Mucosal aspects of primary B-cell deficiency and gastrointestinal infections

Brandtzæg, Per; Nilssen, D E

doi:10.1097/00001574-199511000-00012

Cited by 36 publications

(26 citation statements)

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“…The intestinal epithelial barrier is a crossroads for surface defense and nutrition, and SIgA is apparently essential to keep the balance between these two functions and thus maintain mucosal homeostasis. Lack of SIgA probably explains why patients with common variable immunodeficiency may have a similar gene expression profile in their duodenal mucosa and show malabsorption with fatty stools (Shulzhenko et al, 2011)-despite frequent surface defense compensation with increased intraepithelial lymphocytes, particularly the CD8 + subset (Brandtzaeg and Nilssen, 1995).…”

Section: Figure 7 Hypothetical Depiction Of How the Intestinal Immunementioning

confidence: 99%

“…The activity of the secretory immune system in IgA-deficient subjects is fairly unpredictable on the basis of individual serum IgA levels (Brandtzaeg and Nilssen, 1995;Brandtzaeg et al, 1991). A decreased intestinal IgA + :IgM + PC ratio reflects immaturity of the secretory immune system and also appears to be a good indicator of a significant IgA deficiency after infancy.…”

Section: Selective Iga Deficiency and Related Clinical Problemsmentioning

confidence: 99%

“…Enhanced intestinal production and export of IgM in selective IgA deficiency may partly explain the fact that most subjects with this disorder have no or few gastrointestinal symptoms (Brandtzaeg and Nilssen, 1995;; their problems are rather related to the upper respiratory tract (Brandtzaeg et al, 1987b). In a group of 14 IgA-deficient patients (serum IgA <0.1 g/L) subjected to immunohistochemical studies of their jejunal mucosa in this laboratory, celiac disease was diagnosed in two children and four adults (Nilssen et al, 1992); a good response on gluten-free diet was noted in four of them.…”

Section: Selective Iga Deficiency and Related Clinical Problemsmentioning

confidence: 99%

“…These findings signify increased gastrointestinal permeability, which may explain the relatively high incidence of autoimmunity in IgA deficiency (Cunningham-Rundles et al, 1984). Moreover, the incidence of IgA deficiency is considerably higher among patients with celiac disease than in the general population (Brandtzaeg and Nilssen, 1995), and food allergy may be associated with a defect of the mucosal IgA system in infancy (Brandtzaeg, 2010b). Likewise, mice with pIgR deficiency show decreased epithelial barrier function and predisposition for food allergen-induced anaphylaxis ( Brandtzaeg, 2013;Karlsson et al, 2010).…”

Section: Selective Iga Deficiency and Related Clinical Problemsmentioning

confidence: 99%

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The Mucosal B Cell System

Brandtzæg

2015

Mucosal Immunology

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Section: Figure 7 Hypothetical Depiction Of How the Intestinal Immunementioning

confidence: 99%

Section: Selective Iga Deficiency and Related Clinical Problemsmentioning

confidence: 99%

Section: Selective Iga Deficiency and Related Clinical Problemsmentioning

confidence: 99%

Section: Selective Iga Deficiency and Related Clinical Problemsmentioning

confidence: 99%

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The Mucosal B Cell System

Brandtzæg

2015

Mucosal Immunology

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“…The gut immune system has a more difficult task than most other mucosae because it must distinguish not only between self and non-self but also between potentially dangerous foreign antigens and common harmless foodstuffs to which it is constantly exposed (Brandtzaeg & Nilssen, 1995;Morales et al 1996). The local intestinal immune system is capable of not only a rapid powerful defence against invading organisms but also of active specific suppression of responses against non-invasive antigenic material to avoid potentially damaging reactions to these antigens (Hanson et al 1995).…”

Section: Introductionmentioning

confidence: 99%

Interaction of early diet and the development of the immune system

Gil

Rueda

2002

Nutr. Res. Rev.

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The present review focuses on the specific effects of nutrients on the development of the immune system in early life. There is a big gap regarding the specific mechanisms that regulate immunity at the intestinal level and their impact in the systemic immune function. For this reason, during the last few years there has been great interest in ascertaining the mechanisms that regulate the intestinal immune function, as well as to understand how specific nutrients interact with the gut-associated lymphoid tissue. We have reviewed this topic with special emphasis on how human milk, and its components, influence the early development of intestinal immunity in breast-fed infants compared with formula-fed infants. Interactions between nutrients and intestinal microbiota have also been reviewed. Some micronutrients such as nucleotides and gangliosides, which are present in human milk and also in most foods, are able to influence immune functionality at very low concentrations. The specific action of these micronutrients on some parameters of immunity, as well as their potential mechanisms of action, have been considered in detail. However, there are limited data on how other specific nutrients, namely protein and non-protein N-containing compounds, lipids, carbohydrates, and others, such as minerals, vitamins, fibre, non-nutritional dietary compounds (flavonoids, carotenoids, phyto-oestrogens, etc), influence immunity. In the present review we have provided data regarding the potential effects of these compounds on the immune response in early life. The increasing use of functional foods by the public to improve their general health and prevent the incidence of chronic diseases has become a major area of interest within the nutrition community. Of the many functional foods available, probiotics have been most studied in infancy and childhood, particularly with regard to the prevention of allergic diseases. Infant formulae and fermented milks containing large quantities of probiotics are produced and

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Accumulation of intestinal intraepithelial lymphocytes in association with lack of polymeric immunoglobulin receptor

et al. 2005

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Immunoglobulin A (IgA) is transported by the polymeric immunoglobulin receptor (pIgR) through epithelial cells of the gut, the airways, the tear and salivary glands, and the lactating mammary gland, and IgA accumulates in serum and the intestinal lamina propria of pIgR‐deficient (pIgR–/–) mice. Intraepithelial lymphocytes (IEL) increased in number and Thy‐1+CD8αβ+TCRαβ+ IEL preferentially expanded in the small intestine (SI) of pIgR–/– mice. Cytotoxic activity of SI‐IEL was comparable in pIgR+/+ and pIgR–/– mice. Accumulation and cytotoxic activity of SI‐IEL was attenuated in germ‐free pIgR–/– mice. Furthermore, Thy‐1+CD8αβ+ IEL did not expand in pIgR–/–TCRβδ–/– mice compared with TCRβδ–/– mice, and SI‐IEL from pIgR–/–TCRβδ–/– mice as well as TCRβδ–/– mice expressed perforin and granzyme B mRNA and serine esterase. The proliferative status of SI‐IEL from pIgR+/+ and pIgR–/– mice was similar, but adoptive transfer experiment showed that SI‐IEL from pIgR–/– mice might have a stronger tendency to migrate into the intestinal epithelia than those from pIgR+/+ mice. These results demonstrate that the accumulation of Thy‐1+CD8αβ+TCRαβ+ IEL in pIgR–/– mice triggered by intestinal microorganisms needed the expression of functional TCR and might be caused by lymphocyte migration into the intestinal epithelia.

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Mucosal aspects of primary B-cell deficiency and gastrointestinal infections

Cited by 36 publications

References 0 publications

The Mucosal B Cell System

The Mucosal B Cell System

Interaction of early diet and the development of the immune system

Accumulation of intestinal intraepithelial lymphocytes in association with lack of polymeric immunoglobulin receptor

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