Pregnancy and autoimmunity: Maternal treatment and maternal disease influence on pregnancy outcome

Tincani, Anǵela; Rebaioli, Chiara Biasini; Frassi, Micol; Taglietti, Marco; Gorla, Roberto; Cavazzana, Ilaria; Faden, D; Taddeï, F.; Lojacono, Andrea; Motta, Mario; Trepidi, Laura; Meroni, Pier Luigi; Cimaz, Rolando; Ghirardello, Anna; Doria, Andrea; Pisoni, Maria Pia; Muscarà, Marina; Brucato, Antonio

doi:10.1016/j.autrev.2005.03.001

Cited by 45 publications

(16 citation statements)

References 31 publications

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“…Recently, a murine model of peanut allergy demonstrated that maternal derived anti-peanut IgG 1 is associated with anaphylactic reactions in offspring [47]. In addition, several autoimmune diseases such as systemic lupus erythematosus are known to result in transmission of maternal IgG's that have deleterious effects in progeny [48]. The ability of maternal IgG to mediate differential effects in offspring may be related to affinities for individual FcγRs resulting from Fc glycosylation.…”

Section: Discussionmentioning

confidence: 99%

IgG transmitted from allergic mothers decreases allergic sensitization in breastfed offspring

et al. 2010

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BackgroundThe mechanism(s) responsible for the reduced risk of allergic disease in breastfed infants are not fully understood. Using an established murine model of asthma, we demonstrated previously that resistance to allergic airway disease transmitted from allergic mothers to breastfed offspring requires maternal B cell-derived factors.ObjectiveThe aim of this study was to investigate the role of offspring neonatal Fc receptor for IgG uptake by intestinal epithelial cells (FcRn) in this breast milk transferred protection from allergy.MethodsAllergic airway disease was induced during pregnancy in C57BL/6 female mice. These allergic mothers foster nursed naive FcRn+/- or FcRn-/- progeny born to FcRn+/- females that were mated to C57BL/6J-FcRn-/- male mice. In offspring deficient in FcRn, we expected reduced levels of systemic allergen-specific IgG1, a consequence of decreased absorption of maternal IgG from the lumen of the neonatal gastrointestinal tract. Using this model, we were able to investigate how breast milk IgG affected offspring responses to allergic sensitization.ResultsLevels of maternal antibodies absorbed from the breast milk of allergic foster mothers were determined in weanling FcRn-sufficient or -deficient mice. Maternal transmission of allergen-specific IgG1 to breastfed FcRn-/- offspring was at levels 103-104 lower than observed in FcRn+/- or FcRn+/+ mice. Five weeks after weaning, when offspring were 8 wk old, mice were sensitized and challenged to evaluate their susceptibility to develop allergic airway disease. Protection, indicated by reduced parameters of disease (allergen-specific IgE in serum, eosinophilic inflammation in the airways and lung) were evident in FcRn-sufficient mice nursed as neonates by allergic mothers. In contrast, FcRn-deficient mice breastfed by the same mothers acquired limited, if any, protection from development of allergen-specific IgE and associated pathology.ConclusionsFcRn expression was a major factor in determining how breastfed offspring of allergic mothers acquired levels of systemic allergen-specific IgG1 sufficient to inhibit allergic sensitization in this model.

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Section: Discussionmentioning

confidence: 99%

IgG transmitted from allergic mothers decreases allergic sensitization in breastfed offspring

et al. 2010

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“…The maternal transfer of autoantibodies from the mother to child during pregnancy is well documented, and is associated with a number of factors that can affect both pregnancy and neonatal outcome. 11 The presence of autoantibodies directed against critical neuronal components of fetal brain extracts in a subset of mothers of ASD children provides supporting evidence that one potential mechanism linking maternal immune components with ASD involves the transfer of autoantibodies from mother to the developing fetus during pregnancy 15,16,17,20 (Table 2).…”

Section: Maternal Antibodiesmentioning

confidence: 91%

Immune Dysfunction in Autism: A Pathway to Treatment

2010

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Summary: Autism is a complex and clinically heterogeneous disorder with a spectrum of symptoms. Clinicians, schools, and service agencies worldwide have reported a dramatic increase in the number of children identified with autism. Despite expanding research, the etiology and underlying biological processes of autism remain poorly understood, and the relative contribution from genetic, epigenetic, and environmental factors remains unclear. Although autism affects primarily brain function (especially affect, social functioning, and cognition), it is unknown to what extent other organs and systems are disrupted. Published findings have identified widespread changes in the immune systems of children with autism, at both systemic and cellular levels. Brain specimens from autism subjects exhibit signs of active, ongoing inflammation, as well as alterations in gene pathways associated with immune signaling and immune function. Moreover, many genetic studies have indicated a link between autism and genes that are relevant to both the nervous system and the immune system. Alterations in these pathways can affect function in both systems. Together, these reports suggest that autism may in fact be a systemic disorder with connections to abnormal immune responses. Such immune system dysfunction may represent novel targets for treatment. A better understanding of the involvement of the immune response in autism, and of how early brain development is altered, may have important therapeutic implications.

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“…Corticosteroids and some immunosuppressive drugs (e.g., azathioprine) are used, but may be associated with complications such as preterm delivery, low birth weight, and intrauterine growth restriction [9]. Data on the safety of rituximab during pregnancy are very limited.…”

Section: Discussionmentioning

confidence: 99%

Course of neuromyelitis optica during inadvertent pregnancy in a patient treated with rituximab

et al. 2009

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In neuromyelitis optica (NMO), the monoclonal B-cell antibody rituximab is a therapeutic option. Little is known about the course of NMO and the safety of rituximab during pregnancy. In this study, we report the clinical course of a patient with NMO after application of rituximab 1 week before inadvertent conception. Mother and child did not experience any adverse event, and the postpartum development of the baby was completely normal up to 15 months. Clinical course of NMO was stable during the entire pregnancy. This case illustrates a favorable outcome in a pregnant NMO patient and her child after therapy with rituximab. Multiple Sclerosis 2009; 15: 1006-1008.

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Pregnancy and autoimmunity: Maternal treatment and maternal disease influence on pregnancy outcome

Cited by 45 publications

References 31 publications

IgG transmitted from allergic mothers decreases allergic sensitization in breastfed offspring

IgG transmitted from allergic mothers decreases allergic sensitization in breastfed offspring

Immune Dysfunction in Autism: A Pathway to Treatment

Course of neuromyelitis optica during inadvertent pregnancy in a patient treated with rituximab

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