The receptor for advanced glycation end products (RAGE) affects T cell differentiation in OVA induced asthma.
The receptor for glycation end products (RAGE) has been previously implicated in shaping the adaptive immune response. RAGE is expressed in T cells after activation and constitutively in T cells from patients with diabetes. The effects of RAGE on adaptive immune responses are not clear: Previous rep...
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Public Library of Science (PLoS)
2014-01-01
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Series: | PLoS ONE |
Online Access: | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0095678&type=printable |
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author | Eitan M Akirav Octavian Henegariu Paula Preston-Hurlburt Ann Marie Schmidt Raphael Clynes Kevan C Herold |
author_facet | Eitan M Akirav Octavian Henegariu Paula Preston-Hurlburt Ann Marie Schmidt Raphael Clynes Kevan C Herold |
author_sort | Eitan M Akirav |
collection | DOAJ |
description | The receptor for glycation end products (RAGE) has been previously implicated in shaping the adaptive immune response. RAGE is expressed in T cells after activation and constitutively in T cells from patients with diabetes. The effects of RAGE on adaptive immune responses are not clear: Previous reports show that RAGE blockade affects Th1 responses. To clarify the role of RAGE in adaptive immune responses and the mechanisms of its effects, we examined whether RAGE plays a role in T cell activation in a Th2 response involving ovalbumin (OVA)-induced asthma in mice. WT and RAGE deficient wild-type and OT-II mice, expressing a T cell receptor specific for OVA, were immunized intranasally with OVA. Lung cellular infiltration and T cell responses were analyzed by immunostaining, FACS, and multiplex bead analyses for cytokines. RAGE deficient mice showed reduced cellular infiltration in the bronchial alveolar lavage fluid and impaired T cell activation in the mediastinal lymph nodes when compared with WT mice. In addition, RAGE deficiency resulted in reduced OT-II T cell infiltration of the lung and impaired IFNγ and IL-5 production when compared with WT mice and reduced infiltration when transferred into WT hosts. When cultured under conditions favoring the differentiation of T cells subsets, RAGE deficient T cells showed reduced production of IFNγ but increased production of IL-17. Our data show a stimulatory role for RAGE in T activation in OVA-induced asthma. This role is largely mediated by the effects of RAGE on T cell proliferation and differentiation. These findings suggest that RAGE may play a regulatory role in T cell responses following immune activation. |
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spelling | doaj.art-d215d42236e04f0f9da990da3b2b8f9f2025-02-22T05:33:59ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0194e9567810.1371/journal.pone.0095678The receptor for advanced glycation end products (RAGE) affects T cell differentiation in OVA induced asthma.Eitan M AkiravOctavian HenegariuPaula Preston-HurlburtAnn Marie SchmidtRaphael ClynesKevan C HeroldThe receptor for glycation end products (RAGE) has been previously implicated in shaping the adaptive immune response. RAGE is expressed in T cells after activation and constitutively in T cells from patients with diabetes. The effects of RAGE on adaptive immune responses are not clear: Previous reports show that RAGE blockade affects Th1 responses. To clarify the role of RAGE in adaptive immune responses and the mechanisms of its effects, we examined whether RAGE plays a role in T cell activation in a Th2 response involving ovalbumin (OVA)-induced asthma in mice. WT and RAGE deficient wild-type and OT-II mice, expressing a T cell receptor specific for OVA, were immunized intranasally with OVA. Lung cellular infiltration and T cell responses were analyzed by immunostaining, FACS, and multiplex bead analyses for cytokines. RAGE deficient mice showed reduced cellular infiltration in the bronchial alveolar lavage fluid and impaired T cell activation in the mediastinal lymph nodes when compared with WT mice. In addition, RAGE deficiency resulted in reduced OT-II T cell infiltration of the lung and impaired IFNγ and IL-5 production when compared with WT mice and reduced infiltration when transferred into WT hosts. When cultured under conditions favoring the differentiation of T cells subsets, RAGE deficient T cells showed reduced production of IFNγ but increased production of IL-17. Our data show a stimulatory role for RAGE in T activation in OVA-induced asthma. This role is largely mediated by the effects of RAGE on T cell proliferation and differentiation. These findings suggest that RAGE may play a regulatory role in T cell responses following immune activation.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0095678&type=printable |
spellingShingle | Eitan M Akirav Octavian Henegariu Paula Preston-Hurlburt Ann Marie Schmidt Raphael Clynes Kevan C Herold The receptor for advanced glycation end products (RAGE) affects T cell differentiation in OVA induced asthma. PLoS ONE |
title | The receptor for advanced glycation end products (RAGE) affects T cell differentiation in OVA induced asthma. |
title_full | The receptor for advanced glycation end products (RAGE) affects T cell differentiation in OVA induced asthma. |
title_fullStr | The receptor for advanced glycation end products (RAGE) affects T cell differentiation in OVA induced asthma. |
title_full_unstemmed | The receptor for advanced glycation end products (RAGE) affects T cell differentiation in OVA induced asthma. |
title_short | The receptor for advanced glycation end products (RAGE) affects T cell differentiation in OVA induced asthma. |
title_sort | receptor for advanced glycation end products rage affects t cell differentiation in ova induced asthma |
url | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0095678&type=printable |
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