CXCR4 pos circulating progenitor cells coexpressing monocytic and endothelial markers correlating with fibrotic clinical features are present in the peripheral blood of patients affected by systemic sclerosis

There is still controversy regarding the role of circulating endothelial and progenitor cells (CECs/CEPs) in the pathogenesis of systemic sclerosis (SSc). Using a sequential Boolean gating strategy based on a 4-color flow cytometric protocol, an increased number of CD31(pos)/CD184(pos)(CXCR4)/CD34(pos)/CD45(pos) and CD31(pos)/CD117(pos) (c-kit-R) /CD34(pos)/ CD45(pos) hematopoietic circulating progenitor cells (HCPCs) was detected in SSc patients compared with healthy subjects. In SSc, no circulating mature and progenitor endothelial cells were observed, while an enhanced generation of erythroid progenitor cells was found to be correlated with the presence of CD117+ HCPCs. The presence of freshly detected CXCR4posHCPC was correlated either to the in vitro cultured spindle-shaped endothelial like cells (SELC) with an endo/myelomonocytic profile or to SDF-1 and VEGF serum level. These data are related to more fibrotic clinical features of the disease, thus supporting a possible role of these cells in fibrosis

Connettivite non classificabile e tiroidite autoimmune

none7Abstract n. P83noneRIZZO N; LOCAPUTO A; CASTELLINO G; FOTINIDI M; VOLPINARI S; GOVONI M; TROTTA FRizzo, N; Locaputo, A; Castellino, Gabriella; Fotinidi, Maria; Volpinari, Stefania; Govoni, Marcello; Trotta, Francesc

Studio dei progenitori emopoietici e delle cellule endoteliali in cors di patologie autoimmuni: ruolo della citometria a flusso multicolore

Studio dei progenitori emopoietici e delle cellule endoteliali in cors di patologie autoimmuni: ruolo della citometria a flusso multicolore

Involvement of the Inconstant Bursa of the Fifth Metatarsophalangeal Joint in Psoriatic Arthritis: A Clinical and Ultrasonographic Study

Objective. To evaluate the involvement of the bursa located next to the head of the 5th metatarsal bone in patients with psoriatic arthritis (PsA) in comparison with the other seronegative spondyloarthritis (SpA). Methods. All patients with PsA seen during a period of 24 months were enrolled. The control group included healthy subjects and patients with the other SpA. All subjects underwent clinical and ultrasound (US) examination of the lateral surface of the 5th metatarsal. Results. 150 PsA patients (88 M; 62 F), 172 SpA (107 M; 65 F), and 95 healthy controls (58 M; 37 F) were evaluated. Based on clinical and US evaluation, bursitis was diagnosed in 17/150 (11.3%) PsA patients but in none of the SpA (P < 0.0001) and healthy (P = 0.0002) controls. In detecting bursitis, US was more sensitive than clinical examination, although the difference did not reach statistical significance (P = 0.09). Conclusion. The bursa of the 5th metatarsophalangeal joint appears to be involved in PsA more frequently than by chance. If confirmed by other studies, this finding could be considered as a distinctive clinical sign of PsA, useful for differential diagnosis with the other SpA. In asymptomatic patients, US proved to be more sensitive in the detection of bursiti

Can tumor necrosis factor receptor II gene 676T>G polymorphism predict the response grading to anti-TNFα therapy in rheumatoid arthritis?

none10In this study we analyzed whether the polymorphisms 676T>G in the tumor necrosis factor receptor (TNFR) II gene and -308G>A in the TNFα promoter gene may influence the response grading to anti-TNFα therapy in rheumatoid arthritis. We enrolled and genotyped 105 RA patients treated with etanercept (n=55), infliximab (n=40) and adalimumab (n=10) for one year. The clinical response was evaluated according to the ACR criteria every 3 months. Patients with TNFRII 676TG genotype was significantly associated with lower ACR response compared to 676TT genotype, at 3 (OR 3.78 95%CI 1.07-13.31) and 12 months (OR 4.30 95%CI 1.16-15.99) of treatment. No significant association between TNFα -308G>A polymorphism and the clinical response was found. TNFRII 676TG genotype is associated with a lower response to anti-TNFα therapy, independently from the specific agent used. This polymorphism could become a useful genetic marker for predicting the different response grading to anti-TNFα therapy.noneA. Ongaro; M. De Mattei; A. Pellati; A. Caruso; S. Ferretti; F. F. Masieri; M. Fotinidi; I. Farina; F. Trotta; M. PadovanOngaro, Alessia; DE MATTEI, Monica; Pellati, Agnese; Caruso, Angelo; Ferretti, Stefano; Masieri, Federica Francesca; Fotinidi, Maria; Farina, Ilaria; Trotta, Francesco; Padovan, Meliss

The c.1298A>C polymorphism in the Methylenetetrahydrofolate Reductase (MTHFR) gene is risk factor for Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a common autoimmune disease characterized by chronic inflammation that causes joint deformity, pain, functional limitations and psychological distress leading to work disability and consequent relevant social and individual costs. RA is a complex disease that results from the interplay between genetic and environmental factors. Identification of the genetic factors involved in the pathogenesis of RA could be crucial for early diagnosis and development of treatment strategies directed at the cause of the disease. However, still little is known susceptibility genes for RA. Although HLA-DRB1 is the main RA gene, it accounts for only part of the genetic risk for RA. Association studies suggested that other genes, including TNFR2, PADI4, SLC22A4, RUNX1, and PTPN22 play a role in the etiology of the disease. Metotrexate (MTX) is the first line treatment for RA and its efficacy has been reported to be dependent on gene variant in the Methylenetetrahydrofolate Reductase (MTHFR) gene. To assess the possible role of MTHFR polymorphisms in the etiology of RA, we genotyped the c.677C>T and the c.1298A>C variant in MTHFR gene in a group of 217 Italian RA patients and in a matched group of healthy controls. While no significant difference of c.677C>T genotypes between cases and controls was found, a clear increase of c.1298CC genotype was observed among RA patients (OR=2.59; p=0.0093). Our results suggest that MTHFR c.1298CC genotype may be considered a low-penetrance susceptibility factor for RA and point out a possible role of folate metabolism in the etiology of the disease