Interleukin 2 enhances specific and nonspecific immune responses in experimental Chagas' disease

Choromanski, Leszek; Kuhn, Raymond

doi:10.1128/iai.50.2.354-357.1985

Cited by 44 publications

(13 citation statements)

References 7 publications

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“…The data on in vivo rl L-2 administration are in conflict with the study presented by Choromanski & Kuhn [4]. There are several differences, however, between the two studies, which may explain the different results, such as the choice of parasite strain, infective dose, kinetics, dose of IL-2, and mouse strain.…”

Section: Discussionmentioning

confidence: 75%

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Modulation of Both Interleukin 2 Receptor Expression and Interleukin 2 Production during Experimental Murine Trypanosoma cruzi Infection

et al. 1989

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A massive activation of T cells takes place during the early stages of a Trypanosoma cruzi infection in mice. We present data indicating that substantial amounts of interleukin 2 (IL-2) are secreted and IL-2 receptors are expressed during the period of increased proliferation (4-7 days post infection). Both concanavalin A-induced proliferation and IL-2 production are markedly decreased later in the acute infection (around 3 weeks post infection). This proliferation cannot be restored by externally added IL-2. Simultaneously, there is a drastic reduction in the number of both high- and low-affinity IL-2 receptors. The reduction is not attributable to the elimination of a particular T-cell population. In vivo administration of recombinant IL-2 failed to improve resistance to T. cruzi parasites as measured by parasitaemia and mortality.

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Section: Discussionmentioning

confidence: 75%

“…Spleen cells from acutely 7", (rurf-infected mice have previously been shown to be unable to produce IL-2 in response to eoncanavalin A (Con A) [10], a finding that some groups have eonfirmed by obtaining a partial recovery of immune responsiveness of lymphocytes from T. cruziinfected mice by means of IL-2 [4,31,36].…”

mentioning

confidence: 99%

Modulation of Both Interleukin 2 Receptor Expression and Interleukin 2 Production during Experimental Murine Trypanosoma cruzi Infection

et al. 1989

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“…87,1985). In addition, rIL-2 reduces the number of circulating Trypanosoma cruzi organisms in the blood of mice and prolongs survival (5). Notwithstanding the salutary effects of rIL-2 in these infections, the pleiotropic effects of this lymphokine on CMI in experimental histoplasmosis are insufficient to decrease the CFU of H. capsulatum in spleens of mice whether it is administered early or later during the course of infection.…”

Section: Discussionmentioning

confidence: 99%

Modulation of cellular immune responses in mice with disseminated histoplasmosis by recombinant interleukin-2

Deepe¹,

Taylor²,

Harris³

et al. 1986

Infect Immun

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Depression of the cellular immune responses in mice with disseminated histoplasmosis is associated with deficient production of interleukin-2 (IL-2) by splenocytes. Therefore, we examined whether a highly purified preparation of IL-2, recombinant human IL-2 (rIL-2), could modify the cellular immune responses in infected mice and whether this lymphokine could alter the severity of histoplasmosis in animals. Exogenous rIL-2, at concentrations of up to 1,000 U/ml, failed to augment the proliferative responses to concanavalin A by unfractionated splenocytes or splenic T cells from mice infected for 1 week. In addition, rIL-2 did not modulate the plaque-forming cell response to sheep erythrocytes by splenocytes from these same mice. However, at week 3, rIL-2 in concentrations ranging from 10 to 1,000 U/ml considerably augmented the proliferative response to concanavalin A and plaque-forming cell response to sheep erythrocytes by splenocytes from infected mice. Kinetics studies demonstrated that rIL-2 exerted maximal immunoregulatory activity when added on day 0 or 1 to cultures of splenocytes. In vivo administration of rIL-2, 200 to 20,000 U/day, for 10 days to normal and 3-week-infected mice did not alter the proliferative activity of splenocytes to concanavalin A; 200,000 U of rIL-2 per day actually depressed the proliferative responses of splenocytes from normal and infected mice. In vivo, rIL-2 did not modify delayed-type hypersensitivity responses to sheep erythrocytes or to histoplasmin by normal and infected mice. Moreover, treatment with rIL-2 in vivo did not reduce the number of Histoplasma CFU in spleens of mice. Thus, despite the immunoenhancing effect of rIL-2 in vitro, this lymphokine failed to exert similar effects in vivo.

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“…In a previous study, we were able to demonstrate that maintenance of T. cruzi-infected C3HeB/FeJ mice at 36°C not only increased longevity and decreased parasitemia, but also significantly enhanced both parasite-specific and nonspecific immune responses (2). Whereas immunosuppression during experimental Chagas' disease can be overcome to some degree by a variety of means (2,5,6,27), neither the mechanisms responsible for immunosuppression nor those responsible for overcoming suppression are clearly understood.…”

mentioning

confidence: 98%

Effect of elevated environmental temperature on the antibody response of mice to Trypanosoma cruzi during the acute phase of infection

1991

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When held at 36°C, Trypanosoma cruzi-infected C3H mice survive an otherwise lethal infection with significantly decreased parasitemia levels and enhanced immune responsiveness. Treatment of T. cruzi-infected mice with the immunosuppressive agent cyclophosphamide indicated that the positive effects of increased environmental temperature were primarily due to enhancement of immunity. A parasite-specific, enzyme-linked immunosorbent assay and immunoblot analysis were used to examine the effect of elevated environmental temperature on the production of anti-T. cruzi antibodies. Both the reactivity and diversity of anti-T. cruzi antibodies were found to be lower in infected mice held at 36°C than in infected mice held at room temperature. However, reactivity and diversity could be enhanced by vaccination with culture forms of the parasite.

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Interleukin 2 enhances specific and nonspecific immune responses in experimental Chagas' disease

Cited by 44 publications

References 7 publications

Modulation of Both Interleukin 2 Receptor Expression and Interleukin 2 Production during Experimental Murine Trypanosoma cruzi Infection

Modulation of Both Interleukin 2 Receptor Expression and Interleukin 2 Production during Experimental Murine Trypanosoma cruzi Infection

Modulation of cellular immune responses in mice with disseminated histoplasmosis by recombinant interleukin-2

Effect of elevated environmental temperature on the antibody response of mice to Trypanosoma cruzi during the acute phase of infection

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