For example, CD8αβ did not contact the α2 and β2m domains of H-2D

For example, CD8αβ did not contact the α2 and β2m domains of H-2Dd, which reduced the buried surface area of this complex compared with murine pMHCI–CD8αα. Accumulated structural evidence of TCR–pMHC interactions

has shown that the TCR binds with a conserved general topology, with the TCR α-chain positioned over the N-terminus of the peptide and the TCR β-chain over the C-terminus.[30] It has been postulated that this binding mode is essential to allow co-receptor binding to the same pMHC as the TCR at the cell surface (Fig. 1).[31] Hence, the CD8 co-receptor (and CD4 co-receptor) may have a role in governing the conserved binding mode of the TCR to allow the formation of a functional signalling complex at the T-cell surface.[32] Indeed, Kuhns and Davis[33] have shown that the ectodomains of CD3εδ and CD3εγ, that constitute an important Ivacaftor cell line selleck part of the TCR signalling complex, associate with the Cα DE and

Cβ CC’ loops, respectively, within the constant domain of the TCR (Fig. 3a). In this study, mutation of these conserved loops disrupted the formation of the TCR–CD3 signalling domain and subsequent T-cell activation. So it seems that these CD3 subunits, that contain intracellular tyrosine kinase activation motifs and play an important role in providing T-cell activation signals, form specific interactions with the TCR, fixing their position at the cell surface with respect to the TCR. Yin et al.[32] showed that the structure of the tripartite TCR–pMHCII–CD4 complex is compatible with this notion. Assuming that the TCR and co-receptor co-engage the same pMHC at the cell surface, the fixed polarity of the TCR–pMHC interaction beta-catenin inhibitor could orientate the co-receptor in such a way as to

allow the CD3 molecules to lie between the TCR and co-receptor (Fig. 3a,b). This would position the intracellular signalling domains of CD3 and the co-receptor in close proximity to enable cross-signalling during antigen engagement. If the TCR bound in the reverse polarity, with the TCR β-chain over the peptide N-terminus and the TCR α-chain over the C-terminus, the CD3 complex would lie distal from the co-receptor, and this could presumably reduce the efficiency of the T-cell activation signal between the co-receptor and the CD3 complex (Fig. 3c,d). Adding further support to the idea that the T-cell co-receptors can influence the nature of TCR antigen recognition, Van Laethem et al.[34] have shown that the CD4 and CD8 co-receptors impose MHC-restriction on T cells by preventing Lck availability during TCR interactions with non-MHC antigens. Indeed, in the absence of the co-receptors T cells develop with antibody-like specificities that can respond to other cell surface molecules, such as CD155.

We also developed a bioinformatics method to predict pMHC-I stabi

We also developed a bioinformatics method to predict pMHC-I stability, which suggested that 30% of the nonimmunogenic binders hitherto classified as “holes in the T-cell repertoire” can be explained as being unstably

bound to MHC-I. Finally, we suggest that nonoptimal anchor residues in position 2 of the peptide are particularly prone to cause unstable interactions Ku-0059436 with MHC-I. We conclude that the availability of accurate predictors of pMHC-I stability might be helpful in the elucidation of MHC-I restricted antigen presentation, and might be instrumental in future search strategies for MHC-I epitopes. Major histocompatibility complex class I (MHC-I) plays a pivotal role in the generation of specific immune responses mediated

by cytotoxic T lymphocytes (CTLs). MHC-I molecules sample peptides derived from intracellular proteins, translocate them to the cell surface, and display them to CTLs, allowing immune scrutiny of the ongoing intracellular metabolism leading to the detection of the presence of any intracellular pathogens. To fulfill this crucial antigen presenting function, MHC-I molecules must be endowed with the ability to retain bound peptides at the cell surface while waiting for the arrival of rare circulating CTL clones of the appropriate specificity. Sustained presentation at the cell surface and induction of specific immune T-cell responses therefore requires

some Z-VAD-FMK concentration degree of pMHC-I stability. Indeed, it has been claimed that stability, rather than affinity, of pMHC-I complexes is the better correlate of immunogenicity and immunodominance [[1-5]]. Experimentally, however, affinity remains the most frequently Ureohydrolase established correlate of immunogenicity. Thus, when Assarsson et al. [[6]] recently conducted a quantitative analysis of the variables affecting the repertoire of T-cell specificities recognized after vaccinia virus infection, they found that the vast majority of epitopes (85%) bound their restricting allele with an affinity of 500 nM or better, and most (75%) bound with an affinity of 100 nM or better. Investigating the stability of pMHC-I complexes for a small sample of immunogenic and nonimmunogenic peptides, they found a suggestive, but not statistically significant, trend for off-rates and immunodominance being correlated. The authors concluded that “in our hands, peptide stability did not correlate significantly better with immunodominance than did equilibrium binding measurements”. One reason why pMHC stability has not been addressed more extensively undoubtedly relates to the cumbersome and/or low-throughput nature of current biochemical methods used to measure the dissociation of pMHC complexes [[6-12]]. A particularly interesting dissociation assay developed by Parker et al.

1A) A modest increase in the absolute numbers of Tconv cells was

1A). A modest increase in the absolute numbers of Tconv cells was also seen (Fig. 1D). A similar enhancement in Treg cells was seen in mice treated with a different preparation of Fc-GITR-L [13], but these authors did not observe any increase in Tconv cells. To determine if GITR stimulation modulated Treg-cell function, we purified CD4+CD25+T cells from Fc-GITR-L and IgG1-injected mice and assessed their suppressive capacity in vitro (Supporting Information Fig. 1B). Treg cells from Fc-GITR-L-treated

mice were as suppressive as Treg cells from control human IgG1-treated mice. The increase in Treg cells was transient and the percentage of Foxp3+ T cells returned to normal by day 9 after treatment (Supporting Information Fig. Fer-1 mouse 1C). Previous studies suggested that treatment of mice with an agonist anti-GITR mAb, following anti-CD25 depletion of Treg cells, was capable of enhancing the pathogenicity of autoantigen-specific T cells in an experimental autoimmune encephalomyelitis model [18]. One problem with this approach is that Treg-cell depletion is usually incomplete and Treg cells rapidly

repopulate the treated animals [19]. To more directly address the effects of GITR stimulation on Teff cell numbers and function, we used the IBD model [20] and transferred CD4+CD45RBhi Foxp3− T cells into RAG KO mice buy Idasanutlin followed by weekly treatment with Fc-GITR-L (100 μg/mouse i.v.). Mice treated with Fc-GITR-L exhibited a markedly enhanced loss of weight compared with mice that just received CD4+CD45RBhi T cells (Fig. 2A). The percentage of CD4+ T cells secreting IFN-γ was similar in treated and control animals (Fig. 2B and D), but the absolute number of CD4+ T cells secreting IFN-γ was markedly increased in the mesenteric LN (Fig. 2C). In contrast, we observed no changes in either the percentages or absolute numbers of IL-17-producing T cells (Fig. 2E and F).

Teff-cell expansion was also reflected in enhanced Ki67 staining in the treated mice (Fig. 2G and H). Thus, engagement of the GITR by GITR-L in vivo has no effect on T-cell differentiation, but significantly augments the absolute number of pathogenic IFN-γ producing T cells and disease severity. Our results are similar to the effects of STK38 GITR engagement that have been reported [21] on CD8+ Teff cells in a viral model where GITR engagement increased CD8+ T-cell expansion without enhancing their effector functions. Small percentages of Foxp3+ iTreg cells were observed in mice that received CD4+CD45RBhi Foxp3− T cells, but the percentages were the same in untreated or GITR-L-treated mice (data not shown). The GITR is also expressed on APCs and NK cells at a low levels [2] and it has been suggested [22, 23] that some of the effects of GITR engagement in vivo may be secondary to modulation of innate immune functions. To address this issue, we transferred CD4+CD45RBhi T cells from GITR−/− mice to RAG−/− mice (Supporting Information Fig. 2A).

Some of the mechanisms by that endotoxin can mediate its effects

Some of the mechanisms by that endotoxin can mediate its effects include neutrophil and eosinophil recruitment as well as the activation of macrophages [3, 5, 6]. Chemically, endotoxins consist of lipopolysaccharides (LPS) that exert their effects via the CD14 receptor, a 53-kDa surface glycoprotein [7] expressed on monocytes, macrophages, granulocytes and B lymphocytes [5, 6]. The molecular

interactions underlying the binding of LPS have been extensively studied in recent years. Accordingly, LPS-binding protein (LBP) facilitates the binding of LPS in combination with CD14 to a receptor complex, which consists Smoothened Agonist mouse of Toll-like receptor-4 (TLR-4) and MD-2 [8–10]. The activation of the TLR induces an intracellular

signalling cascade, which results in the release of cytokines such as interleukin (IL)-6, IL-8 and tumour necrosis factor (TNF)-α [6, 11] which have also been shown in elevated concentrations in asthma [12–14]. In vitro, CD14 is constitutively released from mononuclear cell cultures as soluble CD14 (sCD14) [15, 16]. sCD14 can be found in two isoforms, a 49- and a 55-kDa protein. The 55-kDa isoform is produced by a shedding mechanism while the 49-kDa form is thought to derive from the interstitial space [16, 17]. The 49-kDa isoform is found in healthy subjects and is significantly elevated in patients with PD98059 concentration sepsis [18], polytrauma [19] and atopic dermatitis [20]. Shedding is increased by LPS and TNF-αin vitro [21] and also in vivo [22]. The buy Cetuximab function

of sCD14 has been associated with the activation of cells which do not possess membrane-bound CD14 [8]. Elevated levels of sCD14 have been found in bronchoalveolar lavage in several diseases such as tuberculosis, sarcoidosis, allergic alveolitis and idiopathic pulmonary fibrosis [6, 23–27]. sCD14 also seems to play a role in allergic asthma. Dubin et al. [28] showed an increase in sCD14 in bronchoalveolar lavage fluid (BALF) 24 h after allergen provocation which was confirmed by others [29]. Increased concentrations were also found in children with status asthmaticus [30]. In addition, CD14 expression has been correlated to the influx of neutrophils into the airways [22]. It has been suggested that this might be related to a remodelling processes in the airways as has been shown in an animal model with endotoxin-sensitive mice [31]. Moreover, distinct gene-polymorphisms of the C14 gene have been associated with an increased risk to develop an atopic phenotype [32]. It can therefore be hypothesized that an elevated expression of the LPS receptor might be involved in the activation of the inflammatory cascade in asthma which could lead to chronic inflammation, remodelling of the airways and subsequently an accelerated loss in FEV1.

At the remission of the panniculitis, which occurred in about 10 

At the remission of the panniculitis, which occurred in about 10 days, the steroid therapy was suspended, while the orally administered griseofulvin continued for 6 weeks until full recovery. EN is the most frequent clinical form of acute nodular panniculitis and it is considered an epiphenomenon relative to various infectious and non-infectious stimuli. The association of EN with dermatophytosis of the scalp is infrequent, with only 15 cases reported in the Literature.


“Tinea incognito is a dermatophytosis of atypical clinical character, usually misdiagnosed and treated with corticosteroids. We report a case of tinea faciei modified by high potency topical corticosteroids in a 54-year-old woman. Deep, intense inflammatory plaque with boggy, pustular surface located on the right cheek was found. Direct microscopy and culture confirmed

dermatophytosis and led to the identification of Trichophyton mentagrophytes var. https://www.selleckchem.com/products/bmn-673.html mentagrophytes. Complete resolution occurred after treatment with oral terbinafine. “
“Kodamaea ohmeri is an unusual yeast-form fungus that has recently been identified as an important aetiological agent of fungaemia, endocarditis, cellulitis, funguria and peritonitis in immunocompromised patients. We present two new isolated of K. ohmeri. The microorganisms were identified by CHROMagar Candida medium, VitekII system and API ID32C. Biochemical identification of the two yeast isolates was confirmed by sequence analysis of the 26S ribosomal DNA. Antifungal buy LDK378 susceptibility testing done by Sensititre YeastOne showed that the isolates were susceptible to amphotericin B, voriconazole and itraconazole. This work is the first report of isolation of K. ohmeri in immunocompromised patients in Italy. “
“We describe a woman presenting primarily with slowly progressing scarring alopecia. Course, symptoms, and clinical picture were highly suggestive for lichen planus. 4-Aminobutyrate aminotransferase But mycological investigations revealed that cicatricial alopecia was caused by a specific infection with Trichophyton

schoenleinii running a chronic course with minimal skin inflammation. “
“Anecdotal reports have shown that tumour necrosis factor (TNF)-α inhibition may cause unchecked superficial infection with the microorganisms responsible for pityriasis versicolor (PV). We observed several cases of PV, which is frequently resistant to topical therapies, in psoriatic patients undergoing anti-TNF-α monoclonal antibody therapy. To evaluate the incidence and the therapeutic management of PV in this group of individuals, between 1 January and 27 December 2010, we examined 153 psoriatic patients for the hypopigmented/hyperpigmented macular and scaling lesions associated with PV. All patients positive for PV were given topical therapy with miconazole nitrate cream twice daily for 28 days, after which they were re-evaluated. In patients non-responsive to topical therapy, we started systemic therapy with fluconazole, 300 mg week−1 for 3 weeks. We diagnosed seven cases of PV.

No expression of CD4 or CD8 was found on these NK T cells To inv

No expression of CD4 or CD8 was found on these NK T cells. To investigate whether the NK T cells selleck chemical of patients B2 and B7 responded to their tumours, ELISPOT analysis of PBMC-containing NK T cells was performed. Because no CD1d was found on tumour targets (data not shown), not

only tumour cells, but also tumour lysates were tested as targets for which autologous dendritic cells in the PBMC served as antigen-presenting cells. As shown in Table 5, peripheral NK T cells did not react to autologous tumour or lysate and showed IFN-γ, but no IL-4 responses to αGalCer. Several other RCC patients (A1, A2, A3, A4, A6, B1, B3 and B4) and healthy donors did not show any responsiveness to αGalCer (data not shown). Because patient PBMC contained enhanced numbers of Treg, NK T cells were isolated from the cells by FACS sorting and in vitro-cultured NK T cell lines were tested as responders, allowing analysis of anti-tumour reactivity in the absence of potential suppressing Treg. As shown in Fig. 5, isolated NK T cell lines cultured for 1–3 weeks could be typed as TCR Vα24/Vβ11-expressing cells that also bound CD1d tetramer. NK T cell lines were tested in the presence of human CD1d-transfected C1R cells as antigen-presenting cells. Unlike conventional T cells, these purified NK T cell lines did not react to the allogeneic cell line C1R (or C1R-huCD1d) (Table 6). As shown in Table 6, the IFN-γ

responses of the NK T cell lines were induced by αGalCer (but not in its absence) when presented by C1R-huCD1d

cells and not in the presence of the CD1d-negative cell line C1R. B2 autologous tumour did not elicit any response; B7 find more autologous tumour elicited a variable response that was not consistently positive or negative. Tumour lysates did not induce a response (in the Racecadotril absence of αGalCer), did not enhance the αGalCer response and with the B7 NK T cell line as responder even suppressed this response. Enhanced levels of IL-7, IL-12 and IL-15 in the serum of the patients might be an explanation for the high peripheral NK T cell numbers. However, no enhanced levels of these cytokines were found in available plasma samples from patients A1, A2, A4, A5, B1, B3, B5, B6 and B7 (data not shown). In this study, we describe enhanced levels of circulating NK T cells in two of 14 RCC patients treated with IFN-α. The NK T cells expressed TCR Vα24/Vβ11 and the 6B11 NK T cell marker and bound CD1d-presented ligand, confirming their NK T type I character [1]. NK T cells were encountered only sporadically in one of the two patients in the tumour microenvironment. The clinical course of disease in patients B2 and B7 was not exceptional in comparison to the other patients included in this trial, who had similar histological subtypes and extent of metastatic disease. All patients had advanced metastatic RCC, which was the only clinically detectable disease at evaluation.

Where there were sequences associated with two or more isotypes i

Where there were sequences associated with two or more isotypes in a set, averages sequences were generated for each isotype. To investigate the role of antigen selection in the evolution of patterns of mutation within the IgE sequences, the proportion

of replacement mutations within the CDR1 and CDR2 of each sequence was calculated. Broad definitions of CDR1 and CDR2 were used, incorporating the CDR regions of both Kabat [22] and IMGT [23], and analysis was made with reference to a random model of mutations as previously described [13]. In this model, the probability that a random mutation would introduce a replacement mutation in the CDR was estimated to be 0.26, based upon patterns of mutation

and hotspots in a data set of non-productive sequences [13]. Analysis showed that this estimate was appropriate for all IGHV sequences, BMS-777607 manufacturer for there is little variation in the mutability of different IGHV genes (data not shown). Using the binomial distribution, the estimate was then used to establish 95% confidence limits for the proportion of the total mutations that would be replacement mutations in the CDR (RCDR), if the mutation process targeted hotspots, but if these mutations were not subject to antigen selection pressure. Proportions were calculated for varying numbers of total IGHV mutations (Mv). The upper limit (97.5%) was used to distinguish sequences that

showed evidence of antigen selection from sequences that lacked such selleck screening library evidence. Total serum immunoglobulin concentrations were determined for all PNG samples, and the results are summarized in Table 2. Concentrations of serum IgE antibodies were all above the laboratory Reverse transcriptase reference range for healthy Sydney adults, and the mean IgE concentration of the serum samples was 2465 kU/l. IgG subclass concentrations are also shown in Table 2. IgG1 and IgG4 concentrations were particularly high. Nine of the 14 PNG individuals had IgG1 concentrations above the laboratory reference range for healthy Sydney adults, while all but one of the individuals studied had serum IgG4 concentrations that were above the Laboratory Reference Range. In Western populations, IgG4 is typically the least abundant IgG subclass, but IgG4 in these PNG samples was seen at substantially higher concentrations than IgG3. Sequences were aligned against the germline IGHV, IGHD and IGHJ gene repertoires using the iHMMune-align program, while IGHG gene identity was confirmed by blast. PCR error rates were determined by analysis of errors within the IGHG constant region genes and were shown to vary from 0.9‰ (IgG2) to 1.2‰ (IgG4). The amplified constant region of the IgE sequences was too short for such a calculation.

Treatment with TNF-blockers and diabetes mellitus also confer inc

Treatment with TNF-blockers and diabetes mellitus also confer increased risk. It is interesting learn more to note that all these conditions are associated with impaired autophagy: HIV-infected cells block autophagy in bystander macrophages via HIV-1 Tat and IL-10

in a Src-Akt and STAT3-dependent process [25]; cigarette smoke causes a defect in autophagy in alveolar macrophages [78] and TNF induces autophagy [12]. Moreover, early type 2 diabetes is characterized by hyporesponsiveness to insulin and excessive levels of insulin and insulin has been shown to inhibit autophagy [79]. As increasing evidence emerges that autophagy plays a critical role in host immune responses to tuberculosis, the modulation of autophagy either directly or via upstream targets may result in improved outcomes for the millions of individuals infected with Mtb. Vaccine development.  A more effective TB vaccine is needed to achieve global TB elimination. The current TB vaccine is a live attenuated stain of M. bovis: BCG. BCG has variable efficacy, is only 50% effective in preventing tuberculous disease [80] and is not useful as a therapeutic vaccine in promoting the elimination of latent infection. One of the main barriers in designing an effective vaccine is that, as an intracellular organism, Mtb is hidden inside the macrophage, and antigens must be presented to T cells to elicit a response. Autophagic mechanisms

for intracellular antigen processing onto MHC selleck kinase inhibitor class I and class II for enhanced presentation to T cells have been identified. Thus, else a vaccine designed specifically to elicit a strong autophagic response may prove more effective at preventing infection and/or promoting elimination or improved control of latent infection with Mtb. Immunotherapy: targeting autophagy.  Recent years have seen an explosive growth in the incidence of drug resistant Mtb. In

some parts of eastern Europe, up to 50% of TB cases are multi-drug resistant (MDR-TB) [3]. Worldwide, almost one in four cases of MDR-TB results in death [81]. Recent years have also seen numerous outbreaks of extensively drug-resistant TB (XDR-TB), associated with up to 98% fatality rates [82]. The anti-microbials used to treat MDR and XDR-TB are toxic, slow-acting and often ineffective. Immunotherapy which stimulates autophagy could be an answer to the difficulty of treating patients with disease for which there are no good anti-microbial drugs. Adjunctive immunotherapy could also prove useful in shortening the duration of tuberculosis treatment. The current treatment regimen for active tuberculosis is a course of three or four antibiotics, given for a minimum of 6 months. Side effects are common, and up to half of patients fail to adhere to this protracted course of treatment [83]. A minimum of three anti-tuberculous antibiotics are used to treat tuberculosis.

This possibility seemed to be strengthened by the observation

This possibility seemed to be strengthened by the observation

that SIGNR1 physically associates with Dectin-1 constitutively in cells over-expressing SIGNR1 and Dectin-1 (data not shown). Moreover, SIGNR1 and Dectin-1 co-localized to part of the phagosomal membrane in RAW-SIGNR1/Dectin-1 cells (data not shown). This is not the case in rpMϕ, where association/co-localization of SIGNR1 and Dectin-1 was not observed without stimulation, as reported in the case of TNF-α production by collaboration between TLR2 and Dectin-1 8. However, Dectin-1 was recruited to the phagosomal membrane where SIGNR1 captures microbes, and both molecules were detected to physically associate with each other in a time-dependent manner after stimulation. The oxidative burst of RAW-SIGNR1 cells in response to live C. albicans was too weak see more to detect (data not shown). This may be due to the fact that the cell wall in the live microorganism is covered with mannoproteins, preventing Dectin-1 from accessing the β-glucan ligand. However, RAW-SIGNR1 cells showed significant candidacidal

activity, and this activity was substantially dependent www.selleckchem.com/products/abt-199.html on Syk-mediated signaling. When RAW-SIGNR1/Dectin-1 cells (data not shown) and rpMϕ were exposed to live microbes, β-glucan appeared to be accessible to Dectin-1, and SIGNR1 and Dectin-1 co-localized to part of the phagosomal membrane. Therefore, it is feasible that such cellular events effectively induce candidacidal activity. Histidine ammonia-lyase It is not clear how SIGNR1 utilizes Syk-mediated signaling though Dectin-1. It has been reported that cross-linking of SIGNR1 by neo-glycoprotein containing mannose residues and specific antibody induces the activation of JNK and NF-κB, leading to the production of TNF-α 31, IL-12 32 and IL-10 33. Therefore, it is plausible that SIGNR1

transduces the signal by itself. However, RAW264.7 cells expressing the SIGNR1 truncated cytosolic portion were still able to facilitate the oxidative response, suggesting that it is unlikely that there is any direct involvement of the cytosolic portion of SIGNR1 in signal transduction. SIGNR1 in RAW264.7 transfectants is reported to co-localize in lipid rafts with several Src family kinases 31. Therefore, cross-linking of SIGNR1 by ligand/microbes possibly induces activation of the kinases. Alternatively, SIGNR1 might also cooperate with other unidentified molecules than Dectin-1 to induce the Syk-dependent signaling. These possibilities remain to be elucidated in future experiments. In the systemic infection or stimulation, SIGNR1 may not be a major player in the host defense, since SIGNR1 is expressed in limited populations of DCs and Mϕ.

Background: The prevalence of hypertension with hyperuricemia var

Background: The prevalence of hypertension with hyperuricemia varies between 22–38%, with 3–5 fold BAY 57-1293 increased risk for coronary heart disease, peripheral arterial disease or cerebrovascular disease. Hypertension and hyperuricemia condition will trigger an increase in asymmetric dimethyl arginine (ADMA), decrease in nitric oxide and increase in reactive oxygen species, which in turn will lead to endothelial dysfunction. ARBs

losartan in hypertension therapy has the uricosuric agents, anti-inflammatory and antiagregation effects. Methods: The design of this study is a clinical trial before and after, which is done in general and consult policlinic, Internal Medicine Department at RSMH Palembang from May to August 2013. A total of 30 patients with stage 1 hypertension and hyperuricemia was given 50 mg losartan drug once daily for 8 weeks. Before therapy was started, blood pressure, serum uric acid, 24-hour urine uric acid and serum ADMA were measured and repeated after 8 weeks. Blood pressure was measured every 2 weeks. Results: The mean serum ADMA levels prior to administration of losartan was 0.74 μmol/l. The mean ADMA levels after the administration of losartan was 0.56 μmol/l. There was a decrease

in mean serum ADMA levels after the administration of losartan. The results were statistically significant on reduction of serum ADMA levels after the administration of losartan with P = 0.001. Conclusions: There is an influence of losartan on reduction of serum ADMA levels in hypertension patients with asymptomatic Doxorubicin research buy hyperuricemia, and the differences were statistically significant with P = 0.001. 220 RENAL RHEUMATOLOGY LUPUS VASCULITIS CLINIC – 4 YEARS EXPERIENCE G SINGH1, L WHITE2, P FLYNN2, S THOMAS2, L JEYASEELAN3, Reverse transcriptase M THENMOZHI3, G JOHN2, P KUBLER2, D RANGANATHAN2 1Princess Alexandra Hospital, Brisbane, QLD; 2Royal Brisbane and Women’s Hospital,

Brisbane, QLD, Australia; 3Christian Medical College, Vellore, Tamil Nadu, India Aim: To measure the rate of progression of renal disease in patients who attend the Renal Rheumatology Lupus Vasculitis (RRLV) clinic and to compare the results to published studies in Lupus Nephritis (LN) and vasculitis. Background: Patients with connective tissue disorder have multisystem involvement and attend Rheumatology and other sub speciality clinics including Nephrology. In July 2009 a combined RRLV clinic, probably first of its kind for adult patients in Australia, was implemented at Royal Brisbane & Women’s Hospital. Studies have shown patient survival rates at 5 and 10 years for vasculitis patients are 83% and 74% and for LN patients are 88% and 77% respectively. We compared outcome data for patients followed up in our clinic to published studies. Methods: This analysis is a retrospective chart audit of all the patients who attended this clinic from July 2009 to October 2013.