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Objectives. Oligoclonal T-cell infiltrates have been detected in the skin of patients with early dcSSc. Peripheral T cells from patients with early dcSSc co-cultured with autologous fibroblasts have been found to expand the same T-cell clonotypes found in the affected skin. Here, we characterize oligoclonally expanded T lymphocytes and investigate functional changes occurring in early-dcSSc co-cultured T lymphocytes and fibroblasts. [ABSTRACT FROM PUBLISHER]

In recent years several reports have suggested that T cells may have a role in systemic sclerosis (SSc). The aim of our study was to investigate the dynamics of T cell repertoire in early SSc disease analysing a target organ, the skin, and the peripheral blood. To date, indeed, it is not clear if T cell expansions found in SSc reflect a general activation or result from specific antigen stimulation in the target organs. This is an important point to assess in order to characterize the role of T cells in the development of SSc. To address these questions we studied T cell repertoire by CDR3 length analysis in skin biopsies and peripheral blood obtained from patients affected by SSc and we found that a skewed T cell repertoire was present only in the biopsies. In order to characterize more effectively the meaning of these data, we performed co-cultures using fibroblasts and peripheral blood mononuclear cells (PBMCs) obtained from SSc patients. These experiments showed that same T cell expansions were detectable in the skin of SSc patients and in the cultures of PBMCs and autologous fibroblasts of the patients but not in their peripheral blood. Taken together, these data suggest that fibroblasts trigger specific T cell expansions in the early phase of SSc. [ABSTRACT FROM AUTHOR]

Sphingosine 1-phosphate (SIP) is a sphingolipid mediator that is involved in diverse biological functions. Local administration of SI P causes inflammation coupled to a large eosinophil (EO) recruitment in the rat-paw tissue. The inflammatory response is accompanied by an increase in S1P receptors, namely S1P1, S1P2, S1P3, and by an enhanced expression of CCR3, which is the main chemokine receptor known to be involved in EO function. Human EQs constitutively express S1P, and, at a lower extent S1P2, S1P3 receptors. S1P in vitro causes cultured human EO migration and an increase in S1P receptor mRNA copies and strongly up-regulates CCR3 and RANTES (regulated on activation, normal I cell-expressed and secreted) message levels; in particular CCR3 is up-regulated 18,000-fold by S1P. A blocking anti-CCR3 Ab inhibits S1P-induced chemotaxis, implying that S1P acts as specific recruiting signal for EQs not only through its own receptors but also through CCR3. These results show that SIP is involved in EO chemotaxis and contribute to shed light on the complex mechanisms underlying EO recruitment in several diseases such as asthma and some malignancies. [ABSTRACT FROM AUTHOR]

The aim of the present prospective investigation was to study 49 dyspeptic Helicobacter pylori (HP)-positive (HP+) or -negative (HP), CagA+ and CagA- patients with a normal pattern or pure chronic gastritis at initial histology as well as normal features or hyperemic gastropathy at initial endoscopy in a two-year follow up. All the HP+ patients were treated with omeprazole 20 mg twice a day plus amoxicillin 1 g twice a day for two weeks. No substantial change was seen in gastritis in CagA+ patients in whom the infection was not eradicated, and, in contrast, a progressive improvement in 13/14 successfully treated patients was found. At endoscopy, a progressive change to a normal picture was seen in 8 and no change in 6 of 14 patients whose HP infection was eradicated, in contrast a worsening in the 9 HP+ patients who were still infected was observed. In particular, peptic lesions arose in 6 of 21 CagA+ patients in whom the infection was not eradicated. In conclusions, the lack of change in chronic gastritis at histology and the progressive worsening of endoscopic hyperemic gastropathy (with peptic lesions arising in 28,6%) when HP+ CagA+ infection is not eradicated, unlike the progressive improvement of the anatomoclinical condition in the patients whose infection was eradicated, draws attention to the relevance of eradicating HP in CagA+ patients even when no peptic lesion is found at initial endoscopy. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 60-year-old woman presented with paradoxical new-onset psoriasis. It found that the new-onset psoriasis is an adverse effect of treatment with anti-tumor necrosis factor-alpha (TNF) drugs. It suggests that the presence of a positive anti-nuclear antibodies (ANA) titer has no clinical significance, it has to be considered only a not uncommon finding in patients undergoing anti-TNF.