Journal
JOURNAL OF IMMUNOLOGY
Volume 179, Issue 5, Pages 2961-2968Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.179.5.2961
Keywords
-
Categories
Funding
- NHLBI NIH HHS [HL 61005, HL 65410, R01 HL061005, R01 HL065410, HL 36577, P01 HL036577] Funding Source: Medline
- NIAID NIH HHS [AI 057485, AI 44920, R21 AI063400, R01 AI057485-03, R01 AI040611, R01 AI057485, AI 063400, R01 AI044920, AI 40611] Funding Source: Medline
Ask authors/readers for more resources
Mice sensitized and challenged with OVA were used to investigate the role of innate T cells in the development of allergic airway hyperresponsiveness (AHR). AHR, but not eosinophilic airway inflammation, was induced in T cell-deficient mice by small numbers of cotransferred gamma(delta) T cells and invariant NKT cells, whereas either cell type alone was not effective. Only V gamma 1(+)V delta 5(+) gamma delta T cells enhanced AHR. Surprisingly, OVA-specific alpha beta T cells were not required, revealing a pathway of AHR development mediated entirely by innate T cells. The data suggest that lymphocytic synergism, which is key to the Ag-specific adaptive immune response, is also intrinsic to T cell-dependent innate responses.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available