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Depressed T-cell proliferation associated with susceptibility to experimental Taenia crassiceps infection
1Department of Immunology, Universidad Nacional Autónoma de México, México, D.F.
Abstract:
Peritoneal infection with Taenia crassiceps cysticerci of naturally resistant (C57BL/10J and C57BL/6J) and susceptible (BALB/cAnN) mice induces a cellular immune depression. T-cell proliferation in response to concanavalin A (ConA) or anti-CD3 was significantly depressed in infected mice of all strains tested. However, in resistant mice, the diminished response to ConA was transient and animals recovered normal responsiveness at day 40, whereas susceptible mice remained suppressed throughout the 40 days of the experiment. In contrast, the proliferative response to anti-CD3 was lower in infected mice than in noninfected controls regardless of differences in natural susceptibility of the strains. Intraperitoneal injection of mice with a parasite extract also induced a depression of the response to ConA, although not as strong as that produced by the parasite itself. This depression is not due to direct effects by parasite antigens over host lymphocytes, as proliferation is not affected by the presence of cysticercal antigens added in vitro. Diminished interleukin-2 production during the parasitosis accounts at least in part for the diminished responses to ConA. A primary infection favors parasite establishment after a second challenge, pointing to the relevance of the immunodepression in generating a host environment favorable to the parasite.
Insights
Taenia crassiceps infection causes T-cell immune depression in mice, with susceptible strains showing prolonged suppression. This cellular immune depression, linked to reduced interleukin-2, aids parasite establishment.
Area of Science:
- Immunology
- Parasitology
- Cellular Biology
Background:
- Peritoneal infection with Taenia crassiceps cysticerci is known to affect the host immune system.
- Understanding the impact of parasitic infections on T-cell responses is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the effects of Taenia crassiceps cysticerci infection on T-cell proliferation in resistant and susceptible mouse strains.
- To elucidate the mechanisms underlying the observed immune depression and its role in parasite establishment.
Main Methods:
- Infection of C57BL/10J, C57BL/6J (resistant), and BALB/cAnN (susceptible) mice with Taenia crassiceps cysticerci.
- Assessment of T-cell proliferation using concanavalin A (ConA) and anti-CD3 stimulation.
- Measurement of interleukin-2 production.
- In vitro assays to evaluate direct effects of parasite antigens on lymphocyte proliferation.
Main Results:
- Taenia crassiceps infection induced significant T-cell depression in all mouse strains.
- Resistant mice showed transient T-cell suppression, recovering by day 40, while susceptible mice remained suppressed.
- Anti-CD3 response was depressed in infected mice irrespective of strain susceptibility.
- Diminished interleukin-2 production contributed to the reduced T-cell response to ConA.
- Parasite extract induced milder T-cell depression than live parasites.
- In vitro exposure to parasite antigens did not directly inhibit lymphocyte proliferation.
Conclusions:
- Taenia crassiceps infection causes a significant, strain-dependent cellular immune depression in mice.
- Reduced interleukin-2 production is a key factor in the observed T-cell hyporesponsiveness.
- The induced immunodepression creates a favorable environment for parasite establishment, particularly upon secondary challenge.