Abstract:
:Previous work has shown that purified rat macrophages lack both accessory activity for T lymphocyte responses to mitogens and stimulatory activity in a mixed leukocyte reaction, in marked contrast to the potent activity of dendritic cells. This study was designed to re-evaluate macrophages as accessory cells by treating various cell preparations with either silica or L-leucine methyl ester, which have been reported to be toxic to macrophages, and then determining the effect of the treated cells on responses to the mitogens, sodium periodate or concanavalin A. These studies indicated that treatment with L-leucine methyl ester failed to kill rat macrophages or dendritic cells, whereas silica was specifically toxic for rat macrophages. The studies therefore focused on silica. Co-culturing mitogen-treated lymph node cells with silica over a wide range of concentrations had no effect on responses. The same results were obtained if mitogen-treated lymphocytes were enriched with lymph node macrophages and dendritic cells and then co-cultured with silica. Preparations containing both macrophages and dendritic cells were incubated with silica for 24 h to ensure the death of virtually all macrophages; upon the addition of mitogen-treated lymphocytes, the macrophage-depleted accessory cells induced vigorous proliferative responses. Peritoneal exudate cells showed variable, but low accessory activity that increased after incubation with silica. Elimination of more than 90% of the macrophages from peritoneal exudate cells, as determined by staining for non-specific esterase, failed to eliminate this accessory activity. Taken together, these findings confirm and extend the conclusion that rat macrophages lack or have exceedingly low accessory activity.
journal_name
Immunobiologyjournal_title
Immunobiologyauthors
Bowers WE,Ruhoff MS,Goodell EM,Stoltenborg JKdoi
10.1016/S0171-2985(88)80052-4subject
Has Abstractpub_date
1988-02-01 00:00:00pages
179-94issue
3eissn
0171-2985issn
1878-3279pii
S0171-2985(88)80052-4journal_volume
176pub_type
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