4.8 Article

Non-Coated Rituximab Induces Highly Cytotoxic Natural Killer Cells From Peripheral Blood Mononuclear Cells via Autologous B Cells

期刊

FRONTIERS IN IMMUNOLOGY
卷 12, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2021.658562

关键词

rituximab; NK cell; B cell; cytotoxicity; tumor therapy; antibody-dependent cell-mediated cytotoxicity

资金

  1. National Key Research and Development Program of China [2020YFA0707704]
  2. National Natural Science Foundation of China [31700764, 81972684, 81702589]
  3. Jilin Provincial Science and Technology Department [20200201180JC, 20200602032ZP, 20180101009JC, 20190303146SF]
  4. Scientific and Technological Research of Jilin Provincial Education Department [JJKH20190023KJ]
  5. Jilin Province Finance Department [2018SCZWSZX010]
  6. Science and Technology Achievement Transformation Fund Project of the First Hospital of Jilin University [JDYYZH-1902037, JDYYZH-1902038]
  7. China Guanghua Foundation [JDYYGH2019004, JDYYGH2019012]
  8. First Hospital of Jilin University [JDYYGH2019004, JDYYGH2019012]

向作者/读者索取更多资源

The study found that rituximab can independently obtain highly cytotoxic NK cells from PBMCs, without the need for additional feeder cells, and these cells have stronger antitumor activity against cancer cells, depending on autologous living B cells.
Natural killer (NK) cells are becoming valuable tools for cancer therapy because of their cytotoxicity against tumor cells without prior sensitization and their involvement in graft-versus-host disease; however, it is difficult to obtain highly cytotoxic NK cells without adding extra feeder cells. In this study, we developed a new method for obtaining highly cytotoxic NK cells from peripheral blood mononuclear cells (PBMCs) independently of extra feeder cell addition using rituximab not coated on a flask (non-coated rituximab). We found that rituximab could promote both the activation and expansion of NK cells from PBMCs, irrespective of being coated on a flask or not. However, NK cells activated by non-coated rituximab had much greater antitumor activity against cancer cells, and these effects were dependent on autologous living B cells. The antibody-dependent cellular cytotoxicity effect of NK cells activated by non-coated rituximab was also more substantial. Furthermore, these cells expressed higher levels of CD107a, perforin, granzyme B, and IFN-gamma. However, there was no difference in the percentage, apoptosis, and cell-cycle progression of NK cells induced by coated and non-coated rituximab. Non-coated rituximab activated NK cells by increasing AKT phosphorylation, further enhancing the abundance of XBP1s. In conclusion, we developed a new method for amplifying NK cells with higher antitumor functions with non-coated rituximab via autologous B cells from PBMCs, and this method more efficiently stimulated NK cell activation than by using coated rituximab.

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