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An adventitious shoot regeneration protocol from in vitro leaves of the most important dried plum cultivar in the USA, ‘Improved French’, has been established. Factors affecting regeneration were studied in order to optimise regeneration. The proliferation medium in which the shoots, used as the source of leaf explants, were cultured had a strong influence on subsequent regeneration. Shoot regeneration was observed at a mean frequency of 52% when a Murashige-based and Skoog-based shoot culture medium with 3 μM N6-benzylaminopurine and 0.25 μM indole-3-butyric acid (IBA) was employed compared with shoot regeneration frequencies of less than 5% for a Quoirin-based and Lepoivre-based shoot culture medium, with 8.9 μM N6-benzylaminopurine and 0.49 μM IBA. The shoot regeneration medium contained α-naphthaleneacetic acid at 2.0–6.0 μM and thidiazuron at 4.5–15.0 μM. 2,4 Dichlorophenoxy-acetic acid at 9.0 μM was included in the medium but only for the first 4 days of culture. Shoot regeneration frequencies were positively related to thidiazuron concentration and significantly greater (P < 0.05) for 9–15 μM thidiazuron than for the media with 4.5 μM thidiazuron. Leaf explants, incubated in a 16-h-light/8-h-dark photoperiod or in the dark for 1 week followed by exposure to light, showed significantly more organogenic activity (P < 0.01) than was observed for leaves cultured in the dark for 2 or 3 weeks before they were transferred to the light. The utilisation of Bacto agar (0.7%) as the gelling agent increased organogenesis compared with media gelled with TC Agar (0.7%), or an agar–gellan gum blend (Agargel™) (0.45%). The addition of the ethylene inhibitor silver thiosulphate at 60–120 μM also improved organogenesis. When all the studied factors were optimised, a regeneration rate of 65% was achieved. Rooting frequency of regenerated shoots was significantly increased (P < 0.05) by the use of full-strength Murashige and Skoog salts (40%) or 100 mg L−1 phloroglucinol (53%) to the rooting medium. [ABSTRACT FROM AUTHOR]

Plum pox (Sharka) is a serious virus disease of stone fruits caused by the Plum pox virus (PPV). To determine which species could function as potential hosts and virus reservoirs, we used aphid transmission and bud or chip grafting to evaluate the susceptibility of commercial, ornamental, and wild Prunus species to isolates of PPV found in Pennsylvania, USA. Following inoculation, test trees were observed for symptoms, analyzed by enzyme-linked immunosorbent assay (ELISA) and polymerase chain reaction (PCR), back-assayed to healthy peach, and followed through at least four cold-induced dormancy (CID) cycles over 4 years. Thirty-one of 33 Prunus species and cultivars were systemically infected following aphid transmission. Systemic infection could not be detected in P. cerasus (sour cherry) and P × ‘Snofozam’ (Snow Fountains) despite repeated aphid inoculation attempts. Following grafting of PPV-infected budwood, all 40 species and varieties became infected, although species differed in their susceptibility. Within most species, some individual plants remained PPV negative throughout the study despite repeated inoculations. Infection in some species could be detected only through quantitative reverse transcription (RT)-PCR. Most species displayed clear symptoms, were highly positive by ELISA and RT-PCR, and could be back-inoculated into peach seedlings following CID. Our results indicate that a wide range of native and ornamental Prunus species are susceptible to U.S. isolates of PPV-D. [ABSTRACT FROM AUTHOR]

Genetic resistance to Plum pox virus (PPV) is the most viable alternative for long-term control of sharka disease. In addition to the classical approaches to producing resistant germplasm and cultivars, genetic transformation offers a promising genetic approach to resistance. We show, using the example of C5 plum, that genetically engineered resistance can provide durable, stable and high levels of PPV resistance. A review of the results of work with C5 including molecular analyses of resistance and long-term field testing is presented. [ABSTRACT FROM AUTHOR]

We studied HLA antigen distribution of 50 heterosexual partners of HIV+ drug abusers with more than I year of sexual exposure to HIV, 36 children born to seropositive mothers and 61 haemophiliac patients exposed to presumably infectious clotting factor concentrates. B52 and B44 antigens were associated with HIV resistance while B51 was associated with HIV susceptibility. Forty-nine HIV+ drug abusers, spouses of heterosexual partners studied and 25 HIV+ mothers of the children were also typed. DR l1 phenotype was associated with infectiousness of HIV+ subjects. Our data suggest that the HLA region controls susceptibility to infection with HIV and infectiousness of HIV+ subjects in different risk groups. [ABSTRACT FROM AUTHOR]

The development of productive high density peach orchards is often limited by the excessive vegetative growth of the trees that reduces productivity and quality. Dwarfing rootstocks are not available but upright tree architectures have been developed for high density peach production. The purpose of this study was to determine the water use efficiency of upright pillar and standard architecture peach trees in a production setting in order to understand the factors that differentiate transpiration and water use efficiency of the two tree architectures. There were no differences in leaf area index (LAI) of the pillar and standard types but the standards architecture had significantly greater leaf area density (LAD) than the pillar. There was no significant difference in the photosynthetically active radiation (PAR) response of photosynthesis (A) and transpiration (E) for the pillar and standard trees over a range of LAI's and vapor pressure deficits (VPD) for the 3 year period indicating that there was no genetic difference in gas exchange mechanisms between the genotypes of the two tree architectures. For high light conditions, the pillar and standard trees had a similar and non-significantly different E: VPD relationship for LAI < 2.25, however, for LAI > 2.25, the pillar had a significantly ( P = 0.05) greater E than the standard architecture at similar VPD levels due to the decreased LAD of the pillar architecture that more effectively distributed light within the canopy. The increased illumination and interception of PAR by the pillar canopy increased both photosynthesis and transpiration at the same WUE as the standard. The present work demonstrated that as pillar growth types are integrated into production systems, more research will be needed to efficiently schedule the water needs of the pillar architecture in order to maximize fruit size and quality due to the reduced LAD of this tree architecture and the greater illumination of the canopy interior. [ABSTRACT FROM AUTHOR]

Objective To investigate whether polymorphisms in Toll-like receptor (TLR) genes, previously reported to be associated with immune-mediated diseases, are involved in systemic sclerosis (SSc). Methods We genotyped 14 polymorphisms in the genes for TLRs 2, 4, 7, 8, and 9 in a discovery cohort comprising 452 SSc patients and 537 controls and a replication cohort consisting of 1,170 SSc patients and 925 controls. In addition, we analyzed 15-year followup data on 964 patients to assess the potential association of TLR variants with the development of disease complications. We analyzed the functional impact of the associated polymorphism on monocyte-derived dendritic cells. Results In the discovery cohort, we observed that a rare functional polymorphism in TLR2 (Pro631His) was associated with antitopoisomerase (antitopo) positivity (odds ratio 2.24 [95% confidence interval 1.24-4.04], P = 0.003). This observation was validated in the replication cohort (odds ratio 2.73 [95% confidence interval 1.85-4.04], P = 0.0001). In addition, in the replication cohort the TLR2 variant was associated with the diffuse subtype of the disease ( P = 0.02) and with the development of pulmonary arterial hypertension (PAH) (Cox proportional hazards ratio 5.61 [95% confidence interval 1.53-20.58], P = 0.003 by log rank test). Functional analysis revealed that monocyte-derived dendritic cells carrying the Pro63His variant produced increased levels of inflammatory mediators (tumor necrosis factor α and interleukin-6) upon TLR-2-mediated stimulation (both P < 0.0001). Conclusion Among patients with SSc, the rare TLR2 Pro631His variant is robustly associated with antitopoisomerase positivity, the diffuse form of the disease, and the development of PAH. In addition, this variant influences TLR-2-mediated cell responses. Further research is needed to elucidate the precise role of TLR-2 in the pathogenesis of SSc. [ABSTRACT FROM AUTHOR]

A high-throughput transformation system previously developed in our laboratory was used for the regeneration of transgenic plum plants without the use of antibiotic selection. The system was first tested with two experimental constructs, pGA482GGi and pCAMBIAgfp94(35S) that contain selective marker and reporter genes. Transformation was monitored by GUS detection, and estimated transformation efficiencies were 5.7% and 17.7% for pGA482GGi and pCAMBIAgfp94(35S), respectively. Subsequently, an intron-hairpin-RNA (ihpRNA) construct, carrying the Plum Pox Virus coat protein ( ppv-cp) gene, without selectable or reporter marker genes was designed. Five transgenic lines were regenerated as confirmed by DNA blot analysis. We believe that this is the first report on the production of marker-free plants transformed with a potential agronomically important trait in a Prunus species. [ABSTRACT FROM AUTHOR]

Background: Pru p 3 is the major peach allergen recognized by more than 90% of peach-allergic individuals of the Mediterranean area. Identification of the dominant Pru p 3 T-cell epitopes can improve our understanding of the immune responses against this protein and could be helpful in the development of hypoallergenic immunotherapy. For this purpose, we examined the phenotypes, specificities and cytokine secretion profiles of proliferating T cells in response to Pru p 3 in peach-allergic individuals. Methods: Peripheral blood mononuclear cells from 15 peach-allergic patients were incubated with Pru p 3. The proliferation of antigen-specific T-cell lines (TCLs) was assessed by tritiated methylthymidine incorporation. T-cell epitopes were identified by analyzing the reactivity of TCLs against 8 overlapping peptides spanning the entire length of Pru p 3. We characterized the phenotype of Pru-p-3-specific TCLs by flow cytometry and analyzed their production of interleukin (IL) 4 and γ-interferon (IFN-γ) by ELISA. Results: Ninety-two Pru-p-3-specific TCLs were isolated (stimulation index ≥5). These TCLs proliferated mainly in response to Pru p 312–27 and Pru p 357–72. Pru-p-3-specific TCLs were mainly CD4+ (81%) and expressed cell surface CD30. In addition, TCLs produced high levels of IL-4 and low levels of IFN-γ, indicating a Th2 phenotype. Conclusions: Two immunodominant T-cell-reactive regions of Pru p 3 were identified: Pru p 312–27 and Pru p 357–72. These peptides showed a differential ability to elicit a Th2 response. Taken together, our results provide a better understanding of the immunological T-cell reactivity against Pru p 3. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Genetic variation in the interferon regulatory factor 5 (IRF5) gene affects systemic lupus erythematosus (SLE) susceptibility. However, association is complex and incompletely defined. We obtained fourteen European sample collections with a total of 1383 SLE patients and 1614 controls to better define the role of the different IRF5 variants. Eleven polymorphisms were studied, including nine tag single nucleotide polymorphisms (SNPs) and two extra functional polymorphisms. Two tag SNPs showed independent and opposed associations: susceptibility (rs10488631, P<10−17) and protection (rs729302, P<10−6). Haplotype analyses showed that the susceptibility haplotype, identified by the minor allele of rs10488631, can be due to epistasis between three IRF5 functional polymorphisms. These polymorphisms determine increased mRNA expression, a splice variant with a different exon 1 and a longer proline-rich region in exon 6. This result is striking as none of the three polymorphisms had an independent effect on their own. Protection was independent of these polymorphisms and seemed to reside in the 5′ side of the gene. In conclusion, our results help to understand the role of the IRF5 locus in SLE susceptibility by clearly separating protection from susceptibility as caused by independent polymorphisms. In addition, we have found evidence for epistasis between known functional polymorphisms for the susceptibility effect.Genes and Immunity (2007) 8, 429–438. doi:10.1038/sj.gene.6364407; published online 14 June 2007 [ABSTRACT FROM AUTHOR]

Interleukin-10 (IL-10) can favour the development of fibrosis by promoting a relative shift towards T helper 2 responses. Three single base pair substitutions in the 5′ flanking region of the IL-10 gene (G/A −1082, C/T −819 and C/A −592) influence the amount of IL-10 secreted in cell cultures: the GCC haplotype is associated with an increased production, while the ACC and the ATA haplotypes are associated with intermediate and decreased production. Accordingly, three phenotypes have been individuated: high producers (GCC+/GCC+), medium producers (GCC+/GCC−) and low producers (GCC−/GCC−). We hypothesised that IL-10 haplotypes and genotypes are differently expressed in patients with systemic sclerosis (SSc) with the limited cutaneous SSc (lcSSc) subset or the diffuse cutaneous SSc (dcSSc) subset. One hundred and sixty-one unrelated Italian patients with SSc and 94 controls have been included. Their DNA was extracted and stored before being analysed by polymerase chain reaction with sequence-specific primers. The GCC haplotype is overrepresented in patients with SSc; subjects with dcSSc were the primary contributors to these results (dcSSc: 52.2% vs controls: 37.2%; χ2= 8.519, 2 d.f., corrected P= 0.04). In Scl70-positive patients, the GCC haplotype increased the likelihood of presenting the dcSSc subset [χ2= 12.56, P < 0.0005; odds ratio (OR) = 3.89, 95% confidence interval (CI95) = 1.69–9.08]; these results were confirmed at the phenotypic level (χ2= 11.67, 2 d.f., P= 0.003). In Scl70-positve patients, the high-producing phenotype was associated with poor survival, independently from disease subset and gender (hazard ratio = 9.9, CI95= 1.6–61.27, P < 0.05). The IL-10 haplotype and genotype associated with high IL-10 production may alter the susceptibility to SSc and/or its expression, increasing the prognostic value of other well-known markers of disease severity. [ABSTRACT FROM AUTHOR]

We obtained eight collections of DNA samples from ethnically matched systemic lupus erythematosus (SLE) patients and controls from five European countries totaling 783 patients and 1210 controls. A highly significant cline in the frequency of the PD1.3 A allele was found among controls but not among SLE patients. The frequency of the PD1.3 A allele increased from the Northeast to the Southwest of Europe. The cline was clearly apparent (P=1.2 × 10−6) when data from controls of other five SLE susceptibility studies were included in the analysis. This variation has severely biased SLE association studies owing to the lack of parallel changes in SLE patients. As a consequence, the PD1.3 A allele was more common in SLE patients than in controls in the Northeast and Center of Europe, similar to controls in Southeast Europe, and less frequent than in the controls in the Southwest of the Continent. This dissociation in allele frequencies between SLE patients and controls in different subpopulations indicated that programmed cell death 1 variation and disease susceptibility are not independent but the type of relationship is currently unclear. As allele frequency clines are common in other polymorphisms their impact in genetic epidemiology studies should be carefully considered.Genes and Immunity (2007) 8, 138–146. doi:10.1038/sj.gene.6364370; published online 18 January 2007 [ABSTRACT FROM AUTHOR]

Background: Isolated pulmonary hypertension (iPHT) is a near-fatal consequence of systemic sclerosis (SSc); in female patients, the risk of its development is increased during the post-menopausal period, when the protective effects of oestrogens on the endothelium decrease. In many animal and human models, hormone replacement therapy (HRT) and oestrogen administration proved efficacious in counteracting many mechanisms that might be implicated in the pathogenesis of iPHT. Accordingly, it has been hypothesized that HRT might help to prevent the development of iPHT.Methods: A retrospective cohort study was conducted on 61 SSc patients with the limited cutaneous form of the disease and no sign of pulmonary hypertension on echocardiogram (pulmonary artery pressure, PAP > 35 mmHg) at the time of menopause. All the patients had to be stably treated with calcium-channel blockers and not to have risk factors for secondary PHT throughout the duration of the observational period.Results: Twenty patients (32.8%) received HRT for a mean of 6.7 +/- 3.7 years. None of these patients developed iPHT after a mean of 7.2 +/- 3.5 years from menopause, whereas eight out of 41 patients not receiving HRT (19.5%) developed iPHT after a similar time period (7.5 +/- 3.9 years, p = 0.032). These rates were not explained by differences between the two groups with respect to autoantibodies, age, age at onset of SSc, diffusing capacity of the lung for carbon monoxide (DLCO) at menopause, or duration of therapy with calcium-channel blockers.Conclusion: HRT administration may be effective in SSc post-menopausal women, preventing the development of iPHT. [ABSTRACT FROM AUTHOR]

HLA-B35 is associated with an increased risk for developing isolated pulmonary hypertension (iPHT) in systemic sclerosis, but the mechanisms underlying this association have not been fully elucidated yet. Endothelin-1 (ET-1) is the main pathogenetic molecule implied in the development of iPHT; therefore, we sought to determine if ECV304 cells transfected with the HLA-B35 allele produce increased amounts of ET-1 after incubation with physiological concentrations of interleukin-1 beta (IL-1β). ECV304 cells transfected with HLA-B*3501 and HLA-B*0801 polymorphic α chain or with pIRESneo2 were incubated with 100 U/ml of IL-1β for 6, 12, 24, 36 and 48 h. ET-1 levels were determined using EIA kit (CAYMAN Chemical, Ann Arbor, MI) in supernatants from different cell cultures; the relative expression of the preproendothelin-1 (PPET-1) gene was also determined by reverse transcription–polymerase chain reaction. Cells expressing the HLA-B35 allele showed significantly increased levels of ET-1 at all the selected times compared with controls or HLA-B8-transfected cells. The relative expression of the PPET-1 gene was also increased in a proportionally direct manner. The HLA-B35 allele influences the production of ET-1 in HLA-B35-transfected ECV304 cells by promoting the expression of its precursor, PPET-1. Our results provide an explanation for the epidemiological association existing between iPHT and HLA-B35. [ABSTRACT FROM AUTHOR]

Transgenic clones C2, C3, C4, C5, C6, and PT-6, of plum (Prunus domestica L.) transformed with the coat protein (CP) gene of Plum pox virus (PPV), PT-23 transformed with marker genes only, and nontransgenic B70146 were evaluated for sharka resistance under high infection pressure in field trials in Poland and Spain. These sites differed in climatic conditions and virus isolates. Transgenic clone C5 showed high resistance to PPV at both sites. None of the C5 trees became naturally infected by aphids during seven (Spain) or eight (Poland) years of the test, although up to 100% of other plum trees (transgenic clones and nontransgenic control plants) grown in the same conditions showed disease symptoms and tested positively for PPV. Although highly resistant, C5 trees could be infected artificially by chip budding or via susceptible root-stock. Infected C5 trees showed only a few mild symptoms on single, isolated shoots, even up to 8 years post inoculation. These results clearly indicate the long-term nature and high level of resistance to PPV obtained through genetically engineered resistance. [ABSTRACT FROM AUTHOR]

Evergrowing (EVG) peach is one of only two described mutants affecting winter dormancy in woody perennial species. EVG peach does not set terminal buds, cease new leaf growth, nor enter into a dormant resting phase in response to winter conditions. The EVG mutation segregates in F2 progeny as a single recessive nuclear gene. A local molecular genetic linkage map around EVG was previously developed using amplified fragment length polymorphism (AFLP) and simple sequence repeat (SSR) markers, and a bacterial artificial chromosome (BAC) contig that contains the EVG mutation was assembled. A MAIDS box coding open reading frame (ORF) was found in a BAC of this contig and used as a probe. The probe detected a polymorphism between the wild-type and mutant genomes, and the polymorphism is indicative of a deletion in EVG peach. The EVG gene region contained six potential MADS-box transcription factor sequences, and the deletion in EVG affected at least four of these. The deletion was bracketed using RFLP analysis, which showed that it is contained within a segment of the genome no greater than 180 kb. [ABSTRACT FROM AUTHOR]

Our objective was to determine the HLA-DPB1 allele associations of anticardiolipin (aCL) anti-β[sub 2]GPI (aβ[sub 2]GPI) antibodies, and of clinical manifestations of the antiphospholipid syndrome (APS), in systemic lupus erythematosus (SLE). We studied 577 European patients with SLE. aCL and aβ[sub 2]GPI antibodies were measured by ELISA. Molecular typing of HLA-DPB1 locus was performed by polymerase chain reaction-sequence specific oligonucleotide probe (PCR-SSOP) method. aCL showed positive association with -DPB1*1501 (P = 0.005, OR = 7.4), and -DPB1*2301 (P = 0.009, OR 3.3). aβ[sub 2]GPI showed positive association with -DPB1*0301 (P = 0.01, OR = 1.9), and -DPB1*1901 (P = 0.004, OR 8.1). In addition, livedo reticularis was associated with -DPB1*1401, and Raynaud's phenomenon with -DPB1*2001. In conclusion, HLA-DPB1 locus may contribute to the genetic predisposition to develop antiphospholipid antibodies and clinical manifestations of the APS in patients with SLE. [ABSTRACT FROM AUTHOR]

Many lines of evidence suggest that IL10 is a strong candidate gene for systemic lupus erythematosus (SLE) susceptibility. In our previously reported study an allele (IL10.G-140bp) of the microsatellite IL10.G located at position — 1100 was significantly increased in Italian SLE patients in comparison with controls. Starting from this observation, we tested if sequence variations in the vicinity of IL10.G were more strongly associated with SLE. We performed a comprehensive association study including 26 SNPs (of which four were newly identified in the present study by DHPLC analysis) spanning 8.5 Kb of the 5' flanking and the transcribed region of the IL10 gene. The association study was performed by the DNA pool method on an extended panel of Italian patients (205) and controls (631). Haplotypic associations were studied by individual typing of seven selected markers surrounding IL10.G. Gene, genotype and haplotype frequencies were not significantly different in patients and controls. Thus the IL10.G microsatellite remains to date the only IL10 marker associated with SLE in our population. A meta-analysis of all published results indicates a possible direct role of the IL10.G repeat number in SLE susceptibility. [ABSTRACT FROM AUTHOR]

Presents the genetic construction of a local genetic linkage map for the evergrowing gene in peach using amplified fragment length polymorphisms. Methodology; Results; Discussion.

We have previously detected autoantibodies against topoisomerase II α (anti-topo II α) in sera from patients with idiopathic pulmonary fibrosis. To determine whether anti-topo II α is also present in systemic sclerosis (SSc) patients with pulmonary involvement, we screened sera from 92 patients and 34 healthy controls. Presence of anti-topo II α was investigated with respect to clinical and serological features, including the frequencies of HLA class I and II alleles. Anti-topo II α was detected in 20/92 (21.7%) patients. No association was found with either anti-topoisomerase I (Scl-70 or anti-topo I) or anti-centromere antibodies. However, anti-topo II α was associated with the presence of pulmonary hypertension (PHT) (as opposed to pulmonary fibrosis), and with a decrease of carbon monoxide diffusing capacity. Anti-topo II α was strongly associated with the presence of the class I antigen HLA-B35. No significant association was found with HLA class II antigens. HLA-B35 also turned out to be associated with the presence of PHT. These results indicate that in SSc patients, the presence of anti-topo II α is associated with PHT, and that the simultaneous presence of HLA-B35 seems to add to the risk of developing PHT. [ABSTRACT FROM AUTHOR]

Objective: To verify whether features of CNS involvement can be detected in SLE patients without overt neuropsychiatric manifestations. Methods: 114 SLE patients who had never received a diagnosis of neuropsychiatric lupus (never-NPSLE) were studied and compared to 65 SLE patients with known neuropsychiatric involvement (NPSLE). The study relied on evaluation of neurocognitive functions by means of a battery of neuropsychological tests, on psychiatric and neuropsychological assessments and on neuroimaging studies (computed tomography, magnetic resonance, single photon emission computed tomography (SPECT)). Results: Clinical features, including disease duration/activity and pharmacological therapy, of never-NPSLE and NPSLE patients were similar. Short-term and long-term memory, visuo-spatial and verbal information processing were similarly compromised in never-NPSLE and in NPSLE patients; only attention was significantly more compromised in NPSLE patients. Psychiatric morbidity was higher than expected in never-NPSLE patients, although less than in the control neuropsychiatric group. Ischemic lesions, multiple small high intensity lesions and cortical atrophy, detected by CT and MR scans, as well as abnormal SPECT were also frequently detected in never-NPSLE patients. Interestingly, left parietal and occipital area hypoperfusion by SPECT was significantly more frequent in the patients with impaired visuo-spatial intelligence and short-term memory. Conclusions: Most abnormalities detected by available diagnostic tools and characteristics of neuropsychiatric SLE are also present in non-symptomatic patients. They may derive from an unexpected widespread involvement of the CNS and are not per se sufficient, in the absence of clinical manifestations, for a diagnosis of neuropsychiatric SLE. [ABSTRACT FROM AUTHOR]

There is increasing evidence that gene copy number (CN) variation influences clinical phenotype. The low-affinity Fc receptor 3B (FCGR3B) located in the FCGR gene cluster is a CN polymorphic gene involved in the recruitment of polymorphonuclear neutrophils to sites of inflammation and their activation. Given the genetic overlap between systemic lupus erythematosus and systemic sclerosis (SSc) and the strong evidence for FCGR3B CN in the pathology of SLE, we hypothesised that FCGR3B gene dosage influences susceptibility to SSc. We obtained FCGR3B deletion status in 777 European Caucasian cases and 1000 controls. There was an inverse relationship between FCGR3B CN and disease susceptibility. CN of 1 was a significant risk factor for SSc (OR=1.55 (1.13-2.14), P=0.007) relative to CN2. Although requiring replication, these results suggest that impaired immune complex clearance arising from FCGR3B deficiency contributes to the pathology of SSc, and FCGR3B CN variation is a common risk factor for systemic autoimmunity. [ABSTRACT FROM AUTHOR]

The article presents an abstract of a research paper that investigates the role of the Pre B-cell colony-enhancing factor (PBEF)-1001T>G and PBEF -1543C>T polymorphisms in the genetic predisposition to systemic sclerosis (SSc) susceptibilit, submitted at the 5th European Workshop on Immune-Mediated Inflammatory Diseases in Sitges-Barcelona, Spain from December 1-3, 2010.

Examines a case of systemic sclerosis associated with interferon-alpha therapy for chronic myelogenous leukemia. Clinical manifestations; Diagnostic findings; Pathogenesis of interferon-induced autoimmunity.

The article presents an abstract of a research paper that analyzes polymorphisms in the interleukin 4 (IL4), interleukin 13 (IL13) and their corresponding receptors, submitted at the 5th European Workshop on Immune-Mediated Inflammatory Diseases in Sitges-Barcelona, Spain from December 1-3, 2010.