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Site‐specific regulation of tissue dendritic cell function by granulocyte–macrophage colony‐stimulating‐factor
Author(s) -
Lees Joanne,
Boam David,
Proungvitaya Tanakorn,
Wood Peter J.
Publication year - 2004
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2004.01981.x
Subject(s) - spleen , granulocyte macrophage colony stimulating factor , islet , dendritic cell , macrophage , biology , follicular dendritic cells , immunology , microbiology and biotechnology , colony stimulating factor , immune system , granulocyte , antigen presenting cell , t cell , haematopoiesis , endocrinology , cytokine , stem cell , in vitro , diabetes mellitus , biochemistry
Summary Tissue dendritic cells (DC) are usually associated with phagocytic function but poor T‐cell immunostimulatory capacity. Following activation, dendritic cells are stimulated to leave tissue sites and migrate to lymphoid tissue, acquiring immunostimulatory capacity during the process. We provide evidence that the immunostimulatory capacity of tissue DC, but not spleen cells, can be affected in situ by granulocyte–macrophage colony‐stimulating‐factor (GM‐CSF). Initially it was found that islet cells from non‐obese diabetic and BALB/c mice, which produce GM‐CSF, showed significantly higher immunostimulatory capacity than islets from C3H and C57BL/6 mice, which do not produce GM‐CSF. Second, pretreatment of nonobese diabetic mice with anti‐GM‐CSF antibody significantly reduced the immunostimulatory capacity of islet cells, but not spleen cells, although it had no effect on the numbers of cells expressing DC‐associated antigens. Therefore the immunostimulatory function of islet DC is partially dependent on GM‐CSF. By contrast, spleen DC immunostimulatory function does not show the same dependence on GM‐CSF. This may affect the ability of dendritic cells to stimulate autoimmune responses or tolerance.