Journal
NATURE IMMUNOLOGY
Volume 11, Issue 1, Pages 83-U2Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1826
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Funding
- US National Institutes of Health [AI39614, AI66016, AI27998, T32-AI07313, T32-CA9138]
- NATIONAL CANCER INSTITUTE [T32CA009138] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [T32AI007313, R37AI027998, P01AI035296, R01AI039614, R01AI027998] Funding Source: NIH RePORTER
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We used a sensitive method based on tetramers of peptide and major histocompatibility complex II (pMHCII) to determine whether CD4(+) memory T cells resemble the T helper type 1 (T(H)1) and interleukin 17 (IL-17)-producing T helper (T(H)17) subsets described in vitro. Intravenous or intranasal infection with Listeria monocytogenes induced pMHCII-specific CD4(+) naive T cells to proliferate and produce effector cells, about 10% of which resembled T(H)1 or T(H)17 cells, respectively. T(H)1 cells were also present among the memory cells that survived 3 months after infection, whereas T(H)17 cells disappeared. The short lifespan of T(H)17 cells was associated with small amounts of the antiapoptotic protein Bcl-2, the IL-15 receptor and the receptor CD27, and little homeostatic proliferation. These results suggest that T(H)1 cells induced by intravenous infection are more efficient at entering the memory pool than are T(H)17 cells induced by intranasal infection.
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