Mast cell function is not altered by Coronin-1A deficiency.
Coronin-1A is a WD repeat protein family member, highly expressed in all hematopoietic lineages, and acts as a regulator of F-actin dynamics and Ca2+ signaling. In Coro1a(Lmb3) mice results in inactivation of the protein and leads to disease resistance in a model of lupus erythematosus. In Coro1a(-/-) and Coro1a(Lmb3) mice, peripheral T cells exhibit impairments in survival, migration, activation, and Ca2+ flux. In this study, we show that in vitro-differentiated mast cells from Coro1a(Lmb3) mice are viable, developed normally, and are fully functional in assays of degranulation, cytokine secretion, and chemotactic migration, despite increased F-actin levels. In Coro1a(Lmb3) mast cells, Ca2+ flux in response to physiological FcεRI stimulation is unaffected. Finally, Coro1a(Lmb3) mice showed similar in vivo mast cell responses as the WT mice. Coronin-1B and Coronin-1C expression levels were not increased in Coro1a(Lmb3) mast cells but were higher in mast cells than in CD4 T cells or B cells in WT mice. We conclude that Coronin-1A activity is not required for mast cell function.
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- Reverse Transcriptase Polymerase Chain Reaction
- Microfilament Proteins
- Mice, Knockout
- Mice, Inbred C57BL
- Mice
- Mast Cells
- Immunology
- Immunoblotting
- Flow Cytometry
- Cytokines
Citation
Published In
DOI
EISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Reverse Transcriptase Polymerase Chain Reaction
- Microfilament Proteins
- Mice, Knockout
- Mice, Inbred C57BL
- Mice
- Mast Cells
- Immunology
- Immunoblotting
- Flow Cytometry
- Cytokines