Successful treatment of smouldering Human T cell Leukemia Virus Type1 associated bronchiolitis and alveolar abnormalities with amplified natural killer therapy

2021 ◽  
Vol 14 (12) ◽  
pp. e244619
Author(s):  
Kenjiro Nagai ◽  
Sho Nagai ◽  
Yu Hara

In amplified natural killer (ANK) cell immunotherapy, NK cells are extracted from the patient’s blood, cultured for enhancing its anticancer effects and amplified before they are returned to the body. Here, we administered ANK therapy to an 81-year-old female patient diagnosed with smouldering human T cell leukaemia virus-associated bronchioloalveolar disorder. After eight sessions of twice-weekly NK cell infusion, the bilateral diffuse granular shadows on a CT scan and the overall respiratory function improved markedly. Later, the patient received outpatient treatment without serious side effects. Thus, ANK therapy may be safe for elderly patients owing to its infrequent side effects.

Virulence ◽  
2010 ◽  
Vol 1 (1) ◽  
pp. 19-28 ◽  
Author(s):  
Philip J. Norris ◽  
Dale F. Hirschkorn ◽  
Deborah A. DeVita ◽  
Tzong-Hae Lee ◽  
Edward L. Murphy

2007 ◽  
Vol 81 (18) ◽  
pp. 9707-9717 ◽  
Author(s):  
Prabal Banerjee ◽  
Gerold Feuer ◽  
Edward Barker

ABSTRACT Although natural killer (NK) cell-mediated control of viral infections is well documented, very little is known about the ability of NK cells to restrain human T-cell leukemia virus type 1 (HTLV-1) infection. In the current study we show that NK cells are unable to kill HTLV-1-infected primary CD4+ T cells. Exposure of NK cells to interleukin-2 (IL-2) resulted in only a marginal increase in their ability to kill HTLV-1-infected primary CD4+ T cells. This inability of NK cells to kill HTLV-1-infected CD4+ T cells occurred despite the down-modulation of major histocompatibility complex (MHC) class I molecules, one of the ligands for the major NK cell inhibitory receptor, by HTLV-1 p12I on CD4+ T cells. One reason for this diminished ability of NK cells to kill HTLV-1-infected cells was the decreased ability of NK cells to adhere to HTLV-1-infected cells because of HTLV-1 p12I-mediated down-modulation of intercellular adhesion molecule 1 (ICAM-1) and ICAM-2. We also found that HTLV-1-infected CD4+ T cells did not express ligands for NK cell activating receptors, NCR and NKG2D, although they did express ligands for NK cell coactivating receptors, NTB-A and 2B4. Thus, despite HTLV-1-mediated down-modulation of MHC-I molecules, HTLV-1-infected primary CD4+ T cells avoids NK cell destruction by modulating ICAM expression and shunning the expression of ligands for activating receptors.


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