection for colorectal cancer.

2013 ◽  
Vol 31 (4_suppl) ◽  
pp. 404-404
Author(s):  
Graeme JK Guthrie ◽  
Campbell SD Roxburgh ◽  
Colin H Richards ◽  
Paul G. Horgan ◽  
Donald C. Mcmillan
Keyword(s):  
Colorectal Cancer ◽  
Skeletal Muscle ◽  
Inflammatory Response ◽  
Interleukin 6 ◽  
Tumour Necrosis ◽  
Curative Resection ◽  
Inflammatory Cell ◽  
Inflammatory Responses ◽  
Inflammatory Cell Infiltrate ◽  
Cell Infiltrate

404 Background: Cancer-associated inflammation, in the form of systemic and local inflammation, and tumour necrosis are known to have prognostic value in colorectal cancer (CRC). In addition, recent work has reported a direct relationship between the systemic inflammatory response and loss of skeletal muscle in patients with CRC. However, the inter-relationships between these inflammatory responses, tumour necrosis, metabolic upset and circulating biochemical mediators are unclear in CRC. Interleukin-6 and its downstream signalling cascades have been implicated in both cancer-associated inflammation and cancer-associated muscle wasting. The aim of the present study was to examine whether circulating IL-6 concentrations may link tumour necrosis, local and systemic inflammatory responses, and metabolic upset in patients undergoing curative resection for colorectal cancer. Methods: The study included 118 patients undergoing surgery for CRC between 2004 and 2009. Data were collected from pre-operative blood tests. Routine pathology specimens were scored for Klintrup criteria and tumour necrosis. Results: Tumour necrosis was associated with increased T-stage (p<0.01), reduced inflammatory cell infiltrate (p<0.05), increased IL-6 (p<0.001), IL-10 (p<0.01), and VEGF (p<0.001) and with markers of the systemic inflammatory response: mGPS (p<0.001), anaemia (p<0.05); increased white cell (p<0.001), neutrophil (p<0.05) and platelet (p<0.001) counts. Circulating IL-6 was associated with increased IL-10 (p<0.01), VEGF (p<0.001), increased mGPS (p<0.001), increased white cell (p<0.01) and platelet (p<0.01) counts and low skeletal muscle index (p<0.01). On Spearman rank correlation there were significant associations between circulating concentrations of IL-6 and IL-10 (rs= 0.39, p<0.001) and CRP (r= 0.42, p<0.001). Conclusions: Interleukin-6 appears to be associated with systemic inflammation, tumour necrosis, and sarcopenia in colorectal cancer. However, the lack of an association between IL-6 and the local inflammatory response suggests a more complex relationship with the tumour inflammatory cell infiltrate.

Assessment of the tumor inflammatory cell infiltrate in preoperative colonoscopic biopsies of patients with primary operable colorectal cancer.

2015 ◽  
Vol 33 (3_suppl) ◽  
pp. 637-637
Author(s):  
James Hugh Park ◽  
David Mansouri ◽  
Clare Orange ◽  
Paul G. Horgan ◽  
Donald C. Mcmillan ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Cell ◽  
Tumor Resection ◽  
Inflammatory Cell Infiltrate ◽  
Cell Infiltrate ◽  
Elective Resection ◽  
Reliable Assessment ◽  
Resected Tumor ◽  
Tumor Biopsies ◽  
Independent Cohort

637 Background: The tumor inflammatory cell infiltrate is an important and potentially modifiable determinant of outcome in colorectal cancer (CRC). Although a weak inflammatory infiltrate is associated with poor prognosis independent of TNM stage, identifying such patients prior to surgery is problematic. The aim of the present study was to compare the tumor inflammatory cell infiltrate in matched preoperative colonoscopic tumor biopsies and resected tumor specimens from patients undergoing primary elective resection of CRC. Methods: Using an automated scoring system (nuclear h-score) CD3+ T-lymphocyte density was quantified in preoperative tumor biopsies of 76 patients undergoing elective resection of stage I-III CRC and compared to pathological characteristics and manual semi-quantitative (high vs. low) scoring of CD3+density within the invasive margin (IM) intraepithelial (IE) and cancer stroma (CS) compartments of resected tumor specimens. Results: The median h-score was 41 (range 14-85). Patients with a high tumor resection IM, IE and CS CD3+ density had a higher biopsy CD3+ density than patients with a low IM, IE and CS CD3+ density (median h-score: IM – 47 vs. 37, p=0.011; IE – 50 vs. 38, p=0.014, CS – 46 vs. 37, p=0.014). Patients with mismatch repair deficient tumors showed a trend towards a higher biopsy CD3+ density (57 vs. 40, p=0.169). No other pathological factors were associated with biopsy CD3+ density. When biopsy CD3+ density was categorised as high (h-score ≥41) or low (h-score<41), high biopsy CD3+ density was associated with CD3+ density within the IM, IE (both p≤0.05) and CS (p<0.01) and showed a trend towards greater 5-year survival (high – 80% (SE 7), low – 67% (SE 8), p=0.122). Conclusions: The results of the present study suggest that assessment of the inflammatory cell infiltrate in preoperative colonoscopic biopsies may provide reliable assessment of the inflammatory cell infiltrate within resected CRC tumors. Although requiring validation in an independent cohort, this has significant implications for the provision of neoadjuvant therapy, particularly targeting the inflammatory cell infiltrate, in patients with primary operable CRC.

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