Browsing by Author "Santos, P"
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- Expression patterns of HLA-DR+ or HLA-DR- on CD4+/CD25++/CD127low regulatory T cells in patients with allergyPublication . Geraldes, L; Morgado, J; Almeida, A; Todo-Bom, A; Santos, P; Chieira, C; Pais, MLBACKGROUND: Allergic rhinoconjunctivitis induced by pollen is a highly prevalent chronic inflammatory disease in Europe. Parietariajudaica is a frequent trigger in the Mediterranean area. The function of regulatory T cells (Treg cells) in allergy has recently been investigated, but further data are necessary to better understand their role and to find new strategies to treat allergic diseases such as allergic rhinoconjunctivitis. OBJECTIVE: To characterize gene expression of HLA-DR+ or HLA-DR- on peripheral CD4+/CD25++/CD127low Treg cells in patients with allergy. METHODS: Peripheral Treg cells (CD4+/CD25++/CD127low) were quantified using flow cytometry and sorted according to HLA-DR expression during the pollen season in patients with allergic rhinoconjunctivitis caused by P. judaica. The results were compared with those of nonatopic controls. Expression of associated cytokines and their receptors was measured using quantitative reverse transcription-polymerase chain reaction after extraction of mRNA in sorted populations. RESULTS: During the pollen season, no significant differences were observed between allergic patients with rhinoconjunctivitis and healthy controls in terms of the absolute number or the percentage of Treg cells in peripheral blood. All patients had a higher number/percentage of HLA-DR- Treg cells than HLA-DR+ Treg cells. In both groups we found high levels of FOXP3 mRNA expression. Despite being lower in number, HLA-DR+ Treg cells presented higher expression of CD28, PRF1, GZMB, and FASL than HLA-DR-Treg cells. CONCLUSIONS: The most relevant results obtained suggest that HLA-DR+ Treg cells tend to present higher gene expression of molecules associated with contact-dependent cell activation and cytotoxicity.
- Genetic markers in chronic urticariaPublication . Machado, D; Pereira, C; Martinho, A; Loureiro, G; Tavares, B; Santos, P; Calado, G; Chieira, C; Baganha, MF; Pais, M
- Multicentric Genome-Wide Association Study for Primary Spontaneous PneumothoraxPublication . Sousa, I; Abrantes, P; Francisco, V; Teixeira, G; Monteiro, M; Neves, J; Norte, A; Robalo-Cordeiro, C; Moura E Sá, J; Reis, E; Santos, P; Oliveira, M; Sousa, S; Fradinho, M; Malheiro, F; Negrão, L; Feijó, S; Oliveira, SADespite elevated incidence and recurrence rates for Primary Spontaneous Pneumothorax (PSP), little is known about its etiology, and the genetics of idiopathic PSP remains unexplored. To identify genetic variants contributing to sporadic PSP risk, we conducted the first PSP genome-wide association study. Two replicate pools of 92 Portuguese PSP cases and of 129 age- and sex-matched controls were allelotyped in triplicate on the Affymetrix Human SNP Array 6.0 arrays. Markers passing quality control were ranked by relative allele score difference between cases and controls (|RASdiff|), by a novel cluster method and by a combined Z-test. 101 single nucleotide polymorphisms (SNPs) were selected using these three approaches for technical validation by individual genotyping in the discovery dataset. 87 out of 94 successfully tested SNPs were nominally associated in the discovery dataset. Replication of the 87 technically validated SNPs was then carried out in an independent replication dataset of 100 Portuguese cases and 425 controls. The intergenic rs4733649 SNP in chromosome 8 (between LINC00824 and LINC00977) was associated with PSP in the discovery (P = 4.07E-03, ORC[95% CI] = 1.88[1.22-2.89]), replication (P = 1.50E-02, ORC[95% CI] = 1.50[1.08-2.09]) and combined datasets (P = 8.61E-05, ORC[95% CI] = 1.65[1.29-2.13]). This study identified for the first time one genetic risk factor for sporadic PSP, but future studies are warranted to further confirm this finding in other populations and uncover its functional role in PSP pathogenesis.