Specific CD8 T cells in IgE-mediated allergy correlate with allergen dose and allergic phenotype

Juan A. Aguilar-Pimentel, Francesca Alessandrini, Katharina M. Huster, Thilo Jakob, Holger Schulz, Heidrun Behrendt, Johannes Ring, Martin Hrabé De Angelis, Dirk H. Busch, Martin Mempel, Markus Ollert*

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

20 Citations (Scopus)


Rationale: Studies in humans and rodents have indicated a causative role for CD8 + T cells in IgE-mediated allergic inflammation, but their function is still controversial. Objectives: Toanalyze the role of allergen-specific CD8 + T cells during the development of allergic airway inflammation in two parallel but diverging outcome models. Methods: We used H2-Kb SIINFEKL (OVA 257-264) multimers to analyze induction, natural distribution, and phenotype of allergen-specific CD8 + T cells in amurine C57BL/6 model of ovalbumin (OVA)-induced allergic airway inflammation using low-dose or high-dose OVA sensitization. Measurements and Main Results: The low-dose protocol was characterized by a significant induction of total and OVA-specific IgE, eosinophilic airway inflammation, IL-4 levels in bronchoalveolar lavage fluid. And significant alterations in lung function. The high dose protocol was characterizedbya significant reductionof theallergicphenotype. Using OVA 257-264 H2-Kb multimers, we observed lung and airway infiltrating OVA-specific CD8 + T cells showing an effector/effectormemory phenotype. The high-dose protocol caused significantly higher infiltration of allergen-specific CD8 + cells to the airways and enhanced their cytotoxicity. Adoptive transferwith CD8 + T cells from transgenic OT-I mice to TAP1 -/- or wild-type mice showed their migration to the lungs and TAP1-dependent proliferation after OVA aerosol exposure. TAP1 -/- mice defective in CD8 + T cells showed exacerbated symptoms in the low-dose sensitizationmodel. Conclusions: Allergen-specific CD8 + T cells seem to protect from allergic inflammation in the lungs. Their number, which is dependent on the sensitization dose, appears to be a critical predictor for the severity of the allergic phenotype.

Original languageEnglish
Pages (from-to)7-16
Number of pages10
JournalAmerican Journal of Respiratory and Critical Care Medicine
Issue number1
Publication statusPublished - 1 Jan 2010
Externally publishedYes


  • Airway inflammation
  • Asthma
  • Cytotoxicity
  • Immunotherapy
  • Tolerance


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