@article{TEXTUAL,
      recid = {6551},
      author = {McKnight, Christopher G. and Morris, Suzanne C. and  Perkins, Charles and Zhu, Zhenqi and Hildeman, David A. and  Bandelac, Albert and Finkelman, Fred D.},
      title = {NKT cells contribute to basal IL-4 production but are not  required to induce experimental asthma},
      journal = {PLOS ONE},
      address = {2017-11-28},
      number = {TEXTUAL},
      abstract = {CD1d-deficiency results in a selective deletion of NKT  cells in mice that is reported to prevent murine allergic  airway disease (AAD). Because we find 2–3 fold lower basal  IL-4 production in CD1d- mice than in wild-type (WT) mice,  we hypothesized that the contribution made by NKT cells to  AAD would depend on the strength of the stimulus used to  induce the disease. Consequently, we compared  CD1d-deficient mice to WT mice in the development of AAD,  using several models of disease induction that differed in  the type and dose of allergen, the site of sensitization  and the duration of immunization. Surprisingly we found  equivalent allergic inflammation and airway disease in WT  and CD1d- mice in all models investigated. Consistent with  this, NKT cells constituted only ~2% of CD4+ T cells in the  lungs of mice with AAD, and IL-4-transcribing NKT cells did  not expand with disease induction. Concerned that the  congenital absence of NKT cells might have caused a  compensatory shift within the immune response, we  administered an anti-CD1d monoclonal Ab (mAb) to block NKT  function before airway treatments, before or after systemic  sensitization to antigen. Such Ab treatment did not affect  disease severity. We suggest that the differences reported  in the literature regarding the significance of NKT cells  in the induction of allergic airway disease may have less  to do with the methods used to study the disease and more  to do with the animals themselves and/or the facilities  used to house them.},
      url = {http://knowledge.uchicago.edu/record/6551},
}