Mitogenic potentials of bestatin, amastatin, arphamenines A and B, FK-156 and FK-565 on spleen lymphocytes.

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Abstract
The following aminopeptidase (AP) activities are associated with the surface of mouse spleen cells: Leu-AP (138 pmol/105 cells .times. min) and AP-B (16 pmol/105 cells .times. minute with Lys-.beta.-naphthylamide as substrate and 21 pmol/105 cells .times. minute with Arg-.beta.-naphthylamide substrate); AP-A activity was not detected by the assay system applied. The immunoactive peptide bestatin inhibited the Leu-AP, while AP-B activity decreased in the presence of arphamenines A and B and bestatin. No effects on these enzymes were caused by amastatin (an AP-A inhibitor), FK-156, FK-565 and Bu-2743E; the latter peptide turned out to be not an inhibitor of cell surface associated microsomal Leu-AP but an inhibitor of cytosolic Leu-AP. The immunoactive peptides bestatin, arphamenines A and B, and amastatin increased [3H]thymidine incorporation into spleen cells containing lymphocytes and macrophages. These mitogenic actions were not observed when macrophages were removed from the cultures or the cells were stimulated with ConA or LPS. The lactoyl- and heptanoyl peptides FK-156 and FK-565 caused a mitogenic action on lymphocytes independently of the presence of macrophages. The inhibitor of cytosolic Leu-AP did not change the incorporation into lymphocytes.