Fetal mast cells mediate postnatal allergic responses dependent on maternal IgE

Author:

Msallam Rasha1,Balla Jozef2ORCID,Rathore Abhay P. S.3ORCID,Kared Hassen1ORCID,Malleret Benoit14ORCID,Saron Wilfried A. A.2ORCID,Liu Zhaoyuan5ORCID,Hang Jing Wen4ORCID,Dutertre Charles Antoine12,Larbi Anis1,Chan Jerry K. Y.678,St. John Ashley L.2349ORCID,Ginhoux Florent1510ORCID

Affiliation:

1. Singapore Immunology Network (SIgN), A*STAR, Singapore 138648, Singapore.

2. Program in Emerging Infectious Diseases, Duke-NUS Medical School, Singapore 169857, Singapore.

3. Department of Pathology, Duke University Medical Center, Durham, NC 27705, USA.

4. Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117545, Singapore.

5. Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.

6. Department of Reproductive Medicine, KK Women’s and Children’s Hospital, Singapore 229899, Singapore.

7. Academic Clinical Program of Obstetrics and Gynaecology, Duke-NUS Medical School, Singapore 229899, Singapore.

8. Experimental Fetal Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Singapore.

9. SingHealth Duke-NUS Global Health Institute, Singapore 169857, Singapore.

10. Translational Immunology Institute, SingHealth/Duke-NUS Academic Medical Centre, The Academia, Singapore 169856, Singapore.

Abstract

Maternal IgE activates fetal mast cells Mast cells (MCs) are immune cells that participate in allergic reactions through their activation by immunoglobulin E (IgE) antibodies. MCs arise early during mammalian development, but it is unclear whether IgE-mediated activation occurs in fetal tissues and what the source of IgE stimulation is. Msallam et al. show that human and mouse fetal MCs can be sensitized by IgE of maternal origin, which crosses the placental barrier through the fetal neonatal Fc receptor (see the Perspective by Rothenberg). Prenatal maternal sensitization conferred transient allergen sensitivity after birth and resulted in the development of postnatal skin and airway inflammation in the offspring after their first exposure to allergen. Thus, both maternal IgE and fetal MCs may influence mother-to-child transmission of allergic disease during gestation. Science , this issue p. 941 ; see also p. 907

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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