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GM‐CSF‐induced in vivo expansion of splenic dendritic cells and their strong costimulation activity
Author(s) -
Hanada Kenichi,
Tsunoda Rikiya,
Hamada and Hirofumi
Publication year - 1996
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.60.2.181
Subject(s) - biology , dendritic cell , antigen presenting cell , mhc class ii , t cell , antigen presentation , microbiology and biotechnology , cd40 , cytokine , antigen , spleen , in vivo , immunology , major histocompatibility complex , in vitro , immune system , cytotoxic t cell , biochemistry
Dendritic cells (DC), with their potent antigen‐presenting and accessory activities, are involved in the stimulation of naive T cells. To examine the biological functions of DC, we developed a method for generating large numbers of murine splenic DC. First, DC were propagated in vivo by using a granulocyte‐macrophage colony‐stimulating factor‐secreting tumor as a continuous in vivo source of the cytokine. The DC enriched in the spleen, especially in the white pulps, were purified after an overnight culture. We could reproducibly obtain 6 to 10 10 6 splenic DC per mouse. These DC were morphologically similar to interdigitating cells, expressed high levels of MHC class II and costimulatory molecules, and were highly allo‐stimulatory in mixed lymphocyte reactions. Further analysis on T cell stimulation activity revealed that the DC had strong costimulatory activity on human T cells. Activated B cells, which express both B7‐1 and B7‐2, had little T cell costimulatory activity under the same assay conditions. A human histiocytic leukemia cell line, U937, that showed only weak costimulatory activity by itself, worked synergistically with DC and further intensified the T cell stimulation by DC. These findings suggest the presence of a T cell costimulation mechanism in DC, which is activated synergistically by monocytes or macrophages, and deserves further study. J. Leukoc. Biol . 60: 181–190; 1996.