Relevant bibliographies by topics / Common variable immunodeficiency (CVID)

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Common variable immunodeficiency (CVID)'

Author: Grafiati
Published: 4 June 2021
Last updated: 18 February 2022

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Journal articles on the topic "Common variable immunodeficiency (CVID)"

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Suter-Meyer, Nigg, Kolyvanos Naumann, Käser, and Vetter. "Common Variable Immunodeficiency (CVID) – variables humorales Immundefektsyndrom." Praxis 96, no. 1 (January 1, 2007): 3–11. http://dx.doi.org/10.1024/1661-8157.96.1.3.

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Vukas, Emina, Aida Dizdarević, Senka Mesihović - Dinarević, and Adisa Čengić. "Common variable immunodeficiency – case report." Journal of Health Sciences 3, no. 2 (September 15, 2013): 170–72. http://dx.doi.org/10.17532/jhsci.2013.83.

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Common variable immunodeficiency (CVID) or acquired hypogammaglobulinemia is the type of primary immunodeficiency. Deregulation of the immune system, leading to hypogammaglobulinemia, defective activation and proliferation of T cells and dendritic cells, and malfunction of the cytokines are observed in CVID. The clinical picture of CVID varies, any organ or system can be affected, therefore the diagnosis is often difficult and delayed and sometimes is not always possible. This article describes a twelve years old boy with all the clinical signs of immunodeficiency, as confi rmed by laboratory. The main treatment consists of life-long immunoglobulin substitution in intravenous or subcutaneous form.
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Capistrano, Giovany Gomes, Gdayllon Cavalcante Meneses, Fernanda Macedo de Oliveira Neves, Renata de Almeida Leitão, Alice Maria Costa Martins, and Alexandre Braga Libório. "Renal Evaluation in Common Variable Immunodeficiency." Journal of Immunology Research 2018 (2018): 1–6. http://dx.doi.org/10.1155/2018/5841031.

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Introduction. Common variable immunodeficiency (CVID) comprises a heterogeneous group of disorders characterized by impaired antibody production. Kidney involvement in CVID is described in isolated and sporadic case reports. The objective of this study was to study the renal function pattern in CVID patients through glomerular and tubular function tests. Methods. Study of 12 patients with CVID diagnosis and 12 healthy control individuals. Glomerular filtration rate (GFR), fractional excretion of sodium (FENa+) and potassium (FEK+), urinary concentration, and acidification capacity were measured. In addition, microalbuminuria and urinary monocyte chemoattractant protein-1 (MCP-1) were evaluated as markers of selectivity of the glomerular barrier and inflammation, respectively. Results. In relation to glomerular markers, all CVID patients had normal GFR (>90 mL/min/1.73 m2), and microalbuminuria and urinary MCP-1 levels were also similar to those of controls. Interestingly, CVID patients had reduced urinary concentration capacity, as demonstrated by lower U/POsm ratio, when compared to controls. Also, while all control subjects achieved a urinary pH less than 5.3, no CVID patients showed a decrease in urinary pH to such levels in response to acid loading with CaCl2, characterizing impaired urinary acidification capacity. Conclusion. Patients showed a trend towards an elevated prevalence of tubular dysfunction, mainly related to urinary acidification and concentration capacities.
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Caza, Tiffany N., Samar I. Hassen, and Christopher P. Larsen. "Renal Manifestations of Common Variable Immunodeficiency." Kidney360 1, no. 6 (April 21, 2020): 491–500. http://dx.doi.org/10.34067/kid.0000432020.

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BackgroundCommon variable immunodeficiency (CVID) is one of the most common primary immunodeficiency syndromes, affecting one in 25,000–50,000 people. Renal insufficiency occurs in approximately 2% of patients with CVID. To date, there are no case series of renal biopsies from patients with CVID, making it difficult to determine whether individual cases of renal disease in CVID represent sporadic events or are related to the underlying pathophysiology. We performed a retrospective analysis of renal biopsy specimens in our database from patients with a clinical history of CVID (n=22 patients, 27 biopsies).MethodsLight, immunofluorescence, and electron microscopy were reviewed. IgG subclasses, PLA2R immunohistochemistry, and THSD7A, EXT1, and NELL1 immunofluorescence were performed on all membranous glomerulopathy cases. CD3, CD4, CD8, and CD20 immunohistochemistry was performed on cases of tubulointerstitial nephritis.ResultsAKI and proteinuria were the leading indications for renal biopsy in patients with CVID. Immune-complex glomerulopathy was present in 12 of 22 (54.5%) cases, including nine cases with membranous glomerulopathy, one case with a C3 glomerulopathy, and one case with membranoproliferative GN with IgG3κ deposits. All membranous glomerulopathy cases were PLA2R, THSD7A, EXT1, and NELL1 negative. The second most common renal biopsy diagnosis was chronic tubulointerstitial nephritis, affecting 33% of patients. All tubulointerstitial nephritis cases showed tubulitis and a lymphocytic infiltrate with >90% CD3+ T cells. Other renal biopsy diagnoses within our cohort included acute tubular injury (n=1), amyloid light-chain amyloidosis (n=1), diabetic glomerulosclerosis (n=1), thin basement membranes (n=1), pauci-immune GN (n=1), and arterionephrosclerosis (n=1).ConclusionsMembranous glomerulopathy and tubulointerstitial nephritis were the predominant pathologic findings in patients with CVID. Membranous glomerulopathy cases in patients with CVID were IgG1 subclass dominant and showed mesangial immune deposits. Four of the membranous glomerulopathy cases had associated proliferation, with mesangial and/or endocapillary hypercellularity, with or without crescent formation. CVID should be considered as a potential cause when membranous glomerulopathy or chronic tubulointerstitial nephritis is seen in a young patient with a history of recurrent infections.
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Tanir Basaranoglu, Sevgen, Sukru Cekic, Emine Kirhan, Melahat Dirican, and Sara S. Kilic. "Oxidative stress in common variable immunodeficiency." European Journal of Inflammation 19 (January 2021): 205873922110024. http://dx.doi.org/10.1177/20587392211002411.

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Common variable immunodeficiency (CVID) is a heterogenous group of immunologic disorders of unknown etiology. Alterations of the normal cellular balance due to an increase in reactive oxygen species and/or decrease in antioxidant defense may lead to increased oxidative stress. We aimed to evaluate the levels of oxidative stress biomarkers in patients with CVID who had different presentations. We investigated the serum catalase (CAT), erythrocyte superoxide dismutase (SOD), erythrocyte reduced glutathione as antioxidants and serum malondialdehyde levels as lipid peroxidation marker in patients with CVID in Uludag University Hospital Department of Pediatric Allergy and Immunology’s outpatient clinics. In the analysis, there were 21 patients and 27 matched healthy controls. The median levels of CAT in patients with CVID was significantly lower than in healthy controls ( p = 0.04). Among the patients with CVID, 19% had autoimmune disease, one had Sjögren’s syndrome, one had autoimmune alopecia, one had juvenile rheumatoid arthritis, and one had chronic inflammatory demyelinating polyneuropathy. Patients with autoimmune complications had significantly lower CAT levels compared to the ones without autoimmune diseases ( p = 0.03). The patients without non-infectious complications (NICs) had lower SOD levels than the patients with NICs ( p = 0.05). The analysis of oxidative stress markers in the patients with CVID suggested a series of abnormalities in the anti-oxidant system. The clinical syndrome associations may be a useful tool for future studies to set prediction markers for the prognosis of patients with CVID.
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Akkinepally, Sudha, Christian Mendez, and Vijayarama Poreddy. "Giardiasis in Common Variable Immunodeficiency (CVID)." American Journal of Gastroenterology 105 (October 2010): S247—S248. http://dx.doi.org/10.14309/00000434-201010001-00685.

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Coraglia, Ana, Nora Galassi, Diego S. Fernández Romero, M. Cecilia Juri, Marta Felippo, Alejandro Malbrán, and María M. E. de Bracco. "Common Variable Immunodeficiency and Circulating TFH." Journal of Immunology Research 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/4951587.

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CD4+ T follicular helper cells (TFH) were assessed in adult patients with common variable immune deficiency (CVID) classified according to the presence of granulomatous disease (GD), autoimmunity (AI), or both GD and AI (Group I) or the absence of AI and GD (Group II).TFHlymphocytes were characterized by expression of CXCR5 and PD-1.TFHwere higher (in both absolute number and percentage) in Group I than in Group II CVID patients and normal controls (N). Within CXCR5+CD4+ T cells, the percentage of PD-1 (+) was higher and that of CCR7 (+) was lower in Group I than in Group II and N. The percentages of Treg andTFHreg were similar in both CVID groups and in N.TFHresponded to stimulation increasing the expression of the costimulatory molecules CD40L and ICOS as did N. After submitogenic PHA+IL-2 stimulation, intracellular expression ofTFHcytokines (IL-10, IL-21) was higher than N in Group I, and IL-4 was higher than N in Group II. These results suggest thatTFHare functional in CVID and highlight the association of increased circulatingTFHwith AI and GD manifestations.
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Ellwood, Amanda, and Caroline Hamm. "Common Variable Immunodeficiency Presenting with Hodgkin’s Disease." Blood 106, no. 11 (November 16, 2005): 4642. http://dx.doi.org/10.1182/blood.v106.11.4642.4642.

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Abstract We report a case of a 32 year old man with classic Common Variable Immunodeficiency Disease (CVID) and Hodgkin’s disease. Repeated immunoglobulin studies as a child showed hypogammaglobulinemia and decreased mitogen responses, with the suggestion of CVID. He presented to the oncology clinic with nearly three decades of recurrent reactive lymphadenopathy and multiple lymph node biopsies throughout his lifetime, recurrent pulmonary infections, and multiple autoimmune manifestations including diabetes mellitus onset at age 4, autoimmune hemolytic anemia and autoimmune thrombocytopenia. He developed Hodgkin’s disease at the age of 30, which has not previously been described in CVID. We also report two other cases of CVID with the diagnosis of non-Hodgkin’s lymphoma in the same oncology practice. CVID is a relatively common and yet rarely identified syndrome. Specific treatment is recommended. We suggest that oncologists should be aware of this unusual and yet relatively common disorder that carries up to 400 times the risk for the development of lymphoma (Cunningham-Rundles, C, et al. J Clin Immunol1987; 7:294–299).
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Pecoraro, Heidi L., M. Julia B. Felippe, Andrew D. Miller, Thomas J. Divers, Kenneth W. Simpson, Kimberly M. Guyer, and Gerald E. Duhamel. "Neuroborreliosis in a horse with common variable immunodeficiency." Journal of Veterinary Diagnostic Investigation 31, no. 2 (January 19, 2019): 241–45. http://dx.doi.org/10.1177/1040638718824146.

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Common variable immunodeficiency (CVID) is a rare condition in adult horses characterized by hypogammaglobulinemia and increased susceptibility to parasitic and bacterial infections, including recurrent respiratory diseases, septicemia, and meningitis. Lyme disease is often included as a differential diagnosis in CVID horses with signs of meningitis; however, the Borrelia burgdorferi organism has not been demonstrated previously within central nervous system tissues of CVID horses with neurologic disease, to our knowledge. We report herein a case of neuroborreliosis in a CVID horse, confirmed by combined immunologic testing, histopathology, real-time PCR assay, fluorescent in situ hybridization, and immunohistochemical staining. Implications of these findings include heightened monitoring of CVID horses for Lyme disease in endemic areas and appropriate therapy in the case of neurologic disease.
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Montazeri, Maryam, Mohammad Reza Ebadpour, Farideh Kouchak, and Naser Esmaeili. "Common Variable Immunodeficiency (CVID): A Case Report." Internal Medicine and Medical Investigation Journal 2, no. 1 (March 20, 2017): 26. http://dx.doi.org/10.24200/imminv.v2i1.44.

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Common variable immune deficiency disease is the most prevalent acquired immune deficiency in human being after selective immunoglobulin A deficiency. It causes reduction of immunoglobulin levels and specific antibodies production and enhancement of recurrent and chronic infections risk, especially respiratory infections. CVID patients faces increased risk of granulomatous disease, autoimmune and phenomenon and malignancy. The disease involves males and females equally. Some studies showed that early diagnosis of CVID disease and regular treatment of patients with IVIG may have an efficient role in decreasing pneumonia and frequency of hospitalization due to infections and its complications. In this study we report a 16 years old girl with CVID, without clinical history of determined infection with recurrent sinusitis.
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Dissertations / Theses on the topic "Common variable immunodeficiency (CVID)"

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Schönhage, Kai Oliver. "Particle Gel Immuno Assay (ID-PaGIA) zum Nachweis von anti-IgA Antikörpern." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2005. http://dx.doi.org/10.18452/15265.

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Anti-IgA Antikörper werden häufig als Ursache nicht-hämolytischer Transfusionsreaktionen angesehen. Die Inzidenz solcher Reaktionen schwankt zwischen 1:17.000 bis 1:770.000 und beruht größtenteils auf Fallberichten. Die Bedeutung dieser Antikörper, obwohl mit einer Prävalenz von 1: 18 bis 1:1.250 relativ häufig vorkommend, konnte in den circa vierzig Jahren seit ihrer Entdeckung nicht eindeutig geklärt werden; verschiedene Spezifitäten der Antikörper mit unterschiedlichen Reaktionen erschweren die Diagnose und eine klare Schematisierung. Ein Nachteil war bisher das Fehlen einer schnellen und unkomplizierten Nachweismethode, die in vielen Laboratorien angewandt werden kann. Die Ende der sechziger Jahre entwickelte Die Ende der 1960’er Jahre entwickelte Passive Hämagglutination (PHA) ist oft ungenau und unterliegt starken Schwankungen, kann aber relativ einfach durchgeführt werden und ist deshalb die Hauptmethode in der Diagnose von anti-IgA gewesen. Neuere und genauere Methoden wie Radio Immuno Assay (RIA) und Enzyme Linked Immunosorbent Assay (ELISA) sind weder schnell durchzuführen noch in vielen Laboratorien verfügbar. In dieser Arbeit wird eine neue Agglutinationsmethode, Particle Gel Immuno Assay (PaGIA) evaluiert und mit der PHA verglichen. Im ersten Teil wurden die Seren 105 gesunder Spender untersucht: 70 führten zu Reaktionen im PHA mit Titern bis 1:80 während keines im PaGIA reagierte, was die Spezifität des PaGIA unterlegt. Anschließend wurden elf Seren von Patienten mit selektivem IgA Mangel (sDIgA) und 23 Seren von Patienten mit variablem Immundefektsyndrom (CVID) auf das Vorliegen eines anti-IgA Antikörpers untersucht. Fünf Seren beider Patientengruppen führten in beiden Tests zu Agglutinationen und ein Serum (sDIgA) reagierte mit einem Titer von 1:1 in der PHA aber nicht im PaGIA. Die hier gefundenen Prävalenz (22% sDIgA, 45% CVID) und Größe der Titer (sDIgA>CVID) von anti-IgA stimmt mit den bisherigen Erkenntnissen überein. Weitere Untersuchungen konnten die Stabilität des PaGIA bzw. dessen Beads und Reproduzierbarkeit der Ergebnisse über mehrere Monate als auch die Möglichkeit subklassenspezifisches anti-IgA nachzuweisen darlegen. Der PaGIA stellt einen schnell und einfach durchzuführenden Test dar, mit dem anti-IgA Antikörper verschiedener Spezifität verläßlich bestimmt werden können, um Untersuchungen im großen Rahmen durchzuführen, die die Bedeutung der anti-IgA Antikörpern erhellen.
Anti-IgA antibodies are thought to be responsible for non-hemolytic transfusion reactions in one in 17,000 to one in 770,000 number of cases. This incidence is mainly supported by case reports. Despite their relative frequency of one in 18 to one in 1,250, since their discovery approximately forty years ago, the true significance of these antibodies has not yet been determined. Several specificities of these antibodies resulting in different reaction patterns make diagnosis and categorization difficult. Until recently, the lack of a fast and reliable laboratory test was a drawback. This test needed to be easily performed, fast, accurate, reproducible and accessible to many practitioners in many laboratories. The Passive Hemagglutination Assay (PHA), developed in the late 1960’s, is neither precise nor reliable but easy to perform and therefore has been the mainstay in diagnosis of anti-IgA. While newer methods, such as Radio Immuno Assay (RIA) and Enzyme Linked Immunosorbent Assay (ELISA), are neither fast nor easily performed but very precise. This thesis studies and evaluates a new agglutination assay, the Particle Gel Immuno Assay (PaGIA), and compares it to the PHA. In the first part of our study we established the specificity of PaGIA. Sera of 105 healthy blood donors were tested: 70 led to positive reactions with the PHA with titers up to 1:80 while none reacted with the PaGIA. Subsequently, eleven sera of patients with selective deficiency of IgA (sDIgA) and 23 sera of those with Common Variable Immunodeficiency (CVID) were tested for the presence of anti-IgA antibodies. Five sera in each group led to agglutinations in both assays and one serum reacted with a titer of 1:1 in the PHA but not in the PaGIA. The prevalence (22% sDIgA, 45% CVID) and strength of the titers (sDIgA>CVID) of anti-IgA corresponds with current knowledge. Further tests demonstrated the PaGIA’s and its beads stability and reproducibility over several months as well as the possibility for detection of subclass-specific anti-IgA. The PaGIA is a fast and easily performed assay which reliably detects anti-IgA antibodies of different specificities, thereby providing a tool for large scale studies to shed more light on the significance of anti-IgA antibodies.
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Mullighan, Charles Grenfell. "The immunogenetics of common variable immunodeficiency /." Title page, table of contents and summary only, 1997. http://web4.library.adelaide.edu.au/theses/09MD/09mdm959.pdf.

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Wong, Gabriel K. "Haematopoietic clonality in common variable immunodeficiency." Thesis, University of Birmingham, 2016. http://etheses.bham.ac.uk//id/eprint/6935/.

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The aetiology of Common Variable Immunodeficiency (CVID) has fascinated immunologists since Dr. Janeway reported the first case in 1953. While the advances in molecular biology have enlightened us on the aetiology in some patients, the majority is not caused by inherited genetic disorders. A convincing mechanism accounting for the intrinsic variable and partial nature of the condition has yet been proposed. CVID separates itself from other primary antibody deficiencies by the procurement of an abnormal T-cell compartment. Data from this study support that both T-cells and B-cells are subjected to similar deficiency. Investigation of the T-cell receptor repertoire by next-generation sequencing and multi-parametric flow cytometry suggests a severe reduction in naïve T-cell output from the thymus. Similarly, the study of long-lived plasma cell generation and survival highlighted the greatest functional deficits in the naïve B-cell pool, altogether supporting an acquired arrest in lymphogenesis. Using DNA methylation as a surrogate marker for pre-VDJ clonality, this study further shows that some CVID patients exhibited clonal haematopoiesis, adjoining CVID to other clonal haematopoiesis related acquired haematological disorders. Further work is being focused on using high resolution techniques to confirm this association and mechanistically define the development of antibody deficiency in adulthood.
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Kuntz, Martin [Verfasser], and Robert [Akademischer Betreuer] Thimme. "CD8-T-Zell-Differenzierung bei Patienten mit Common Variable Immunodeficiency." Freiburg : Universität, 2011. http://d-nb.info/1123465452/34.

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Rezaei, Nima. "B-Cell and T-Cell interaction in common variable immunodeficiency." Thesis, University of Sheffield, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.512017.

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Koopmans, Wijntje Jeltje. "Common variable immunodeficiency in New Zealand : finding the molecular and cellular foundations." Thesis, University of Auckland, 2012. http://hdl.handle.net/2292/19414.

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Common Variable Immunodeficiency Disorder (CVID) is a disorder characterised by low level of serum immunoglobulin and increased susceptibility to infection. The aim of this study was to develop a better understanding and prognosis for CVID patients. Clinical details and disease histories were analysed in 39 CVID patients. The time taken to diagnose CVID when symptoms first appear was in steady decline for the past 80 years. Those who develop CVID at a young age were more likely to develop bronchiectasis. Ten genes known to cause CVID in human or mouse were analysed in 95 patients (45 CVID, 50 hypogammaglobulinaemia). Thirty one SNPs and one deletion were identified with certain mutations already reported in literature. The following new mutations were identified: R20H and K186del in TACI; G42V in Bob-1; S77N in IL-15; T75M and N146T in IL-15R��. The C104R mutation in TACI is linked to susceptibility to CVID. Segregation analysis was performed for a family with this mutation. Having one or both copies of the C104R allele is not a reliable predictor of CVID since the allele is not always present in family members with CVID. A healthy brother with the C104R/C104R genotype was identified. His markedly reduced immunoglobulin levels and reduced vaccine response requires close monitoring. The total CD8 central memory T cell or marginal zone B cell numbers could be potential health indicators in this family because these cell numbers are related to health status. B and T cell phenotyping were reported to predict clinical outcomes in CVID. The question is how consistent these assays are over time. The three B and one T cell assays were evaluated monthly over 6 and 3 months respectively. The EUROclass B cell classification system was the most consistent. CCR7 was the more reliable marker than CD62L for the memory T cell assay. Several potential markers for CVID were identified in this work. Certain cell subsets were significantly (p ��� 0.01) elevated (CD38low CD21low B cells, transitional B cells, CD4+ effector memory T cells and CD4+ Tim3+) or decreased (switched memory B cells and CD4+ nai��ve T cells) compared to normal donors.
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Rodríguez, Cortez Virginia Carolina. "Epigenetic Mechanisms in two primary immunodeficiencies: Hyper-IgM Syndrome and Common Variable Immunodeficiency." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/311631.

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The proper function of the immune system requires complex regulatory mechanisms and a highly strict balance in the amount and function of immune and non-immune elements. Part of the primary immunodeficiencies result from mutations in specific genes and their clinical manifestations can be recapitulated through the generation of knockout mice models that support the role of these genes. However, an important number of these disorders cannot be explained by genetic alterations and, to date, there is not an alternative explanation to understand it. This makes difficult the diagnosis process, the establishment of prognosis markers and complicates the finding of specific treatments or the improvement of the existing ones. Epigenetic mechanisms, mainly DNA methylation and histone modifications, are elements of gene control and have emerged to provide explanation to a wide variety of diseases including those related to the immune system. For that reason, this doctoral thesis was focused on investigating the influence of the epigenetic mechanisms in two primary immunodeficiencies: Hyper-IgM Syndrome and Common Variable Immunodeficiency. This was achieved by the establishment of the following specific objectives: 1. To investigate the influence of activation-induced cytidine deaminase (AID), commonly mutated in Hyper-IgM Syndrome, in the setting of epigenetic modifications in an inducible B cell model. 2. To analyze the effects of AID mutations in the acquisition of epigenetic alterations. 3. To determine the participation of epigenetic alterations in CVID by focusing on the DNA methylation profiling of B cells isolated from monozygotic twins discordant for CVID. 4. To expand the results obtained with monozygotic twins discordant for CVID in three different B cell subsets from a cohort of healthy donors and CVID patients.
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Lo, Ching-ha, and 盧靜霞. "Study of B lymphocyte subset phenotypes and clinical features of common variable immunodeficiency patients in Hong Kong." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B42924959.

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Lo, Ching-ha. "Study of B lymphocyte subset phenotypes and clinical features of common variable immunodeficiency patients in Hong Kong." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B42924959.

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Marashi, S. M. "Functional competence of CD8+ T cell responses specific to human cytomegalovirus in common variable immunodeficiency." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1306764/.

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This PhD investigated the role of human cytomegalovirus (HCMV) in inflammatory disease associated with common variable immunodeficiency (CVID) by examining the functional competence of HCMV specific CD8+ T cell responses. The project was based on the hypothesis that HCMV is a major factor driving the expansion of CD8+ T cells that contribute to the inflammatory pathology. HCMV specific CD8+ T cell frequencies were significantly elevated in inflammatory patients compared to non-inflammatory patients or healthy subjects. The frequency of EBV (GLC) epitope specific CD8+ T cells did not differ between patient groups. HCMV CD8+ T cells from inflammatory patients displayed a distinct cytokine expression profile with the majority of cells producing IFN-γ only or IFN-γ and TNF-α in response to antigen stimulation. These cells did not show evidence of exhaustion, with low PD-1 expression; rather, they showed high functionality, high TCR avidity and high proliferative potential. CD8+ T cells from inflammatory patients but not non-inflammatory patients or healthy donors expressed high levels of Ki-67 and proliferated in response to antigen stimulation in vitro without co-stimulation. Further phenotypic analysis revealed striking correlations between the frequencies of HCMV specific CD8+ T cells expressing PD-1 or granzyme B and the overall frequency of CD8+ CD27-CD28- T cells. Consistent with their hypothesized role in the inflammatory disease, the CD8+ T cells from inflammatory patients expressed reduced levels of the anti-inflammatory marker CD73. Further support for the involvement of HCMV in driving the inflammatory pathology came from collaborative work in which viral antigen was detected at the sites of inflammation. The results support the hypothesis that HCMV and HCMV-specific T cells are key factors in CVID associated inflammation. They explain previously reported T cell ‘abnormalities’ seen in CVID and provide an evidence base for clinical trials of anti-TNF therapy and/or antiviral therapy in these patients.
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Books on the topic "Common variable immunodeficiency (CVID)"

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Case Studies in Immunology: Common Variable Immunodeficiency. Garland Science, 2010. http://dx.doi.org/10.4324/9780203853542.

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Book chapters on the topic "Common variable immunodeficiency (CVID)"

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Warnatz, Klaus, and Eric Oksenhendler. "Common Variable Immunodeficiency (CVID)." In Encyclopedia of Medical Immunology, 1–5. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-9209-2_22-1.

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Warnatz, Klaus, and Eric Oksenhendler. "Common Variable Immunodeficiency (CVID)." In Encyclopedia of Medical Immunology, 192–96. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-8678-7_22.

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Ebert, Suzahn, Sonali Bracken, John Woosley, Kevin G. Greene, Jonathan Hansen, Leonard Jason Lobo, and Teresa Kathleen Tarrant. "Common Variable Immunodeficiency (CVID)." In Rare Rheumatic Diseases of Immunologic Dysregulation, 59–85. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-99139-9_3.

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Gartler, Stanley M., R. Scott Hansen, Vinzenz Oji, Heiko Traupe, Julia Horn, Bodo Grimbacher, Srijita Sen-Chowdhry, et al. "Immunodeficiency, Common Variable." In Encyclopedia of Molecular Mechanisms of Disease, 1039–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_378.

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Peters, Nils, Martin Dichgans, Sankar Surendran, Josep M. Argilés, Francisco J. López-Soriano, Sílvia Busquets, Klaus Dittmann, et al. "Common Variable Immunodeficiency." In Encyclopedia of Molecular Mechanisms of Disease, 396. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_9103.

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Ameratunga, Rohan, Caroline Allan, and See-Tarn Woon. "Common Variable Immunodeficiency-Like Disorders." In Primary and Secondary Immunodeficiency, 91–104. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57157-3_7.

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Farrant, J., and A. David B. Webster. "Different Categories of Common Variable Immunodeficiency." In Symposium in Immunology III, 91–101. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78438-5_10.

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Warnatz, Klaus, and Michael Schlesier. "Diagnostics for Common Variable Immunodeficiency Syndrome." In Cellular Diagnostics, 540–57. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000209179.

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Lehman, Heather K., and Parteet Sandhu. "Common Variable Immunodeficiency, Hypogammaglobulinemia, and Specific Antibody Deficiency." In Primary and Secondary Immunodeficiency, 15–36. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57157-3_2.

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Aiuti, F., G. Luzi, E. Scala, A. Oliva, R. Rosso, and F. Pandolfi. "Clinical and Immunological Aspects of Common Variable Immunodeficiency." In Symposium in Immunology III, 71–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78438-5_8.

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Conference papers on the topic "Common variable immunodeficiency (CVID)"

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Dirks, Jackie, Richard Warrington, and Sat Sharma. "Respiratory Manifestations Of Common Variable Immunodeficiency (CVID)." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4157.

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Alves Moreira, Ana Catarina, Carina Lopes, Natália Melo, Hélder Bastos, Patrícia Mota, and António Morais. "Lung involvement in common variable immunodeficiency (CVID): a case series." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa3677.

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Elborn, J. S., D. Mooney, M. M. Tunney, J. D. Edgar, S. McGrath, L. McIlreavey, and E. Johnston. "Impaired neutrophil function in patients with common variable immunodeficiency (CVID)." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2621.

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Baleeiro, Carlos, and Nathan Mull. "Prevalence Of Common Variable Immunodeficiency (CVID) Among Patients With Recurrent Respiratory Tract Infections." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3187.

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Wasala, Rani, and Noman Khan. "P108 A rare case report with alopecia, onycodystrophy and hypogammaglobulinaemia- common variable immunodeficiency (CVID)." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.463.

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Mohammed, A., S. Mazher, A. Yelisetty, Y. Sheinin, R. A. Franco, and V. S. Ramalingam. "A Serious Complication of Common Variable Immunodeficiency." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1368.

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Low, TB, I. Singh, K. Boland, SH Chotirmall, P. Branagan, NG McElvaney, and SJ O'Neill. "Prevalence of Common Variable Immunodeficiency Masquerading as Sarcoidosis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2271.

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Burini Lobo, Vanessa, Fernanda Freire Kosac, Tiere Costa Bravim, Isabela Taveira Mouzinho, Luciana Nunes de Assis Daameche, Jamille Nascimento Carneiro, Gustavo de Paiva Costa, et al. "PATIENT WITH COMMON VARIABLE IMMUNODEFICIENCY AND RHEUMATOID ARTHRITIS." In Congresso Brasileiro de Reumatologia 2020. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2020.16861.

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LACERDA, DIOGO CUNHA, RODRIGO ZUBER MACIEL, LUCAS ANDROCZEVECZ SILVA, JEAN TAFAREL BOBATO, RAFAELA SORPILE ARAUJO, BRENDA ZAPPELINI PEZZI, AUREO ANTÔNIO AURELIO JUNIOR, LUCIANE MARTIGNONI, and CASSIANO EDUARDO T. GOULART. "COMMON VARIABLE IMMUNODEFICIENCY MIMETIZING CASE OF SPONDILOARTROPATHY – CASE REPORT." In 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-059.

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Bron, C., M. Wislez, E. Catherinot, E. Rivaud, J. Cadranel, and L. Couderc. "Pulmonary Non Infectious Diseases in Adult Patients with Common Variable Immunodeficiency." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2865.

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You might also be interested in the extended bibliographies on the topic 'Common variable immunodeficiency (CVID)' for particular source types:
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