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The expression of NK cell inhibitory receptors on cytotoxic T cells in B-cell chronic lymphocytic leukaemia (B-CLL).

Artikel i vetenskaplig tidskrift
Författare Katarina Junevik
Olle Werlenius
Sverker Hasselblom
Stefan Jacobsson
Herman Nilsson-Ehle
Per-Ola Andersson
Publicerad i Annals of hematology
Volym 86
Nummer/häfte 2
Sidor 89-94
ISSN 1432-0584
Publiceringsår 2007
Publicerad vid Institutionen för biomedicin, avdelningen för klinisk kemi och transfusionsmedicin
Institutionen för medicin, avdelningen för invärtesmedicin
Sidor 89-94
Språk en
Länkar dx.doi.org/10.1007/s00277-006-0198-...
Ämnesord Adult, Aged, Aged, 80 and over, Antigens, CD, metabolism, Female, Humans, Leukemia, Lymphocytic, Chronic, B-Cell, metabolism, Male, Middle Aged, Neoplasm Staging, Receptors, Immunologic, metabolism, Receptors, KIR, Receptors, KIR2DL1, Receptors, KIR2DL2, Receptors, KIR2DL3, Receptors, KIR3DL1, T-Lymphocytes, Cytotoxic, metabolism
Ämneskategorier Tumörbiologi, Hematologi

Sammanfattning

Immune surveillance of tumours is mediated by cytotoxic T cells (CTL) that recognise tumour antigen. Reduced reactivity of CTL towards tumour cells could thus lead to disease progression and loss of tumour control. In B-cell chronic lymphocytic leukaemia (B-CLL), the function of tumour-reactive CTL seems to correlate inversely to disease stage. Inhibitory NK cell receptors are known to suppress the CTL response upon interaction with major histocompatibility complex (MHC) class I and increased expression of such receptors on CTL may inhibit the anti-tumour response. So, the aim of this study was to investigate the expression of NK cell inhibitory receptors on CTL in B-CLL patients and if such expression correlated to disease stage. CD8+ T cells from B-CLL patients in Binet stage A (n = 26) and stage C (n = 14) and healthy controls (n = 14) were analysed for the expression of killer immunoglobulin-like receptors (KIR) CD158a (KIR2DL1), CD158b (KIR2DL2), CD158e (KIR3DL1) and the C-type lectin receptor CD94, by flow cytometry analysis. Patients with advanced disease (Binet stage C) had a significantly greater percentage of CTL expressing CD158b, CD158e and CD94 than patients with non-progressive disease (Binet stage A) and healthy controls. Stage C patients also had a significantly higher percentage of CTL expressing CD158a than stage A patients. No statistically significant differences were found between Binet A patients and healthy controls. Our results suggest that increased expression of KIR and CD94 on CTL in advanced stage B-CLL may potentially contribute to the impaired anti-tumour immune response in these patients.

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