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Updated: Jun 3, 2026
08:05
Murine Model of Allergen Induced Asthma
Published on: May 14, 2012
Tim1 and Tim3 are not essential for experimental allergic asthma
J L Barlow1, S H Wong, S J Ballantyne
1MRC Laboratory of Molecular Biology, Cambridge, UK. jbarlow@mrc-lmb.cam.ac.uk
Summary
Tim-1 and Tim-3 are not essential for inducing type-2 responses in lung allergy, contrary to previous antibody studies. This finding questions their clinical relevance for developing new allergy therapies.
Area of Science:
- Immunology
- Allergy Research
- T-cell Regulation
Background:
- Previous studies suggested Tim-1 and Tim-3 polymorphisms are linked to airway hyperreactivity (AHR) in asthma models and atopic populations.
- Antibody and fusion protein studies indicated Tim-1 and Tim-3 may regulate type-1 and type-2 immunity, but their role in AHR and airway inflammation was unclear.
Purpose of the Study:
- To investigate the role of Tim-1 and Tim-3 in regulating antigen-driven lung allergy and inflammation.
- To determine if Tim-1 and Tim-3 are essential for the development of allergic lung inflammation and AHR.
Main Methods:
- Utilized Tim-1 and Tim-3 deficient mice to assess allergic lung inflammation development.
- Analyzed airway hyperreactivity (AHR) and cellular infiltration in the lungs and blood.
Main Results:
- Airway hyperreactivity (AHR) developed normally in mice lacking both Tim-1 and Tim-3.
- Tim-1 deficient mice showed a minor but significant reduction in lung cell infiltration and blood eosinophilia.
- Tim-3 was expressed on CD4(+) T cells, while Tim-1 expression was limited to CD86(+) B cells in allergic lungs.
Conclusions:
- Tim-1 and Tim-3 are not critical for initiating type-2 responses in lung allergy.
- These findings challenge previous research using neutralizing/activating antibodies.
- The clinical relevance of Tim-1 and Tim-3 for novel allergy therapies is questioned.
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