Peripheral blood mononuclear cells (PBMC) from patients with systemic sclerosis (SSc) produced increased amounts of interleukin-2 (IL-2), in a dosedependent manner, in response to stimulation with human type I collagen, whereas PBMC from normal subjects did not. At a dose of 50 p g human type I collagen/106 PBMC, PBMC from SSc patients (n = 17) produced 8 times as much IL-2 as did PBMC from 16 normal subjects (P < 0.005) and 3 times as much as did PBMC from a group of 13 rheumatoid arthritis patients (P < 0.05). In contrast, IL-2 production by PBMC after nonspecific stimulation with the mitogen, phytohemagglutinin, did not differ among the SSc, rheumatoid arthritis, and normal control groups. Cell depletion experiments indicated that the IL-%producing cells in SSc patients are CD4+. Thus, SSc patients have CD4 cells that are specifically sensitized to human type I collagen and can produce increased levels of IL-2.
The dimensions of a BCG-potentiated antitumor response against the poorly immunogenic murine mastocytoma, P815 (MA), are described for a model in which the tumor immunogen is injected into subcutaneous sites previously infected with BCG; a distantly located tumor challenge is subsequently monitored for evidence of regression. A comparison of concomitant immunity and the immunity elicited by injection of varying doses of live MA into sites previously infected with BCG revealed similar antitumor effects. The subcutaneous site was the most effective route for immunization with BCG and irradiated tumor cells. Antitumor immunity was maximally expressed at intravascular sites and in the footpad. Complete tumor suppression was limited to footpadchallenge with 10-4-10-5 MA. Not only did the iv injection of BCG and immunogen fail to elicit immunity against subcutaneous challenge, but also systemically administered immunogens abrogated antitumor immunity elicited by subcutaneous immunization. These effects were reversed by prior splenectomy. Immunity was specific for the evoking tumor immunogen, but challenge with the specific tumor did not elicit nonspecific resistance against another 3-methylcholanthrene-induced tumor. In another strain of mice, immunity potentiated by BCG against the highly antigenic tumor, Meth A, was more effective than that potentiated against the poorly immunogenic MA.
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