NDLI: Regulatory T cells migrate to airways via CCR4 and attenuate the severity of airway allergic inflammation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Florsheim, Esther Borges Takenaka, Maisa Carla Silva, João Santana Russo, Momtchilo da Fonseca, Denise Morais Faustino, Lucas Guereschi, Marcia Grando Basso, Alexandre Salgado Mirotti, Luciana
Description	Country affiliation: Brazil Author Affiliation: Faustino L ( Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, Sao Paulo, SP 05508-900, Brazil.)
Abstract	We have previously shown that regulatory T (Treg) cells that accumulate in the airways of allergic mice upregulate CC-chemokine receptor 4 (CCR4) expression. These Treg cells suppressed in vitro Th2 cell proliferation but not type 2 cytokine production. In the current study, using a well-established murine model of allergic lung disease or oral tolerance, we evaluated the in vivo activity of Treg cells in allergic airway inflammation with special focus on CCR4 function. We found that allergic, but not tolerant, mice treated with anti-CD25 Ab showed increased airway eosinophilia and IL-5- or IL-4-producing Th2 cells when compared with untreated mice. Notably, mice with CCR4 deficiency displayed an augmented airway allergic inflammation compared with wild-type or CCR2 knockout (KO) mice. The allergic phenotype of CCR4KO mice was similar to that observed in anti-CD25-treated mice. The exacerbated allergic inflammation of CCR4KO mice was directly associated with an impaired migration of Treg cells to airways and augmented frequency of pulmonary Th2 cells. Adoptive transfer of CD25(+)CD4(+) T cells expressing high levels of CCR4, but not CCR4KO CD25(+)CD4(+) T cells, attenuated the severe airway Th2 response of CCR4KO mice. Our results show that CCR4 is critically involved in the migration of Treg cells to allergic lungs that, in turn, attenuate airway Th2 activation and allergic eosinophilic inflammation.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	6
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-03-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cell Movement Immunology Eosinophilia Pneumonia Receptors, Ccr4 Physiology Severity Of Illness Index T-lymphocytes, Regulatory Animals Genetics Pathology Inflammation Mice Mice, Inbred C57bl Mice, Knockout Deficiency Metabolism Th2 Cells Up-regulation Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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