help button home button Am J Pathol ASIP MEMBERSHIP
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hubeau, C.
Right arrow Articles by Kobzik, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hubeau, C.
Right arrow Articles by Kobzik, L.
(American Journal of Pathology. 2006;168:1931-1939.)
© 2006 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2006.051231

Adoptively Transferred Allergen-Specific T Cells Cause Maternal Transmission of Asthma Risk

Cedric Hubeau*, Irina Apostolou{dagger} and Lester Kobzik*{ddagger}

From the Department of Environmental Health,* Physiology Program, Harvard School of Public Health; the Department of Pathology,{dagger} Dana-Farber Cancer Institute; and the Department of Pathology,{ddagger} Brigham & Women’s Hospital, Boston, Massachusetts

In addition to genetics and environment, maternal asthma is an identified risk factor for developing the disease during childhood. The mechanisms of this maternal effect remain poorly understood. We tested the role of allergen-specific T cells in the maternal transmission of asthma risk by modifying a model where offspring of asthmatic mothers are more prone to develop asthma after an intentionally suboptimal asthma induction. Normal BALB/c females were injected with allergen-specific T cells from ovalbumin-specific T cell receptor (TCR) transgenic DO11.10 donors before mating. Using the protocol of suboptimal asthma induction, offspring of normal and recipient mothers were tested for their susceptibility to develop asthma. Only pups of recipient mothers showed increased airway responsiveness (Penh), allergic airway inflammation with eosinophilia, and local Th2-skewed cytokine production. Although recipient mothers did not develop asthma, serum levels of interferon-{gamma}, interleukin (IL)-4, IL-10, and IL-13 were significantly increased during pregnancy. Consistent with this finding, a subset of DO11.10 T cells persisted in the spleen and placenta of expectant recipient mothers. We conclude that allergen-specific T cells are sufficient to orchestrate the maternal transmission of asthma risk. Because overt maternal asthma was not required, our results suggest that similar maternal-fetal interactions may occur in other allergic disorders.




This article has been cited by other articles:


Home page
 Am. J. Respir. Cell Mol. Bio.Home page
A. V. Fedulov, A. Leme, Z. Yang, M. Dahl, R. Lim, T. J. Mariani, and L. Kobzik
Pulmonary Exposure to Particles during Pregnancy Causes Increased Neonatal Asthma Susceptibility
Am. J. Respir. Cell Mol. Biol., January 1, 2008; 38(1): 57 - 67.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
A. P. Matson, L. Zhu, E. G. Lingenheld, C. M. Schramm, R. B. Clark, D. M. Selander, R. S. Thrall, E. Breen, and L. Puddington
Maternal Transmission of Resistance to Development of Allergic Airway Disease
J. Immunol., July 15, 2007; 179(2): 1282 - 1291.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
C. Hubeau, I. Apostolou, and L. Kobzik
Targeting of CD25 and Glucocorticoid-Induced TNF Receptor Family-Related Gene-Expressing T Cells Differentially Modulates Asthma Risk in Offspring of Asthmatic and Normal Mother Mice
J. Immunol., February 1, 2007; 178(3): 1477 - 1487.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2006 by the American Society for Investigative Pathology.