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CCR2 expression determines T1 versus T2 polarization during pulmonary Cryptococcus neoformans infection
T R Traynor1, W A Kuziel, G B Toews
1Pulmonary Division, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|February 5, 2000
Summary
The chemokine receptor CCR2 is essential for controlling Cryptococcus neoformans lung infections. Its absence impairs T1 immunity, leading to increased fungal burden and dissemination.
Area of Science:
- Immunology
- Microbiology
- Infectious Diseases
Background:
- Pulmonary clearance of Cryptococcus neoformans relies on T1-type immunity.
- The role of chemokine receptor 2 (CCR2) in host defense against C. neoformans is not fully understood.
Purpose of the Study:
- To investigate the function of CCR2 in leukocyte recruitment and T1-type cell-mediated immunity during pulmonary C. neoformans infection.
Main Methods:
- Intratracheal inoculation of C. neoformans into CCR2 knockout (CCR2-/-) and wild-type (CCR2+/+) mice.
- Assessment of fungal burden (CFU), dissemination, and immune cell populations in the lungs.
- Analysis of cytokine production (IFN-gamma, IL-4, IL-5) and delayed-type hypersensitivity.
Main Results:
- CCR2-/- mice exhibited prolonged pulmonary infection and significant dissemination to spleen and brain.
- Reduced recruitment of macrophages and CD8+ T cells into the lungs of CCR2-/- mice.
- CCR2 deficiency led to chronic pulmonary eosinophilia, IL-4/IL-5 production, and high IgE levels, indicating a T2-type immune response.
Conclusions:
- CCR2 is critical for developing a T1-type immune response against C. neoformans.
- Lack of CCR2 promotes a detrimental switch to a T2-type response, impairing fungal clearance.