Role of apoptosis in common variable immunodeficiency and selective immunoglobulin A deficiency

Yazdani, Reza; Fatholahi, Maryam; Ganjalikhani‐Hakemi, Mazdak; Abolhassani, Hassan; Azizi, Gholamreza; Hamid, Kabir Magaji; Rezaei, Nima; Aghamohammadi, Asghar

doi:10.1016/j.molimm.2015.12.016

Cited by 37 publications

(27 citation statements)

References 120 publications

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“…Most studies show that almost 90% of CVID patients have normal B-cell counts, [35,36], indicating that the major defect is likely related to alterations of the terminal stages of B-cell differentiation. Furthermore, several groups, including our own, have shown that disturbed B-cell subsets could result from an increase of terminal B-cell apoptosis [37,38]. Impaired antibody production despite normal B-cell counts also suggests a defect in the differentiation of B cells into memory and plasma cells in many CVID patients [35].…”

Section: B-cell Subsetsmentioning

confidence: 86%

Common Variable Immunodeficiency: Epidemiology, Pathogenesis, Clinical Manifestations, Diagnosis, Classification, and Management

Yazdani¹,

Habibi²,

Sharifi³

et al. 2020

J Investig Allergol Clin Immunol

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Common variable immunodeficiency (CVID) is a heterogeneous disorder characterized by hypogammaglobulinemia and increased susceptibility to recurrent bacterial infections. It is the most frequent symptomatic antibody deficiency, with a wide variety of infectious and noninfectious complications. Numerous studies have demonstrated that immunological and genetic defects are involved in the pathogenesis of CVID. However, in most cases, the genetic background of the disease remains unidentified. This review aims to discuss various aspects of CVID, including epidemiology, pathogenesis, symptoms, diagnosis, classification, and management.

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Section: B-cell Subsetsmentioning

confidence: 86%

Common Variable Immunodeficiency: Epidemiology, Pathogenesis, Clinical Manifestations, Diagnosis, Classification, and Management

Yazdani¹,

Habibi²,

Sharifi³

et al. 2020

J Investig Allergol Clin Immunol

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“…[58] T and B cells have a higher rate of spontaneous and induced apoptosis in patients with CVID, and Yazdani and colleagues have recently suggested that the same mechanism may be present in those with SIgAD, although this mechanism has yet to be confirmed in individuals with SIgAD. [59] Additionally, SIgAD has been transferred between patients via bone marrow grafting, which further suggests a defect in immune cells. [46] The monogenic hypothesis suggests that certain as-yet undiscovered monogenic mutations predispose both to the development of SIgAD and autoimmune conditions.…”

Section: Mechanisms Of Autoimmunity In Iga Deficiencymentioning

confidence: 99%

The Epidemiology and Clinical Manifestations of Autoimmunity in Selective IgA Deficiency

Odineal

Gershwin

2019

Clinic Rev Allerg Immunol

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Selective Immunoglobulin A Deficiency (SIgAD) is the most common primary immunodeficiency, defined as an isolated deficiency of IgA (less than 0.07 g/L). Although the majority of people born with IgA deficiency lead normal lives without significant pathology, there is nonetheless a significant association of IgA deficiency with mucosal infection, increased risks of atopic disease, and a higher prevalence of autoimmune disease. To explain these phenomena, we have performed an extensive literature review to define the geoepidemiology of IgA deficiency and particularly the relative risks for developing Systemic Lupus Erythematosus, hyperthyroidism, hypothyroidism, type 1 diabetes mellitus, Crohn's Disease, ulcerative colitis, rheumatoid arthritis, juvenile idiopathic arthritis, ankylosing spondylitis, and vitiligo; these diseases have strong data to support an association. We also note weaker associations with scleroderma, celiac disease, autoimmune hepatitis, immune thrombocytopenic purpura, and autoimmune hemolytic anemia. Minimal if any associations are noted with myasthenia gravis, lichen planus, and multiple sclerosis. Finally, more recent data provide clues on the possible immunologic mechanisms that lead to the association of IgA deficiency and autoimmunity; these lessons are important for understanding the etiology of autoimmune disease. 2 3 Introduction:

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“…In this regard, Hammarström and colleagues [45] reported that SIgAD patients lack surface IgA B cells, and the combination of IL-4, IL-21, and the anti-CD40 monoclonal antibody can prevent apoptosis of these cells in SIgAD patients, and result in reconstitution of IgA secretion. A notable point is that in spite of the intact genes and molecular mechanisms of IgA recombination, and in addition to the reports that show low surface IgA-positive B cells in patients with SIgAD, the existence of a defect in the long-term survival of IgA secreting cells and memory B cells should be considered [14]. …”

Section: Pathogenesis Of Sigadmentioning

confidence: 99%

The Heterogeneous Pathogenesis of Selective Immunoglobulin A Deficiency

Bagheri¹,

Sanaei²,

Yazdani³

et al. 2019

Int Arch Allergy Immunol

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Selective immunoglobulin A deficiency (SIgAD) is the most prevalent type of primary immunodeficiency disorder. The phenotypic feature of SIgAD is related to a defect in B lymphocyte differentiation into plasma cell-producing immunoglobulin A (IgA). In this review, we summarize the recent advances in this regard. Genetic (including major histocompatibility complex [MHC] and non-MHC genes), immunologic (including B and T lymphocyte subsets abnormality), cytokines/chemokines and their related receptors, apoptosis and microbiota defects are reviewed. The mechanisms leading to SIgAD are most likely multifactorial and it can be speculated that several pathways controlling B cells functions or regulating epigenetic of the IGHA gene encoding constant region of IgA heavy chain and long-term survival of IgA switched memory B cells and plasma cells may be defective in different SIgAD patients.

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Role of apoptosis in common variable immunodeficiency and selective immunoglobulin A deficiency

Cited by 37 publications

References 120 publications

Common Variable Immunodeficiency: Epidemiology, Pathogenesis, Clinical Manifestations, Diagnosis, Classification, and Management

Common Variable Immunodeficiency: Epidemiology, Pathogenesis, Clinical Manifestations, Diagnosis, Classification, and Management

The Epidemiology and Clinical Manifestations of Autoimmunity in Selective IgA Deficiency

The Heterogeneous Pathogenesis of Selective Immunoglobulin A Deficiency

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