I have not come across this in the literature though have not studied it specifically. This is a very interesting observation although I presume this assay was carried out on PBLs rather than pulmonary lymphocytes. Alveolar lymphocytes express high levels of CD69, according to one paper even in normal subjects, but definitely where there is an alveolitis (Soluble and cellular markers of T cell activation in patients with pulmonary sarcoidosis. Am Rev Respir Dis 1993 Sep;148(3):643-9 Hol BE etal ) This is consistent with their presence at a mucosal site of antigen exposure. Research by Holt and colleagues suggests that the alveolar environment, in particular the presence of alveolar macrophages, permits activation but specifically keeps the lid on proliferation of alveolar T-cells, as excessive proliferation would affect the gas exchange mechanism. Obviously if sufficient activation takes place, such antiproliferative machanisms can be overcome, leading to recruitment of monocytes and appropriate t cell responses (Huffnagle et al, J Immunol). Now if the patient you are investigating has (perhaps) a problem with initial T cell activation then normal proliferative responses may not ensue in pulmonary defence and the defect may predispose to pulmonary infections. Have you looked at later activation markers eg CD25 or HLA-DR expression? It would be very interesting to look at BAL Tcells and their CD69 expression but on the other hand perhaps a BAL would be risky in her setting. You din't say what kind of pulmonary infections she is getting: are they specifically associated with defective Tcell immunity? Dr. D O Donnell, Lung Fibrosis Unit, University College Dublin, Ireland
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