Tolerance of NK and LAK activity for HLA class I deficient targets in a TAP1-deficient patient (bare lymphocyte syndrome type I)

Citation
H. Furukawa et al., Tolerance of NK and LAK activity for HLA class I deficient targets in a TAP1-deficient patient (bare lymphocyte syndrome type I), HUMAN IMMUN, 60(1), 1999, pp. 32-40
Citations number
26
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Immunology
Journal title
HUMAN IMMUNOLOGY
ISSN journal
0198-8859 → ACNP
Volume
60
Issue
1
Year of publication
1999
Pages
32 - 40
Database
ISI
SICI code
0198-8859(199901)60:1<32:TONALA>2.0.ZU;2-M
Abstract
NK cells recognize target cells that lack HLA class I molecules and lyse th em, according to the 'missing self' hypothesis. It was previously reported that a TAP2-deficient patient with an HLA class I-deficiency, had a normal number of NK cells but chat the lymphocytes of this patient had lose their NK activity against K562 cells.[1] In this study, we investigated the HLA c lass I-recognizing NK receptor expressions and the NK and LAK activities of the lymphocytes of a TAP1-deficient patient. The patient had a normal numb er of NK cells. Although the lymphocytes showed LAK activity against class I expressing targets following IL-2, IL-12 and IL-15 stimulation for 3 days , neither NK nor LAK activity against targets lacking class I molecules was induced. The NK cells of the patient expressed class I-recognizing NK rece ptors, although the percentages of such cells were low. However, no differe nces were observed in the expression levels of inhibitory and activating NK receptors between lymphocytes of the patient and chose of healthy controls , suggesting that the modulation of the NK receptor expression is not prima rily responsible for this tolerance. These results also suggest that the ly mphocytes of the patient are defective in the recognition of class I-defici ent target cells in order to promote the induction of self tolerance. (C) A merican Society for Histocompatibility and Immunogenetics, 1999. Published by Elsevier Science Inc.