{'fraction_non_alphanumeric': 0.023237179487179488, 'fraction_numerical': 0.0016025641025641025, 'mean_word_length': 5.245, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Mechanism of the A/Ph.MC.S1 tumor graft rejection in syngeneic mice.

A considerable number of normal mice injected with a low dose of A/Ph.MC.S1 syngeneic methylcholanthrene-induced tumor cells showed regression of the tumor after a transient period of growth. The regressor mice eliminated a challenge inoculum in an accelerated fashion. Splenic lymphocytes from such regressor mice inhibited the growth of the same tumor in the local adoptive transfer assay. This capacity required the presence of thymus-derived cells. The regressor animals developed a delayed-type hypersensitivity response against the tumor In vivo and their lymph-node cells produced macrophage migration inhibitory factor in the presence of tumor cells in vitro. The growth of this tumor was facilitated by treating the primary recipients with carrageenan, and the strong tumor-inhibitory capacity of regressors was also depressed by this agent. Early macrophage infiltration of the tumor in regressor mice was demonstrable histochemically, preceding the inhibition of tumor growth. A lymphokine-producing T cell-mediated, macrophage-dependent delayed-type hypersensitivity-like mechanism is proposed to be the dominant mechanism of the resistance in this tumor-host model.