Phong, B and Kane, LP
(2016)
Mast cell activation is enhanced by Tim1: Tim4 interaction but not by Tim-1 antibodies.
F1000Research, 5.
ISSN 2046-1402
Abstract
Polymorphisms in the T cell (or transmembrane) immunoglobulin and mucin domain 1 (TIM-1) gene, particularly in the mucin domain, have been associated with atopy and allergic diseases in mice and human. Genetic- and antibody-mediated studies revealed that Tim-1 functions as a positive regulator of Th2 responses, while certain antibodies to Tim-1 can exacerbate or reduce allergic lung inflammation. Tim-1 can also positively regulate the function of B cells, NKT cells, dendritic cells and mast cells. However, the precise molecular mechanisms by which Tim-1 modulates immune cell function are currently unknown. In this study, we have focused on defining Tim-1-mediated signaling pathways that enhance mast cell activation through the high affinity IgE receptor (FceRI). Using a Tim-1 mouse model lacking the mucin domain (Tim-1 Dmucin;), we show for the first time that the polymorphic Tim-1 mucin region is dispensable for normal mast cell activation. We further show that Tim-4 cross-linking of Tim-1 enhances select signaling pathways downstream of FceRI in mast cells, including mTOR-dependent signaling, leading to increased cytokine production but without affecting degranulation.
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Item Type: |
Article
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Status: |
Published |
Creators/Authors: |
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Contributors: |
Contribution | Contributors Name | Email | Pitt Username | ORCID |
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Reviewer | August, Avery | UNSPECIFIED | UNSPECIFIED | UNSPECIFIED | Reviewer | Wilson, Bridget S | UNSPECIFIED | UNSPECIFIED | UNSPECIFIED |
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Date: |
1 January 2016 |
Date Type: |
Publication |
Journal or Publication Title: |
F1000Research |
Volume: |
5 |
DOI or Unique Handle: |
10.12688/f1000research.8132.2 |
Schools and Programs: |
School of Medicine > Immunology |
Refereed: |
Yes |
ISSN: |
2046-1402 |
Date Deposited: |
09 Aug 2016 20:00 |
Last Modified: |
22 Jun 2021 11:55 |
URI: |
http://d-scholarship.pitt.edu/id/eprint/29115 |
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