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Tissue localization and frequency of antigen‐specific effector CD4 + T cells determines the development of allergic airway inflammation
Author(s) -
Harris Nicola L,
Holloway John,
Fitzharris Penny,
McDonald Michael,
Camberis Mali,
Fazekas De St Groth Barbara,
Ronchese Franca,
Le Gros Graham
Publication year - 2005
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1111/j.1440-1711.2005.01357.x
Subject(s) - immunology , allergen , priming (agriculture) , allergic inflammation , antigen , inflammation , medicine , population , effector , sensitization , lymph node , lung , allergy , biology , botany , germination , environmental health
Previous activation of effector Th2 cells is central to the development of allergic inflammatory responses. We have observed that priming of allergen‐specific Th2 cells in C57BL/6 or B10.A mice with allergen delivered via the i.p. or s.c. routes results in very different outcomes following subsequent airway exposure to the same allergen. Systemic allergen immunization (via the i.p. route) resulted in the formation of a lung‐resident population of allergen‐specific T cells, and mice developed severe allergic airway inflammation in response to inhaled allergen. The localization of cells to the lung did not require the presence of antigen at this site, but reflected a large pool of circulating activated allergen‐specific T cells. In contrast, localized immunization (via the s.c. route) resulted in a small T‐cell response restricted to the draining lymph node, and mice were not responsive to inhaled allergen. These data indicate that prior sensitization to an allergen alone was not sufficient for the induction of allergic inflammation; rather, responsiveness was largely determined by precursor frequency and tissue localization of the allergen‐specific effector Th2 cells.