1,518 research outputs found
IgA in the horse: cloning of equine polymeric Ig receptor and J chain and characterization of recombinant forms of equine IgA
Get PDFAs in other mammals, immunoglobulin A (IgA) in the horse has a key role in immune defense. To better dissect equine IgA function, we isolated complementary DNA (cDNA) clones for equine J chain and polymeric Ig receptor (pIgR). When coexpressed with equine IgA, equine J chain promoted efficient IgA polymerization. A truncated version of equine pIgR, equivalent to secretory component, bound with nanomolar affinity to recombinant equine and human dimeric IgA but not with monomeric IgA from either species. Searches of the equine genome localized equine J chain and pIgR to chromosomes 3 and 5, respectively, with J chain and pIgR coding sequence distributed across 4 and 11 exons, respectively. Comparisons of transcriptional regulatory sequences suggest that horse and human pIgR expression is controlled through common regulatory mechanisms that are less conserved in rodents. These studies pave the way for full dissection of equine IgA function and open up possibilities for immune-based treatment of equine diseases
IGA Nephropathy : From Molecules to Men /
No full textThe author of this volume has studied IgA nephropathy for nearly 25 years, almost as long as primary IgA nephropathy has been recognized as a new disease. IgA nephropathy, considered to be an immune-complex-mediated glomerulonephri tis, is characterized by granular deposition of IgA (mainly IgA1) and C3 in the glomerular mesangial areas and is defined as nephropathy showing pro- liferative changes in the glomerular mesangial cells and increases in the mesangial matrices. Apart from being one of the most common types of chronic glomerulonephritis, it is also the most frequent case of end-stage renal disease. Since the pathogenesis of IgA nephropathy is still obscure, specific treatment is not yet available. Previous approaches have included tonsillectomy, anticoagulants, prednisolone, immunosuppressants, angiotensin-converting enzyme inhibitors and others. During his career, the author of this book has studied many aspects of IgA nephropathy, shedding much light on the mechanism of development and progression of this disease. He also undertook new treatments for patients and developed animal models for IgA nephropathy. The purpose of the present volume is to review the authors work on pathogenesis and treatment of the disease and to provide the most up-to-date findings on this subject, constituting a valuable source of information for nephrologists, general practitioners, residents and interns.The author of this volume has studied IgA nephropathy for nearly 25 years, almost as long as primary IgA nephropathy has been recognized as a new disease. IgA nephropathy, considered to be an immune-complex-mediated glomerulonephri tis, is characterized by granular deposition of IgA (mainly IgA1) and C3 in the glomerular mesangial areas and is defined as nephropathy showing pro- liferative changes in the glomerular mesangial cells and increases in the mesangial matrices. Apart from being one of the most common types of chronic glomerulonephritis, it is also the most frequent case of end-stage renal disease. Since the pathogenesis of IgA nephropathy is still obscure, specific treatment is not yet available. Previous approaches have included tonsillectomy, anticoagulants, prednisolone, immunosuppressants, angiotensin-converting enzyme inhibitors and others. During his career, the author of this book has studied many aspects of IgA nephropathy, shedding much light on the mechanism of development and progression of this disease. He also undertook new treatments for patients and developed animal models for IgA nephropathy. The purpose of the present volume is to review the authors work on pathogenesis and treatment of the disease and to provide the most up-to-date findings on this subject, constituting a valuable source of information for nephrologists, general practitioners, residents and interns.Print version recor
Murine models of renal disease: Possibilities and problems in studies using mutant mice
Get PDFThe elucidation of the pathogenesis of human renal disease at the molecular level has been facilitated by the growing field of gene targeting and the development of mouse strains with single-gene deletions - the `knock-out' mice. Experimental nephrology, therefore, requires well-characterized and reliable models of human renal disease that can be induced reproducibly in mice. Today surgical procedures for the induction of renal ischemia, chronic renal failure, and ureter obstruction are feasible in mice. Models of mesangioproliferative or crescentic glomerulonephritis, glomerulosclerosis, and tubulointerstitial disease are readily available; however, these depend heavily on the mouse genetic background. Attention to the genetic background and appropriate backcrossing are, therefore, of great importance in the design and interpretation of experimental studies, especially in transgenic mice. Simple murine models displaying the clinical features of other human renal diseases such as IgA nephropathy, membranous glomerulonephritis, and renal vasculitis are still lacking. Mouse strains that spontaneously develop distinct renal pathologies similar to lupus nephritis and focal-segmental glomerulosclerosis can be intercrossed with transgenic mice to study the impact of single-gene deletions on the renal phenotype. The present review provides a survey about currently available spontaneous and inducible murine models of renal disease with special attention to problems and future perspectives for their use in transgenic animals. Copyright (C) 2000 S. Karger AG, Basel
Cutaneous IgA subclasses in dermatitis herpetiformis and linear IgA disease.
No full textThe subclasses of the cutaneous IgA were studied in 8 patients with dermatitis herpetiformis and 4 with linear IgA disease. The cutaneous IgA in dermatitis herpetiformis consisted of both IgA1 and IgA2, although IgA1 predominated. This demonstrated that the IgA is polyclonal and may be both mucosal and blood derived. The IgA in linear IgA disease was exclusively IgA1, confirming previous work, and suggesting that mucosal IgA may not make a major contribution to the skin deposits
Acute reduction in secretory immunoglobulin A following smoking cessation
No full textSmokers report an increase in upper respiratory infections in the early phase of stopping smoking. One possible cause is a depletion in secretory immunoglobulin A (S-IgA) which has been observed in one study. The present study sought to establish this finding in smokers using nicotine patches. Ninety-two smokers, trying to stop smoking, were assessed whilst smoking and for up to six weeks of abstinence. All smokers were prescribed 15 mg 16-h nicotine patches. Among abstinent smokers, changes in S-IgA and saliva volume were assessed. During the preliminary analyses, we observed that for the pre-smoking cessation measure a longer time since the last cigarette was significantly related to Lower S-IgA levels (P = 0.006). Consequently, the main analysis, of changes in S-IgA from pre-cessation to post-cessation, was confined to those who had smoked within 0.5-1.5 h of the pre-cessation measure (n = 51). There was a significant decline in S-IgA, relative to pre-smoking abstinence levels, following abstinence of one day (P = 0.027), but Levels returned to pre-abstinence values after one week. There was no evidence of any significant changes in saliva volume following smoking cessation, relative to pre-cessation levels. Users of 15 mg patches are likely to experience a decline in S-IgA levels on the first day of smoking cessation, independent of saliva volumes, and this decline in S-IgA is Likely to occur acutely, within the first few hours of smoking abstinence. This acute drop in S-IgA appears to stem from a factor other than depletion of nicotine from the body. The observed decrease in S-IgA may help to explain the increased susceptibility of smokers to upper respiratory tract infections in the immediate post-cessation period. (C) 2004 Elsevier Ltd. ALL rights reserved
Assessment of humoral immunity in workers occupationally exposed to low levels of ionizing radiation
Get PDFBackground: The aim of this study was investigating the effect of low levels of ionizing radiation on immunoglobulin, complement levels in radiology workers occupationally exposed to ionizing radiation. Materials and Methods: The present study was conducted in the Department of immunology, college of medicine, Tabriz University of medical sciences, Iran. during the year of 2006-2007. Blood samples were taken from 45 radiology staff and from 35 subjects who had never been exposed to radiation. Samples were analyzed for immunoglobulin, complement levels. Results: Serum total IgA, IgM, c3, c4 levels were as significantly lower in the radiology workers exposed to ionizing radiation compared to the controls (p<0.05). A significant difference was observed in IgA, IgM levels and age in radiology workers (p<0.05). A statistical significant difference between IgA, IgM and c3 and working period was found in this study. Conclusion: The present study suggests that exposure to low levels of ionizing radiation causes decreased IgA, IgM, c3, c4 levels in radiology workers. Further studies are needed for determining the appropriateness of periodic check-ups of immune functions for detecting early changes in the immune system
The dynamic influence of the DRB1*1101 allele on the resistance of sheep to experimental Teladorsagia circumcincta infection
Get PDFSuffolk sheep carrying the DRB1*1101 (previously referred to as-DRB1*0203 or G2) allele have been reported to show increased resistance to natural Teladorsagia circumcincta infection compared to non-carriers. The objective of this study was to compare the biochemical and physiological responses of DRB1*1101 carrier and non-carrier twin lambs to an experimental infection with 3 x 10 [superscript 4] L3 Teladorsagia circumcincta. The variables studied included worm burden, faecal egg count, abomasal mast cells, IgA, IgE, IgG1 plus IgG2 and haematological parameters at 0, 3, 7, 21 and 35 days post infection (dpi), and duodenal smooth muscle contractility at 0 and 35 dpi. DRB1*1101 carrier lambs had significantly lower worm burden, higher mast cell and plasma platelet counts than the DRB1*1101 non-carriers (P < 0.05). Before infection, the non-carrier lambs exhibited significantly higher mucosal levels of all antibody isotypes measured compared to the carriers; these levels remained relatively stable over the course of infection in the non-carriers while there was a slow build up of these antibodies in the carriers up to day 21 post infection (pi). The DRB1*1101 non-carrier lambs had a significantly higher plasma lymphocyte count, and produced greater duodenal contractile force relative to the carrier lambs (P < 0.05). There was no significant difference between genotypes in the level of plasma eosinophils, monocytes, neutrophils or FEC. This evidence suggests that resistance conferred by DRB1*1101 is acquired rather than innate, depends on worm expulsion rather than fecundity and is dependent on mucosal mast cell proliferation, platelet activation, and IgA and IgE antibody responses.Teagasc (Organization). Walsh Fellowshi
Acquired selective IgA deficiency induced by dietary bovine IgA
No full textSelective IgA deficiency (sIgAD) is the most common immunodeficiency in humans. Auto-reactive antibodies to human IgA are found in the serum of 20-40% of individuals with sIgAD. It is unknown whether these antibodies play a role in the pathogenesis of this immunodeficiency, and most researchers believe that they are secondary to the onset of sIgAD. However, it is possible that in these individuals, the anti-IgA antibodies are in fact responsible for the removal of IgA from serum, and are originally generated against xenogeneic IgA. To examine this hypothesis, the presence of anti-bovine and anti-human IgA antibodies was tested by ELISA in serum samples from IgA-deficient and control individuals. All 14 of the IgA-deficient individuals that were tested had IgG anti-bovine IgA antibodies (100%), whereas only 8 had IgG anti-human IgA antibodies (57%). Individuals with both anti-bovine and anti-human IgA antibodies always had a higher titre against bovine IgA than against human IgA. Of 18 control individuals who have normal serum levels of IgA and no anti-human IgA antibodies, a surprisingly high proportion (61%) had IgG anti-bovine IgA antibodies in their serum. These results strongly support the hypothesis that the anti-human IgA antibodies found in IgA-deficient individuals are originally produced against xenogeneic IgA, specifically bovine IgA found in dietary beef products. These antibodies can be found in many normal individuals, but only those that cross-react with endogenous human IgA will lead to the removal of IgA from circulation, and to sIgAD. Thus, sIgAD with anti-IgA antibodies is an acquired immunodeficiency, initiated by cross-reactive antibodies consumed in the diet.M.S.Includes bibliographical references (p. 28-32)
Serum IgA contributes to the comprehension of Anisakis simplex associated chronic urticaria
No full textThe phenotype of allergic diseases associated with Anisakis determines the pattern of cytokines related to antibody production. However, the role of serum IgA and the immunomodulatory mechanisms exerted by active infection of L3 or passive mucosal contact with A. simplex specific antigens has not been studied before. We measured serum cytokine by flow cytometry (IL-2, IL-4, IL-6, IL-10, TNF-α, IFN-γ, IL-17A, TGF-β1) and antibody levels (IgE, IgG4, IgA) by ELISA against total and excretory-secretory (ES) antigens, Ani s 3,and the group of major allergens Ani s 1, Ani s 7, and Ani s 13 in sera from 10 patients with gastro-allergic anisakiasis (GAA), 11 Anisakis sensitization associated chronic urticaria (CU+) as well as 17 non-Anisakis-sensitized patients with chronic urticaria (CU-), compared with the urticaria control group (18 subjects). Specific IgE, IgG4 and IgA were high in the GAA, but IgA levels were significantly higher in the CU+ with respect the CONTROL group. We observed higher levels of the ratio IgA/IgG4 in CU+ than GAA group for Ani s 1, Ani s 7, Ani s 13 and ES. Furthermore, chronic urticaria (CU) patients showed significant lower levels of IL-10, IFN-γ and IL-17A than patients without CU. The anti-Ani s 13 IgA/IgG4 ratio correlated positively with pro-inflammatory cytokines and ratios (TNF-α, IL-17A, Th17/Th2, Type1/Type2 and TNF-α/IL-10) in CONTROL group. In general, Anti-Anisakis IgA/G4 ratio was high in CU patients. In conclusion, this study demonstrates the importance of serum IgA because it is associated with chronic urticaria independently of Anisakis sensitization.Sociedad Española de Alergología e Inmunología ClínicaFundación Mutua MadrileñaDepto. de Microbiología y ParasitologíaFac. de FarmaciaTRUEpu
Case-Control Study of Dietary Pattern and Other Risk Factors for Gastric Cancer
Get PDFThe rates of gastric cancer reported from Ardabil Province of Iran, are among the highest in the world. The aim of this study was to investigate the risk factors for gastric cancer in Ardabil Province. This case-control study was conducted on 128 adults with mean age of 56.5 ± 12.8 yr old in Ardebil City, Iran in 2010 – 2011. Forty-two people with gastric cancer and 86 healthy people were recruited. Participants were interviewed using a structured questionnaire. Fasting blood samples were taken for measurement of IgG and IgA indices against Helicobacter pylori infection. Data were analyzed using the Chi-square and Independent sample t-test.Diet and H. pylori infection indices had the significant relationship with gastric cancer (P<0.05). Among dietary patterns, drinking hot tea, low intake of fresh vegetables and fruits, and unsaturated fat were the most significant risk factors (P<0.05). In gastric cancer patients, the levels of serum IgG and IgA as indicator of H. pylori infection were significantly (P<0.05) higher than the healthy subjects (IgG 37.7 ± 29.3 vs. 16.9 ± 11.1 U/ml and IgA 50.5 ± 44.7 vs. 22.9 ± 15.8 U/ml). No significant relationship was observed between tobacco smoking and alcohol consumption with gastric cancer.Dietary pattern especially drinking hot tea and low consumption of unsaturated fat, fresh vegetables, and fruits, as well as H. pylori infection were the most important risk factors in gastric cancer patients
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