Database : MEDLINE
Search on : IgA and Deficiency [Words]
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[PMID]: 29484746
[Au] Autor:Hauge SC; Jensen CK; Nielsen LK; Pedersen OB; Sørensen E; Thørner LW; Hjalgrim H; Erikstrup C; Nielsen KR; Kaspersen KA; Didriksen M; Dziegiel M; Ullum H
[Ad] Address:Department of Clinical Immunology, Copenhagen University Hospital, Copenhagen, Denmark.
[Ti] Title:The association of IgA deficiency on infection rate, self-perceived health, and levels of C-reactive protein in healthy blood donors.
[So] Source:APMIS;126(3):248-256, 2018 Mar.
[Is] ISSN:1600-0463
[Cp] Country of publication:Denmark
[La] Language:eng
[Ab] Abstract:The clinical importance of immunoglobulin A (IgA) deficiency in otherwise healthy individuals is not well described. We aimed to investigate the self-reported mental and physical health and the risk of infection in IgA-deficient blood donors compared to healthy control blood donors. Infectious events, recorded in public health registries either as prescriptions filled of any antimicrobial medicine or as hospital infections, were compared between 177 IgA-deficient blood donors and 1770 control blood donors. A subset of the IgA-deficient donors were further characterized by self-reported health (Short Form-12, n = 28) and circulating C-reactive protein (CRP) (n = 10). IgA-deficient individuals had lower self-reported mental health (p = 0.01) and higher CRP (p < 0.05). A strong trend was found regarding prescription of antimicrobial medicine (hazard ratio = 1.19, p = 0.05). No association was found with hospital infections (hazard ratio = 1.02, p = 0.95) or self-reported physical health (p = 0.86). IgA-deficient blood donors have impaired self-reported mental health, enhanced inflammation and possibly an increased risk of infection. Despite these findings, this study does not provide sufficient evidence to warrant specific health precautions for donors with IgA deficiency.
[Mh] MeSH terms primary: C-Reactive Protein/metabolism
Diagnostic Self Evaluation
Genetic Predisposition to Disease
IgA Deficiency/immunology
Immunoglobulin A/immunology
Infection/epidemiology
[Mh] MeSH terms secundary: Adult
Blood Donors
Denmark/epidemiology
Female
Humans
IgA Deficiency/genetics
Immunoglobulin A/genetics
Infection/immunology
Male
Middle Aged
Risk
Surveys and Questionnaires
Young Adult
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Immunoglobulin A); 9007-41-4 (C-Reactive Protein)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180228
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12807

  2 / 5245 MEDLINE  
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[PMID]: 29321370
[Au] Autor:Tan Q; Tai N; Li Y; Pearson J; Pennetti S; Zhou Z; Wong FS; Wen L
[Ad] Address:Section of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.
[Ti] Title:Activation-induced cytidine deaminase deficiency accelerates autoimmune diabetes in NOD mice.
[So] Source:JCI Insight;3(1), 2018 Jan 11.
[Is] ISSN:2379-3708
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:B cells play an important role in type 1 diabetes (T1D) development. However, the role of B cell activation-induced cytidine deaminase (AID) in diabetes development is not clear. We hypothesized that AID is important in the immunopathogenesis of T1D. To test this hypothesis, we generated AID-deficient (AID-/-) NOD mice. We found that AID-/-NOD mice developed accelerated T1D, with worse insulitis and high levels of anti-insulin autoantibody in the circulation. Interestingly, neither maternal IgG transferred through placenta, nor IgA transferred through milk affected the accelerated diabetes development. AID-/-NOD mice showed increased activation and proliferation of B and T cells. We found enhanced T-B cell interactions in AID-/-NOD mice, with increased T-bet and IFN-γ expression in CD4+ T cells in the presence of AID-/- B cells. Moreover, excessive lymphoid expansion was observed in AID-/-NOD mice. Importantly, antigen-specific BDC2.5 CD4+ T cells caused more rapid onset of diabetes when cotransferred with AID-/- B cells than when cotransferred with AID+/+ B cells. Thus, our study provides insights into the role of AID in T1D. Our data also suggest that AID is a negative regulator of immune tolerance and ablation of AID can lead to exacerbated islet autoimmunity and accelerated T1D development.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  3 / 5245 MEDLINE  
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[PMID]: 29511864
[Au] Autor:Tallantyre EC; Whittam DH; Jolles S; Paling D; Constantinesecu C; Robertson NP; Jacob A
[Ad] Address:University Hospital of Wales, Cardiff, UK.
[Ti] Title:Secondary antibody deficiency: a complication of anti-CD20 therapy for neuroinflammation.
[So] Source:J Neurol;, 2018 Mar 06.
[Is] ISSN:1432-1459
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:B-cell depleting anti-CD20 monoclonal antibody therapies are being increasingly used as long-term maintenance therapy for neuroinflammatory disease compared to many non-neurological diseases where they are used as remission-inducing agents. While hypogammaglobulinaemia is known to occur in over half of patients treated with medium to long-term B-cell-depleting therapy (in our cohort IgG 38, IgM 56 and IgA 18%), the risk of infections it poses seems to be under-recognised. Here, we report five cases of serious infections associated with hypogammaglobulinaemia occurring in patients receiving rituximab for neuromyelitis optica spectrum disorders. Sixty-four per cent of the whole cohort of patients studied had hypogammaglobulinemia. We discuss the implications of these cases to the wider use of anti-CD20 therapy in neuroinflammatory disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher
[do] DOI:10.1007/s00415-018-8812-0

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[PMID]: 29335801
[Au] Autor:Langereis JD; Henriet SS; Kuipers S; Weemaes CMR; van der Burg M; de Jonge MI; van der Flier M
[Ad] Address:Section Pediatric Infectious Diseases, Laboratory of Medical Immunology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands. Jeroen.Langereis@radboudumc.nl.
[Ti] Title:IgM Augments Complement Bactericidal Activity with Serum from a Patient with a Novel CD79a Mutation.
[So] Source:J Clin Immunol;38(2):185-192, 2018 Feb.
[Is] ISSN:1573-2592
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Antibody replacement therapy for patients with antibody deficiencies contains only IgG. As a result, concurrent IgM and IgA deficiency present in a large proportion of antibody deficient patients persists. Especially patients with IgM deficiency remain at risk for recurrent infections of the gastrointestinal and respiratory tract. The lack of IgM in the current IgG replacement therapy is likely to contribute to the persistence of these mucosal infections because this antibody class is especially important for complement activation on the mucosal surface. We evaluated whether supplementation with IgM increased serum bactericidal capacity in vitro. Serum was collected from a patient with agammaglobulinemia and supplemented with purified serum IgM to normal levels. Antibody and complement deposition on the bacterial surface was determined by multi-color flow cytometry. Bacterial survival in serum was determined by colony-forming unit counts. We present a patient previously diagnosed with agammaglobulinemia due to CD79A (Igα) deficiency revealing a novel pathogenic insertion variant in the CD79a gene (NM_001783.3:c.353_354insT). Despite IgG replacement therapy and antibiotic prophylaxis, this patient developed a Campylobacter jejuni spondylodiscitis of lumbar vertebrae L4-L5. We found that serum IgM significantly contributes to complement activation on the bacterial surface of C. jejuni. Furthermore, supplementation of serum IgM augmented serum bactericidal activity significantly. In conclusion, supplementation of intravenous IgG replacement therapy with IgM may potentially offer greater protection against bacterial infections, also in the context of increasing antibiotic resistance.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review
[do] DOI:10.1007/s10875-017-0474-7

  5 / 5245 MEDLINE  
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[PMID]: 29506643
[Au] Autor:Larsen CS; Katzenstein TL
[Ad] Address:carslars@rm.dk.
[Ti] Title:[Diagnosis and treatment of primary antibody deficiency syndromes].
[So] Source:Ugeskr Laeger;180(9), 2018 Feb 26.
[Is] ISSN:1603-6824
[Cp] Country of publication:Denmark
[La] Language:dan
[Ab] Abstract:Primary antibody deficiencies (PAD) make up more than half of primary immunodeficiencies. PAD is characterized by low levels of one or more immunoglobulin (Ig) classes or impaired vaccine response. Recurrent infections are the predominant presenting symptoms, but autoimmune disorders are also frequent. Onset of symptoms is often after the age of six. Screening for PAD with measurement of the levels of serum IgG, IgM, and IgA is simple and can be done in general practice. Replacement therapy with Ig is the cornerstone in treatment of PAD and reduces the frequency of infections and mortality.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:In-Data-Review

  6 / 5245 MEDLINE  
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[PMID]: 29475900
[Au] Autor:Sullivan A; Bland RM; Hague R
[Ad] Address:Paediatric Department, Wishaw General Hospital, Wishaw, UK.
[Ti] Title:Fifteen-minute consultation: The child with an incidental finding of low IgA.
[So] Source:Arch Dis Child Educ Pract Ed;, 2018 Feb 23.
[Is] ISSN:1743-0593
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Low or absent immunoglobulin A (IgA) levels are frequently found in children in whom immunodeficiency is not suspected. IgA deficiency is the most common primary immunodeficiency disorder in the UK affecting approximately 1 in 600 people. Isolated IgA deficiency is often identified coincidentally when investigating a child for conditions such as coeliac disease. The aim of this article is to provide a structured approach to the history, investigation and management of an isolated IgA deficiency.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180224
[Lr] Last revision date:180224
[St] Status:Publisher

  7 / 5245 MEDLINE  
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[PMID]: 29465626
[Au] Autor:Wulandari EAT; Saraswati H; Adawiyah R; Djauzi S; Wahyuningsih R; Lee S; Price P
[Ad] Address:Virology and Cancer Pathobiology Research Center, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia.
[Ti] Title:Evaluation of the protective role for C. albicans-reactive IgA against oral fungal infection.
[So] Source:J Acquir Immune Defic Syndr;, 2018 Feb 20.
[Is] ISSN:1944-7884
[Cp] Country of publication:United States
[La] Language:eng
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180221
[Lr] Last revision date:180221
[St] Status:Publisher
[do] DOI:10.1097/QAI.0000000000001657

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[PMID]: 29389970
[Au] Autor:Glaesener S; Jaenke C; Habener A; Geffers R; Hagendorff P; Witzlau K; Imelmann E; Krueger A; Meyer-Bahlburg A
[Ad] Address:Department of Pediatric Pneumology, Allergy and Neonatology, Hannover Medical School, Hannover, Germany.
[Ti] Title:Decreased production of class-switched antibodies in neonatal B cells is associated with increased expression of miR-181b.
[So] Source:PLoS One;13(2):e0192230, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The increased susceptibility to infections of neonates is caused by an immaturity of the immune system as a result of both qualitative and quantitative differences between neonatal and adult immune cells. With respect to B cells, neonatal antibody responses are known to be decreased. Accountable for this is an altered composition of the neonatal B cell compartment towards more immature B cells. However, it remains unclear whether the functionality of individual neonatal B cell subsets is altered as well. In the current study we therefore compared phenotypical and functional characteristics of corresponding neonatal and adult B cell subpopulations. No phenotypic differences could be identified with the exception of higher IgM expression in neonatal B cells. Functional analysis revealed differences in proliferation, survival, and B cell receptor signaling. Most importantly, neonatal B cells showed severely impaired class-switch recombination (CSR) to IgG and IgA. This was associated with increased expression of miR-181b in neonatal B cells. Deficiency of miR-181b resulted in increased CSR. With this, our results highlight intrinsic differences that contribute to weaker B cell antibody responses in newborns.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180218
[Lr] Last revision date:180218
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0192230

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[PMID]: 27776452
[Au] Autor:Vo Ngoc DT; Krist L; van Overveld FJ; Rijkers GT
[Ad] Address:a Department of Science , University College Roosevelt , Middelburg , The Netherlands.
[Ti] Title:The long and winding road to IgA deficiency: causes and consequences.
[So] Source:Expert Rev Clin Immunol;13(4):371-382, 2017 04.
[Is] ISSN:1744-8409
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:INTRODUCTION: The most common humoral immunodeficiency is IgA deficiency. One of the first papers addressing the cellular and molecular mechanisms underlying IgA deficiency indicated that immature IgA-positive B-lymphocytes are present in these patients. This suggests that the genetic background for IgA is still intact and that class switching can take place. At this moment, it cannot be ruled out that genetic as well as environmental factors are involved. Areas covered: A clinical presentation, the biological functions of IgA, and the management of IgA deficiency are reviewed. In some IgA deficient patients, a relationship with a loss-of-function mutation in the TACI (transmembrane activator and calcium-modulating cyclophilin ligand interaction) gene has been found. Many other genes also have been associated. Gut microbiota are an important environmental trigger for IgA synthesis. Expert commentary: Expression of IgA deficiency is due to both genetic and environmental factors and a role for gut microbiota cannot be excluded.
[Mh] MeSH terms primary: B-Lymphocytes/physiology
IgA Deficiency/immunology
Immunity, Mucosal
Immunoglobulin A/metabolism
Microbiota/immunology
Precursor Cells, B-Lymphoid/physiology
Transmembrane Activator and CAML Interactor Protein/genetics
[Mh] MeSH terms secundary: Animals
B-Cell Activating Factor/genetics
Gene-Environment Interaction
Genetic Predisposition to Disease
Humans
IgA Deficiency/etiology
Immunoglobulin Class Switching
Polymorphism, Genetic
Tumor Necrosis Factor Ligand Superfamily Member 13/genetics
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (B-Cell Activating Factor); 0 (Immunoglobulin A); 0 (TNFRSF13B protein, human); 0 (Transmembrane Activator and CAML Interactor Protein); 0 (Tumor Necrosis Factor Ligand Superfamily Member 13)
[Em] Entry month:1706
[Cu] Class update date: 180215
[Lr] Last revision date:180215
[Js] Journal subset:IM
[Da] Date of entry for processing:161026
[St] Status:MEDLINE
[do] DOI:10.1080/1744666X.2017.1248410

  10 / 5245 MEDLINE  
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[PMID]: 29436447
[Au] Autor:Webb C; Norris A; Hands K
[Ad] Address:NHS Tayside, Dundee, UK.
[Ti] Title:An acute transfusion reaction.
[So] Source:Clin Med (Lond);18(1):95-97, 2018 Feb.
[Is] ISSN:1473-4893
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:We present the case of a 67-year-old man who suffered an acute anaphylactic reaction during red cell transfusion due to the presence of anti-IgA antibodies. The incidence and clinical relevance of anti-IgA antibodies in IgA deficiency is reviewed, and the wider investigation and management of acute transfusion reactions is also discussed. This case highlights the need to consider the potential risks of blood component transfusion against the purported benefit.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180213
[Lr] Last revision date:180213
[St] Status:In-Data-Review
[do] DOI:10.7861/clinmedicine.18-1-95


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