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, M.D.
Background The number of type 2 helper CD4+ T cells is increased in the airways of persons with asthma. Whether the majority of these cells are class II major-histocompatibility-complex–restricted cells or are among the recently identified CD1d-restricted invariant natural killer T cells is a matter of controversy. We studied the frequency of invariant natural killer T cells in the airways of subjects with mild or moderately severe asthma to investigate the possibility of an association between the number of invariant natural killer T cells in the airway and disease severity. We also studied whether an increased number of these cells is a feature of chronic obstructive pulmonary disease (COPD).
Methods We enumerated invariant natural killer T cells by flow cytometry with the use of CD1d tetramers loaded with
Results Fewer than 2% of the T cells obtained from all subjects on airway biopsy, bronchoalveolar lavage, and sputum induction were invariant natural killer T cells, with no significant differences among the three groups of subjects. No expression of messenger RNA for the invariant natural killer T-cell–receptor domains V
Conclusions Invariant natural killer T cells are found in low numbers in the airways of subjects with asthma, subjects with COPD, and controls.
-galactosylceramide and antibodies specific to the invariant natural killer T-cell receptor in samples of bronchoalveolar-lavage fluid, induced sputum, and bronchial-biopsy specimens obtained from subjects with mild or moderately severe asthma, subjects with COPD, and healthy control subjects. Real-time polymerase-chain-reaction analysis was performed on bronchoalveolar-lavage cells for evidence of gene expression of the invariant natural killer T-cell receptor. 24 and V
11 was detected in bronchoalveolar-lavage cells from subjects with asthma.
Source Information
From the Division of Infection, Inflammation, and Repair, University of Southampton, Southampton General Hospital (P.V., G.S., C.P., G.A., D.S., P.S.F., R.D.); and PrimerDesign, Roger Brooke Laboratory, University of Southampton, Southampton General Hospital (R.M.P.) — both in Southampton, United Kingdom; and University of Bern, Inselspital, Bern, Switzerland (S.D.G.).
Dr. Vijayanand and Mr. Seumois contributed equally to this article.
Address reprint requests to Dr. Vijayanand at the Inflammatory Cell Biology Group, Division of Infection, Inflammation, and Repair, Level F, South Block, Mail Point 810, Southampton General Hospital, Tremona Rd., Southampton SO16 6YD, United Kingdom, or at vijay{at}soton.ac.uk.
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