Abstract:
:The role of major histocompatibility complex (MHC) and adhesion molecule expression by alveolar epithelium on the modulation of immune responses in the lung is not understood. We have developed efficient methods to isolate, purify and culture human alveolar epithelial cells (type II pneumocytes) in vitro. The expression of MHC and adhesion molecules by isolated, cultured and cytokine-stimulated alveolar epithelial cells was quantified by flow cytometry, and demonstrated the presence of T-cell ligands including class I MHC, HLA-DR and HLA-DP, intracellular adhesion molecule-1 (ICAM-1; CD54) and lymphocyte function-associated antigen (LFA-3; CD58), but not vascular cell adhesion molecule-1 (VCAM-1) (CD106) or B7 (CD80). The proinflammatory cytokine interferon-gamma (IFN-gamma) caused an up-regulation of class I MHC and ICAM-1. In contrast, tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) had little effect on the expression of these surface antigens by human alveolar epithelial cells. The functional activity of alveolar epithelial adhesion molecules was then studied by determining their ability to bind allogeneic lymphocytes. An increase in lymphocyte adherence to monolayers of alveolar epithelial cells was observed following in vitro activation. However, up-regulation of alveolar epithelial counter receptors with the proinflammatory cytokine gamma-IFN did not enhance adhesion. The adhesive interaction between CD18 on lymphocytes and ICAM-1 on alveolar epithelial cells was demonstrated by the use of blocking antibodies specific for both ligands. Blockade of LFA-3 on alveolar monolayers also suppressed lymphocyte adherence. In conclusion, alveolar epithelial cells expressed MHC HLA-A, B, C, HLA-DR and -DP, and functional adhesion molecules including ICAM-1 and LFA-3.
journal_name
Immunologyjournal_title
Immunologyauthors
Cunningham AC,Kirby JAsubject
Has Abstractpub_date
1995-10-01 00:00:00pages
279-86issue
2eissn
0019-2805issn
1365-2567journal_volume
86pub_type
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