Epithelia: lymphocyte interactions in the gut

Dahan, Stéphanie; Roth‐Walter, Franziska; Arnaboldi, Paul M.; Agarwal, Shradha; Mayer, Lloyd

doi:10.1111/j.1600-065x.2006.00484.x

Cited by 112 publications

(91 citation statements)

References 114 publications

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“…This process confers specificity to CSR 38 , because the promoter upstream of each C H gene responds only to a specific set of signal-induced transcription factors 10 . Promoters upstream of C α genes, or I α promoters, become activated in response to transforming growth factor-β1 (TGFβ1) [39][40][41] , a cytokine that is secreted by many cell types, including various subsets of CD4 + T cells 42,43 . Together with CD40L, TGFβ1 is essential for the induction of T-cell-dependent IgA class switching 10 .…”

Section: T-cell-dependent Iga Class Switchingmentioning

confidence: 99%

The regulation of IgA class switching

2008

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IgA class switching is the process whereby B cells acquire the expression of IgA, the most abundant antibody isotype in mucosal secretions. IgA class switching occurs via both T-celldependent and T-cell-independent pathways, and the antibody targets both pathogenic and commensal microorganisms. This Review describes recent advances indicating that innate immune recognition of microbial signatures at the epithelial-cell barrier is central to the selective induction of mucosal IgA class switching. In addition, the mechanisms of IgA class switching at follicular and extrafollicular sites within the mucosal environment are summarized. A better understanding of these mechanisms may help in the development of more effective mucosal vaccines.IgA has been selected throughout evolution to provide a first line of immune protection at mucosal surfaces -vulnerable frontline sites that are exposed to potentially harmful commensal, airborne, ingested and sexually transmitted agents. Growing evidence indicates that IgA uses a high-affinity binding system to neutralize microbial toxins and pathogens, and a low-affinity binding system to prevent commensal bacteria from breaching the mucosal surface 1 . This latter process is known as immune exclusion and has a fundamental role in the intestine, which is home to a number of commensal bacteria exceeding that of human cells by an estimated order of magnitude 2 .Remarkably, intestinal IgA achieves both immune protection and immune exclusion in a non-inflammatory manner, thereby promoting the establishment of a sustainable hostmicrobial mutualism 3 . The complex relationship between IgA and the intestinal microbiota is further exemplified by the fact that IgA responses are highly dependent on intestinal colonization by commensal microorganisms. Indeed, the number of IgA-secreting B cells is dramatically reduced in the intestine of germ-free animals and these cells are virtually absent in neonates before their exposure to bacteria 3 .In this Review, I summarize recent advances in our understanding of the function, regulation and geography of IgA class switching. In addition to analysing the signalling pathways underlying IgA class switching, I discuss new evidence indicating that commensal bacteria Competing interests statementThe author declares no competing financial interests. DATABASES Function of IgA class switchingAntibody diversification is essential for the immune system to mount protective humoral responses. B cells diversify their antibody repertoire through three main genetic alterations that occur in two distinct phases of B-cell development. In the antigen-independent phase, B-cell precursors lodged in the bone marrow generate antigen recognition diversity by assembling the exons that encode immunoglobulin heavy (H) and light (L) chain variable regions from individual variable (V), diversity (D) and joining (J) gene segments through V(D)J gene recombination 4 . This process is initiated by a lymphoid-cell-and sequencespecific RAG1 (recombination-activating gene 1...

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Section: T-cell-dependent Iga Class Switchingmentioning

confidence: 99%

The regulation of IgA class switching

2008

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“…In the intestine, two major lymphocyte populations exist: the intraepithelial lymphocytes (IEL) which remain associated with the basolateral membrane of the IECs, and the LPL which localize to the subepithelial lamina propria and are in contact with IECs via basolateral projections through the semi-porous basement membrane 1,2 . Previous studies from our lab suggested that IECs function as antigen-presenting cells (APCs) and, as such, can promote regulatory T-cell responses in the mucosa [3][4][5][6][7][8] .…”

Section: Introductionmentioning

confidence: 99%

Epithelial: Lamina Propria Lymphocyte Interactions Promote Epithelial Cell Differentiation

et al. 2008

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“…Food allergy to wheat is typically characterized by a T helper type 2 (Th2) lymphocytic inflammation [124][125][126][127][128] in genetically predisposed [125,129,130] individuals. The subsequent cascade of Th2 activation could either lead to an IgE mediated (immediate response with wheatspecific IgE antibodies) or a non IgE mediated allergy (chronic cellular inflammation with presence of lymphocytes and eosinophils) [124][125][126][127][128].…”

Section: Wheat Allergymentioning

confidence: 99%

“…The subsequent cascade of Th2 activation could either lead to an IgE mediated (immediate response with wheatspecific IgE antibodies) or a non IgE mediated allergy (chronic cellular inflammation with presence of lymphocytes and eosinophils) [124][125][126][127][128].…”

Section: Wheat Allergymentioning

confidence: 99%

Gluten and the Gut: A Brief Review of Gluten-Related Gastrointestinal Disorders

Shah¹

2017

SOJI

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We conducted online electronic searches (published manuscripts in English) of the Cochrane Library, pub med and manual searches of selected specialty journals to identify any pertinent literature. The search was conducted using the key words 'celiac disease', 'gluten related disorder', 'non celiac gluten sensitivity', 'wheat allergy', 'gluten', , 'gluten free diet'. Studies not published in English or published only in the abstract form were excluded. We also conducted a focused review of available references to identify subsequent pertinent papers. AbstractCeliac disease (CD) was the first gluten-related disorder to be described. Presently the realm of gluten-related disorders also includes non-celiac gluten sensitivity (NCGS) and wheat allergy (WA). CD is a multisystem immune mediated enteropathy observed in genetically susceptible individuals exposed to dietary gluten present in barley, rye and wheat. Although the prevalence of CD is on the rise, it still largely remains under diagnosed given that many cases can be silent, subtle or atypical. The Pathophysiology of CD includes both innate and adaptive immune response to dietary gluten. Patients present with a wide variety of intestinal and extra-intestinal symptoms and are at risk for non-Hodgkin's lymphoma and small intestinal adenocarcinoma. The corner stone for treatment of CD is a gluten-free diet (GFD). NCGS is an emerging condition associated with gluten ingestion and the diagnosis of which is based on exclusion of CD and WA. Further evidence and studies are required to fully appreciate the clinical entity of NCGS and WA to detail its epidemiology and pathogenesis. The symptoms of NCGS and WA may overlap with CD and hence it is imperative to differentiate these clinical entities and select patients for appropriate management.Keywords: Celiac disease, gluten related disorder, non-celiac gluten sensitivity, wheat allergy, gluten, epidemiology, clinical features, Pathophysiology, management, gluten free diet.Core tip: CD is largely under-diagnosed while the incidence and prevalence of gluten-related disorders are on the rise. A clear understanding of the various clinical presentations of gluten-related disorders can help differentiate CD from NCGS and WA. The management for these conditions differs and hence accurate diagnosis leads to improved patient outcomes with avoidance of longterm complications as well as unnecessary testing which can be both invasive and expensive. Celiac DiseaseThe term celiac is derived from the Greek word "koiliaks" meaning "abdominal". It was first described in the second century in modern day Turkey by a Greek physician Aretaeus of Cappadocia [1]. In 1888, Samuel Gee; a pediatrician from the United Kingdom gave the first modern-day description of the condition and associated diet to the treatment of celiac disease EpidemiologyCeliac disease occurs in about 1% of the general population worldwide [7]. Data from the USA suggests CD to be more common in Caucasians as compared to African-Americans and Hispanics [8,9]. The initial ...

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Epithelia: lymphocyte interactions in the gut

Cited by 112 publications

References 114 publications

The regulation of IgA class switching

The regulation of IgA class switching

Epithelial: Lamina Propria Lymphocyte Interactions Promote Epithelial Cell Differentiation

Gluten and the Gut: A Brief Review of Gluten-Related Gastrointestinal Disorders

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