P.10.8 T-HELPER LYMPHOCYTES AND MAST CELLS: AN IMMUNOHISTOCHEMICAL TOOL FOR NON-CELIAC GLUTEN SENSITIVITY?

2018 ◽  
Vol 50 (2) ◽  
pp. e231
Author(s):  
G. Losurdo ◽  
D. Piscitelli ◽  
F. Pezzuto ◽  
F. Fortarezza ◽  
C. Covelli ◽  
...  
2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Giuseppe Losurdo ◽  
Domenico Piscitelli ◽  
Federica Pezzuto ◽  
Francesco Fortarezza ◽  
Claudia Covelli ◽  
...  

Background and Aims. Nonceliac gluten sensitivity (NCGS) is a gluten-related emerging condition. Since few data about NCGS histopathology is available, we assessed the markers of lymphocyte and innate immunity activation. Materials and Methods. We retrieved duodenal biopsy samples of patients with NCGS diagnosis according to the Salerno criteria. We selected specimens of positive (seropositive celiac disease/Marsh 1-2 stage) and negative (normal microscopic picture) controls. Immunohistochemistry for CD3 (intraepithelial lymphocytes-IELs), CD4 (T helper lymphocytes), CD8 (T cytotoxic lymphocytes), and CD1a/CD117 (Langerhans/mast cells) was performed. ANOVA plus Bonferroni’s tests were used for statistical analysis. Results. Twenty NCGS, 16 celiac disease, and 16 negative controls were selected. CD3 in NCGS were higher than negative controls and lower than celiac disease (18.5 ± 6.4, 11.9 ± 2.8, and 40.8 ± 8.1 IELs/100 enterocytes; p<0.001). CD4 were lower in NCGS than controls and celiac disease (31.0 ± 22.1, 72.5 ± 29.5, and 103.7 ± 15.7 cells/mm2; p<0.001). CD8 in NCGS were similar to negative controls, but lower than celiac disease (14.0 ± 7.4 and 34.0 ± 7.1 IELs/100 enterocytes, p<0.001). CD117 were higher in NCGS than celiac disease and negative controls (145.8 ± 49.9, 121.3 ± 13.1, and 113.5 ± 23.4 cells/mm2; p=0.009). Conclusions. The combination of CD4 and CD117, as well as IEL characterization, may be useful to support a clinical diagnosis of NCGS.


2015 ◽  
Vol 21 (4) ◽  
pp. 1-13
Author(s):  
Maha Abd El-wahed ◽  
Ebtesam Ahmed ◽  
Mohamed Mohamed ◽  
Nora Said

2021 ◽  
Vol 12 ◽  
Author(s):  
Yoan Eliasse ◽  
Edouard Leveque ◽  
Lucile Garidou ◽  
Louise Battut ◽  
Brienne McKenzie ◽  
...  

Acne is a multifactorial disease driven by physiological changes occurring during puberty in the pilosebaceous unit (PSU) that leads to sebum overproduction and a dysbiosis involving notably Cutibacterium acnes. These changes in the PSU microenvironment lead to a shift from a homeostatic to an inflammatory state. Indeed, immunohistochemical analyses have revealed that inflammation and lymphocyte infiltration can be detected even in the infraclinical acneic stages, highlighting the importance of the early stages of the disease. In this study, we utilized a robust multi-pronged approach that included flow cytometry, confocal microscopy, and bioinformatics to comprehensively characterize the evolution of the infiltrating and resident immune cell populations in acneic lesions, beginning in the early stages of their development. Using a discovery cohort of 15 patients, we demonstrated that the composition of immune cell infiltrate is highly dynamic in nature, with the relative abundance of different cell types changing significantly as a function of clinical lesion stage. Within the stages examined, we identified a large population of CD69+ CD4+ T cells, several populations of activated antigen presenting cells, and activated mast cells producing IL-17. IL-17+ mast cells were preferentially located in CD4+ T cell rich areas and we showed that activated CD4+ T cells license mast cells to produce IL-17. Our study reveals that mast cells are the main IL-17 producers in the early stage of acne, underlying the importance of targeting the IL-17+ mast cell/T helper cell axis in therapeutic approaches.


2005 ◽  
Vol 201 (12) ◽  
pp. 1869-1873 ◽  
Author(s):  
Joshua A. Boyce ◽  
K. Frank Austen

Mouse models of T helper type 2 (Th2) cell–biased pulmonary inflammation have elucidated mechanisms of sensitization, cell traffic, and induced airway hyperresponsiveness (AHR). Nonetheless, most mice lack intrinsic AHR, a central property of human asthma, and disparities persist regarding the contributions of eosinophils and mast cells and the sensitivity to induced AHR in the commonly used mouse strains. We suggest that these discordances, reflecting methodological and genetic differences, may be informative for understanding heterogeneity of human asthma.


2021 ◽  
Author(s):  
Alexandre GUILHEM ◽  
Pierre Portalès ◽  
Sophie Dupuis-Girod ◽  
Sophie Rivière ◽  
Thierry Vincent

Abstract Background: Hereditary hemorrhagic telangiectasia (HHT) is a rare genetic disease characterized by a deregulated neo-angiogenesis. Besides a mainly vascular phenotype (telangiectasia, arteriovenous malformations), patients exhibit a specific infectious risk and a deficit of T and natural killer (NK) lymphocytes. As the CXCR4/CXCL12 chemotactic axis is dysregulated in HHT endothelial cells, we hypothesized that a similar phenomenon could occur on lymphocytes.Results: Eighteen HHT patients with history of severe infection (HSI) were matched in age and sex with 18 HHT without HSI and 18 healthy control subjects (HC). We assessed the cell count and the surface expression of CXCR4 and CD26 (CXCL12 inactivating peptidase) of circulating helper and cytotoxic T lymphocytes (including naive, memory and activated subsets) and NK cells.The overall HHT group of 36 patients exhibited a reduction of circulating T-helper lymphocytes compared to HC (median: 517 vs 1026 cells/mm3, p<0.0001), correlated with age (r=-0.46, p=0.005), requirement of intravenous iron or blood transfusions (median: 291 vs 627 cells/mm3, p=0.03) and CXCR4 surface expression (r=0.353, p=0.0345). CXCR4 and CD26 membrane expression were both decreased on HHT T-helper lymphocytes (median MFI ratio: 4.49 vs 5.74 for CXCR4 and 3.21 vs 4.33 for CD26, p=0.03 and 0.0018 respectively) with an unchanged CXCR4/CD26 ratio. The HHT group with HSI had a higher CXCR4/CD26 ratio on the naive T-helper lymphocytes (median: 2.34 vs 1.32, p=0.0002), also observed on the T and T-helper populations.Conclusions: Our findings support a dysregulation of the CXCL12/CXCR4 chemotaxis of T-helper lymphocytes in HHT patients, potentially linked to their T-helper lymphopenia and susceptibility to infection.


2016 ◽  
Vol 291 (52) ◽  
pp. 26707-26721 ◽  
Author(s):  
Ioannis Panagoulias ◽  
Tassos Georgakopoulos ◽  
Ioanna Aggeletopoulou ◽  
Marios Agelopoulos ◽  
Dimitris Thanos ◽  
...  

2019 ◽  
Vol 71 (10) ◽  
pp. 1756-1765 ◽  
Author(s):  
Kristyna Hradilkova ◽  
Patrick Maschmeyer ◽  
Kerstin Westendorf ◽  
Heidi Schliemann ◽  
Olena Husak ◽  
...  

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