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The effect of all‐trans retinoic acid on myeloid dendritic cell adhesion
Author(s) -
Lackey Denise E,
Ashley Shanna L,
Duriancik David M,
Hoag Kathleen A
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a125
Subject(s) - retinoic acid , myeloid , dendritic cell , microbiology and biotechnology , chemistry , cell adhesion , tretinoin , bone marrow , cell culture , cancer research , immune system , biology , immunology , cell , biochemistry , genetics
Myeloid dendritic cells (DC) are specialized antigen presenting cells. Activation of DC by antigen triggers migration to secondary lymphoid tissues where DC activate naive T cells. Vitamin A has long been known for its role in immune function. We investigated the effect of all‐ trans retinoic acid (atRA), a bioactive metabolite of vitamin A, on DC adhesion. Mouse bone marrow cells cultured with granulocyte‐macrophage colony‐stimulating factor in the presence of a retinoic acid receptor‐alpha antagonist (AGN) demonstrated increased adherence compared to cell cultures rescued with atRA treatment for the final 48 hours of culture. When floating cells, predominantly granulocytes, are removed on day 6 and 8 of the 10‐day culture period, there is no difference in percentage of adherent cells between the AGN and atRA rescued treatments, indicating that atRA and granulocytes act together to cause loss of DC adherence. AtRA rescue treatment is found to result in decreased surface expression of the cellular adhesion molecule CD11a. Adherent cells and floating DC treated with atRA produce more matrix metalloproteinase (MMP) mRNA and protein and lower levels of MMP inhibitor than adherent cells cultured with AGN. However, there is no difference in RNA expression of CD11a between treatment groups. These data suggest that atRA up‐regulates MMPs to release DC for migration, partly through degradation of CD11a. Supported by NIH grant 5R21AI58994‐2 to KAH.