期刊
JOURNAL OF IMMUNOLOGY
卷 164, 期 4, 页码 2021-2027出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.164.4.2021
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资金
- NHLBI NIH HHS [R01-HL63670, R01-HL51082] Funding Source: Medline
- NIAID NIH HHS [R29-AI38190] Funding Source: Medline
Pulmonary clearance of the encapsulated yeast Cryptococcus neoformans requires the development of T1-type immunity. The objective of this study was to determine the role of CCR2 in leukocyte recruitment and development of T1-type cell-mediated immunity during pulmonary C, neoformans infection. Intratracheal inoculation of C. neoformans into CCR2 knockout (CCR2(-/-)) mice produced a prolonged pulmonary infection (5000-fold CFU at 6 wk compared with CCR2(+/+) mice) and significant dissemination to the spleen and brain (160- and 800-fold greater). In addition, CCR2 deficiency resulted in significantly reduced recruitment of macrophages (weeks 1-3) and CD8(+) T cells (weeks 1-2) into the lungs. The immune response in CCR2(-/-) mice was characterized by chronic pulmonary eosinophilia, crystal deposition in the lungs, pulmonary leukocyte production of IL-4 and IL-5 but not IFN-gamma, lack of anticryptococcal delayed-type hypersensitivity, and high levels of serum IgE, These results demonstrate that expression of CCR2 is required for the development of a T1-type response to C. neoformans infection and lack of CCR2 results in a switch to a T2-type response. Thus, CCR2 plays a critical role in promoting the development of T1- over T2-type immune responses in the lung following cryptococcus infection.
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