NDLI: Abr, a negative regulator of Rac, attenuates cockroach allergen-induced asthma in a mouse model.

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Abr, a negative regulator of Rac, attenuates cockroach allergen-induced asthma in a mouse model.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Heisterkamp, Nora Fei, Fei Gong, Dapeng Lim, Min Groffen, John Yu, Min
Description	Author Affiliation: Gong D ( Division of Hematology and Oncology, Children's Hospital Los Angeles, Los Angeles, CA 90027.)
Abstract	Abr deactivates Ras-related C3 botulinum toxin substrate (Rac), a master molecular switch that positively regulates many immune cell functions, by converting it to its GDP-bound conformation. In this article, we report that, in the absence of Abr function, cockroach allergen (CRA)-immunized mice experienced a fatal asthma attack when challenged with CRA. The asthma in abr(-/-) mice was characterized by increased pulmonary mucus production, elevated serum IgE, and leukocyte airway infiltration. Decreased pulmonary compliance was further documented by increased airway resistance upon methacholine challenge. Peribronchial and bronchoalveolar lavage eosinophils, key cells associated with allergic asthma, were increased in abr(-/-) mice, but adoptive transfer of this cell type from immunized mice to naive controls, followed by CRA challenge, showed that eosinophils are not primarily responsible for differences in airway resistance between controls and abr-null mutants. CD4(+) T cell numbers in the airways of CRA-challenged abr(-/-) mice also were significantly increased compared with controls, as were the Th2 T cell-secreted cytokines IL-4 and IL-5 in total lung. Interestingly, when control and abr(-/-) CD4(+) T cells from CRA-immunized mice were transferred to wild-type animals, airway resistance upon challenge with CRA was significantly higher in mice transplanted with T cells lacking Abr function. CD4(+) T cells from CRA-immunized and challenged abr(-/-) mice contained elevated levels of activated GTP-bound Rac compared with wild-type controls. Functionally, abr(-/-) CD4(+) T cells from CRA-exposed mice showed significantly enhanced chemotaxis toward CCL21. These results identify Abr-regulated CD4(+) T cell migration as an important component of severe CRA-evoked allergic asthma in mice.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1202603
Journal	The Journal of Immunology
Issue Number	9
Volume Number	191
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Allergens Immunology Asthma Cd4-positive T-lymphocytes Gtpase-activating Proteins Metabolism Adoptive Transfer Animals Cell Movement Chemokine Ccl21 Disease Models, Animal Eosinophils Deficiency Genetics Immunoglobulin E Blood Interleukin-4 Secretion Interleukin-5 Lung Methacholine Chloride Mice Mice, Knockout Rac Gtp-binding Proteins Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Abr, a negative regulator of Rac, attenuates cockroach allergen-induced asthma in a mouse model.