Alternative spliced CD1d transcripts in human bronchial epithelial cells.

MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom.
PLoS ONE (Impact Factor: 3.53). 08/2011; 6(8):e22726. DOI: 10.1371/journal.pone.0022726
Source: PubMed

ABSTRACT CD1d is a MHC I like molecule which presents glycolipid to natural killer T (NKT) cells, a group of cells with diverse but critical immune regulatory functions in the immune system. These cells are required for optimal defence against bacterial, viral, protozoan, and fungal infections, and control of immune-pathology and autoimmune diseases. CD1d is expressed on antigen presenting cells but also found on some non-haematopoietic cells. However, it has not been observed on bronchial epithelium, a site of active host defence in the lungs. Here, we identify for the first time, CD1D mRNA variants and CD1d protein expression on human bronchial epithelial cells, describe six alternatively spliced transcripts of this gene in these cells; and show that these variants are specific to epithelial cells. These findings provide the basis for investigations into a role for CD1d in lung mucosal immunity.

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    ABSTRACT: The epithelium, once considered a simple inert barrier against foreign bodies and responsible merely for maintaining tissue structural integrity, is now viewed as a tissue involved in bona fide immune processes, including homeostasis and during the course of microbial insults. At respiratory alveolar surfaces, epithelial cells and alveolar macrophages interact through the production of surfactant, regulatory cytokines and endogenous antimicrobial molecules, to ensure a non-inflammatory regulatory phenotype. Following microbial infection, this regulatory ‘brake’ is released and these cells participate in the orchestration of pro-inflammatory and adaptive immune mechanisms, leading to the containment of the microbial infection and the restoration of tissue homeostasis. We will review here some of the molecular mechanisms operative in this ‘switch’ from regulatory to effector immune phenotypes.
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