CpG oligodeoxynucleotide stimulates production of anti-neutrophil cytoplasmic antibodies in ANCA associated vasculitis-4

G-B and IL-2. Each patient assay was paired with a healthy control. After 12 days of culture, supernatants were harvested. IgG concentration and supernatant reactivity to either PR3 or MPO was measured by ELISA. The amount of IgG detected in the supernatants was of 5.5 ± 2.2 μg mLin the patients compared to 4.1 ± 1.2 μg mLin the control group (. Figure shows the reactivity of the supernatants from PR3ANCA patients towards PR3 antigen. The difference against control individuals was highly significant (P = 0.0082). Figure shows the reactivity of the supernatants from MPOANCA patients towards MPO antigen. The difference was not significant (P = 0.072) although their supernatants showed a clear tendency towards higher reactivity compared to controls. There was no correlation between patients' serum ANCA titre at the time of the assay and their production of ANCA in response to CpG-B as shown in (r= 0.172).<p><b>Copyright information:</b></p><p>Taken from "CpG oligodeoxynucleotide stimulates production of anti-neutrophil cytoplasmic antibodies in ANCA associated vasculitis"</p><p>http://www.biomedcentral.com/1471-2172/9/34</p><p>BMC Immunology 2008;9():34-34.</p><p>Published online 14 Jul 2008</p><p>PMCID:PMC2483256.</p><p></p

CpG oligodeoxynucleotide stimulates production of anti-neutrophil cytoplasmic antibodies in ANCA associated vasculitis-5

D mitogen (PWM) + IL2, or inactivated + IL2. A representative set of results is shown from a PR3ANCA patient (and a MPOANCA patient ().<p><b>Copyright information:</b></p><p>Taken from "CpG oligodeoxynucleotide stimulates production of anti-neutrophil cytoplasmic antibodies in ANCA associated vasculitis"</p><p>http://www.biomedcentral.com/1471-2172/9/34</p><p>BMC Immunology 2008;9():34-34.</p><p>Published online 14 Jul 2008</p><p>PMCID:PMC2483256.</p><p></p

CpG oligodeoxynucleotide stimulates production of anti-neutrophil cytoplasmic antibodies in ANCA associated vasculitis-1

D mitogen (PWM) + IL2, or inactivated + IL2. A representative set of results is shown from a PR3ANCA patient (and a MPOANCA patient ().<p><b>Copyright information:</b></p><p>Taken from "CpG oligodeoxynucleotide stimulates production of anti-neutrophil cytoplasmic antibodies in ANCA associated vasculitis"</p><p>http://www.biomedcentral.com/1471-2172/9/34</p><p>BMC Immunology 2008;9():34-34.</p><p>Published online 14 Jul 2008</p><p>PMCID:PMC2483256.</p><p></p

CpG oligodeoxynucleotide stimulates production of anti-neutrophil cytoplasmic antibodies in ANCA associated vasculitis-0

G-B and IL-2. Each patient assay was paired with a healthy control. After 12 days of culture, supernatants were harvested. IgG concentration and supernatant reactivity to either PR3 or MPO was measured by ELISA. The amount of IgG detected in the supernatants was of 5.5 ± 2.2 μg mLin the patients compared to 4.1 ± 1.2 μg mLin the control group (. Figure shows the reactivity of the supernatants from PR3ANCA patients towards PR3 antigen. The difference against control individuals was highly significant (P = 0.0082). Figure shows the reactivity of the supernatants from MPOANCA patients towards MPO antigen. The difference was not significant (P = 0.072) although their supernatants showed a clear tendency towards higher reactivity compared to controls. There was no correlation between patients' serum ANCA titre at the time of the assay and their production of ANCA in response to CpG-B as shown in (r= 0.172).<p><b>Copyright information:</b></p><p>Taken from "CpG oligodeoxynucleotide stimulates production of anti-neutrophil cytoplasmic antibodies in ANCA associated vasculitis"</p><p>http://www.biomedcentral.com/1471-2172/9/34</p><p>BMC Immunology 2008;9():34-34.</p><p>Published online 14 Jul 2008</p><p>PMCID:PMC2483256.</p><p></p

table_1_Delayed Diagnosis and Complications of Predominantly Antibody Deficiencies in a Cohort of Australian Adults.docx

Background<p>Predominantly antibody deficiencies (PADs) are the most common type of primary immunodeficiency in adults. PADs frequently pass undetected leading to delayed diagnosis, delayed treatment, and the potential for end-organ damage including bronchiectasis. In addition, PADs are frequently accompanied by comorbid autoimmune disease, and an increased risk of malignancy.</p>Objectives<p>To characterize the diagnostic and clinical features of adult PAD patients in Victoria, Australia.</p>Methods<p>We identified adult patients receiving, or having previously received immunoglobulin replacement therapy for a PAD at four hospitals in metropolitan Melbourne, and retrospectively characterized their clinical and diagnostic features.</p>Results<p>179 patients from The Royal Melbourne, Alfred and Austin Hospitals, and Monash Medical Centre were included in the study with a median age of 49.7 years (range: 16–87 years), of whom 98 (54.7%) were female. The majority of patients (116; 64.8%) met diagnostic criteria for common variable immunodeficiency (CVID), and 21 (11.7%) were diagnosed with X-linked agammaglobulinemia (XLA). Unclassified hypogammaglobulinemia (HGG) was described in 22 patients (12.3%), IgG subclass deficiency (IGSCD) in 12 (6.7%), and specific antibody deficiency (SpAD) in 4 individuals (2.2%). The remaining four patients had a diagnosis of Good syndrome (thymoma with immunodeficiency). There was no significant difference between the age at diagnosis of the disorders, with the exception of XLA, with a median age at diagnosis of less than 1 year. The median age of reported symptom onset was 20 years for those with a diagnosis of CVID, with a median age at diagnosis of 35 years. CVID patients experienced significantly more non-infectious complications, such as autoimmune cytopenias and lymphoproliferative disease, than the other antibody deficiency disorders. The presence of non-infectious complications was associated with significantly reduced survival in the cohort.</p>Conclusion<p>Our data are largely consistent with the experience of other centers internationally, with clear areas for improvement, including reducing diagnostic delay for patients with PADs. It is likely that these challenges will be in part overcome by continued advances in implementation of genomic sequencing for diagnosis of PADs, and with that opportunities for targeted treatment of non-infectious complications.</p