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Journal articles on the topic 'Killer cells'

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Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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1

WOODS, D. R., I. W. ROSS, and D. A. HENDRY. "A New Killer Factor Produced by a Killer/Sensitive Yeast Strain." Microbiology 81, no. 2 (February 1, 2000): 285–89. http://dx.doi.org/10.1099/00221287-81-2-285.

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Summary: The isolation of a new killer/sensitive phenotype of the yeast, Saccharomyces cerevisiae, is described. Killer/sensitive yeast cells are killed by the killer factor (KF1) secreted by killer yeast cells. The killer/sensitive cells also secrete a new killer factor (KF2) which kills sensitive cells. The production of KF2 by killer/sensitive cells renders them less sensitive to KF1, than sensitive cells. Sensitive cells are most susceptible to the action of KF2 in log phase. KF2 is a thermostable protein-containing killer factor.

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2

Abramova, V. A., A. Kali, N. Abdolla, O. Yu Yurikova, Yu V. Perfilyeva, Ye O. Ostapchuk, R. T. Tleulieva, S. K. Madenova, and N. N. Belyaev. "Influence of tumor cells on natural killer cell phenotype and cytotoxicity." International Journal of Biology and Chemistry 8, no. 1 (2015): 9–14. http://dx.doi.org/10.26577/2218-7979-2015-8-1-9-14.

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3

Mueller, K. L. "Killer Cells for Killer Bacteria." Science 333, no. 6051 (September 29, 2011): 1803. http://dx.doi.org/10.1126/science.333.6051.1803-b.

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4

Seaman, William E. "Natural killer cells and natural killer T cells." Arthritis & Rheumatism 43, no. 6 (June 2000): 1204–17. http://dx.doi.org/10.1002/1529-0131(200006)43:6<1204::aid-anr3>3.0.co;2-i.

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5

Perussia, Bice. "Lymphokine-activated killer cells, natural killer cells and cytokines." Current Opinion in Immunology 3, no. 1 (January 1991): 49–55. http://dx.doi.org/10.1016/0952-7915(91)90076-d.

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6

Kay, Neil E. "Natural Killer Cells." CRC Critical Reviews in Clinical Laboratory Sciences 22, no. 4 (January 1985): 343–59. http://dx.doi.org/10.3109/10408368509165790.

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7

Herberman, R. B. "Natural Killer Cells." Annual Review of Medicine 37, no. 1 (February 1986): 347–52. http://dx.doi.org/10.1146/annurev.me.37.020186.002023.

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8

Bevan, Michael J. "Stimulating killer cells." Nature 342, no. 6249 (November 1989): 478–79. http://dx.doi.org/10.1038/342478a0.

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9

Gardiner, Clair M. "Natural killer cells." Current Biology 9, no. 19 (October 1999): R716. http://dx.doi.org/10.1016/s0960-9822(99)80464-3.

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10

Lanier, Lewis L., and Joseph H. Phillips. "Natural killer cells." Current Biology 2, no. 3 (March 1992): 134. http://dx.doi.org/10.1016/0960-9822(92)90254-8.

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11

Burns, Gordon F., C. Glenn Begley, Ian R. Mackay, Tony Triglia, and Jerome A. Werkmeister. "‘Supernatural’ killer cells." Immunology Today 6, no. 12 (December 1985): 370–73. http://dx.doi.org/10.1016/0167-5699(85)90097-0.

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12

Lanier, Lewis L., and Joseph H. Phillips. "Natural killer cells." Current Opinion in Immunology 4, no. 1 (February 1992): 38–42. http://dx.doi.org/10.1016/0952-7915(92)90121-t.

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13

&NA;. "Lymphokine-activated killer cells see Interleukin 2 ?? lymphokineactivated killer cells." Reactions Weekly &NA;, no. 305 (June 1990): 7. http://dx.doi.org/10.2165/00128415-199003050-00031.

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14

Lebow, L. T., A. Jewett, and B. Bonavida. "Killer cell recruitment and renewal capacity of purified cytolytic and noncytolytic human peripheral blood natural killer cell subsets." Journal of Immunology 150, no. 1 (January 1, 1993): 320–29. http://dx.doi.org/10.4049/jimmunol.150.1.320.

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Abstract The inability to isolate NK precursors at different stages of development has impeded understanding of the processes involved in NK maturation. The present studies utilize a flow cytometric technique that enables the isolation of operationally defined cell subsets, lytic (killers) and nonlytic conjugate-forming (binders), and nonconjugate-forming (free) cells, within NK-enriched preparations to test whether these might represent cells in different stages of NK development. To characterize both the steps involved in NK maturation and the cells responsible for IL-2 induced proliferation, these purified subsets were analyzed for their killer cell recruitment and renewal capacity. After a 2-h exposure to IFN-alpha or IL-2, induction of lytic function was developed only in the binder subset as detected in the single cell assay. Neither enhancement of killer cell recycling nor induction of binding function among the subsets was observed. However, after an 18-h culture period, with or without rIL-2, killer cells preferentially expressed activation Ag CD69 (Leu-23) and the IL-2R alpha-chain, TAC (CD25). In addition, all cells in contact with K562 targets displayed enhanced expression of these Ag. Killer cells also showed an enhanced capacity to proliferate in response to rIL-2 in a 6-day [3H]TdR incorporation assay. Additional irradiated K562 targets enhanced the proliferative capacity of all the subsets, with only a marginal effect on sorted free cells. Nevertheless, sorted free cells, in addition to binders, developed potent binding and lytic function when tested in the single-cell assay after 4 days of IL-2 culture. The lytic activity of killers was reduced, as compared with freshly isolated killers. The results are consistent with a two-step model for NK maturation, involving the acquisition of lytic function before proliferative capacity, and specific triggering of killer cells through interaction with target cells for induction of a proliferative competent state.

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15

Bandey, Irfan N., Jay R. T. Adolacion, Gabrielle Romain, Melisa Martinez Paniagua, Xingyue An, Arash Saeedi, Ivan Liadi, et al. "Designed improvement to T-cell immunotherapy by multidimensional single cell profiling." Journal for ImmunoTherapy of Cancer 9, no. 3 (March 2021): e001877. http://dx.doi.org/10.1136/jitc-2020-001877.

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BackgroundAdoptive cell therapy based on the infusion of chimeric antigen receptor (CAR) T cells has shown remarkable efficacy for the treatment of hematologic malignancies. The primary mechanism of action of these infused T cells is the direct killing of tumor cells expressing the cognate antigen. However, understanding why only some T cells are capable of killing, and identifying mechanisms that can improve killing has remained elusive.MethodsTo identify molecular and cellular mechanisms that can improve T-cell killing, we utilized integrated high-throughput single-cell functional profiling by microscopy, followed by robotic retrieval and transcriptional profiling.ResultsWith the aid of mathematical modeling we demonstrate that non-killer CAR T cells comprise a heterogeneous population that arise from failure in each of the discrete steps leading to the killing. Differential transcriptional single-cell profiling of killers and non-killers identified CD137 as an inducible costimulatory molecule upregulated on killer T cells. Our single-cell profiling results directly demonstrate that inducible CD137 is feature of killer (and serial killer) T cells and this marks a different subset compared with the CD107apos (degranulating) subset of CAR T cells. Ligation of the induced CD137 with CD137 ligand (CD137L) leads to younger CD19 CAR T cells with sustained killing and lower exhaustion. We genetically modified CAR T cells to co-express CD137L, in trans, and this lead to a profound improvement in anti-tumor efficacy in leukemia and refractory ovarian cancer models in mice.ConclusionsBroadly, our results illustrate that while non-killer T cells are reflective of population heterogeneity, integrated single-cell profiling can enable identification of mechanisms that can enhance the function/proliferation of killer T cells leading to direct anti-tumor benefit.

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16

&NA;. "Lymphokine-activated killer cells see Interleukin 2 ?? lymphokine-activated killer cells." Reactions Weekly &NA;, no. 292 (March 1990): 7. http://dx.doi.org/10.2165/00128415-199002920-00028.

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17

&NA;. "Lymphokine activated killer cells see Interleukin 2 + lymphokine activated killer cells." Reactions Weekly &NA;, no. 365 (August 1991): 9. http://dx.doi.org/10.2165/00128415-199103650-00044.

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18

Vosshenrich, Christian A. J., Sarah Lesjean-Pottier, Milena Hasan, Odile Richard-Le Goff, Erwan Corcuff, Ofer Mandelboim, and James P. Di Santo. "CD11cloB220+ interferon-producing killer dendritic cells are activated natural killer cells." Journal of Experimental Medicine 204, no. 11 (October 8, 2007): 2569–78. http://dx.doi.org/10.1084/jem.20071451.

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Interferon-producing killer dendritic cells (IKDCs) are a recently described subset of CD11cloB220+ cells that share phenotypic and functional properties of DCs and natural killer (NK) cells (Chan, C.W., E. Crafton, H.N. Fan, J. Flook, K. Yoshimura, M. Skarica, D. Brockstedt, T.W. Dubensky, M.F. Stins, L.L. Lanier, et al. 2006. Nat. Med. 12:207–213; Taieb, J., N. Chaput, C. Menard, L. Apetoh, E. Ullrich, M. Bonmort, M. Pequignot, N. Casares, M. Terme, C. Flament, et al. 2006. Nat. Med. 12:214–219). IKDC development appears unusual in that cytokines using the interleukin (IL)-2 receptor β (IL-2Rβ) chain but not those using the common γ chain (γc) are necessary for their generation. By directly comparing Rag2−/−γc−/y, Rag2−/−IL-2Rβ−/−, Rag2−/−IL-15−/−, and Rag2−/−IL-2−/− mice, we demonstrate that IKDC development parallels NK cell development in its strict IL-15 dependence. Moreover, IKDCs uniformly express NK-specific Ncr-1 transcripts (encoding NKp46), whereas NKp46+ cells are absent in Ncr1gfp/+γc−/y mice. Distinguishing features of IKDCs (CD11cloB220+MHC-II+) were carefully examined on developing NK cells in the bone marrow and on peripheral NK cells. As B220 expression was heterogeneous, defining B220lo versus B220hi NK1.1+ NK cells could be considered as arbitrary, and few phenotypic differences were noted between NK1.1+ NK cells bearing different levels of B220. CD11c expression did not correlate with B220 or major histocompatibility complex (MHC) class II (MHC-II) expression, and most MHC-II+ NK1.1+ cells did not express B220 and were thus not IKDCs. Finally, CD11c, MHC-II, and B220 levels were up-regulated on NK1.1+ cells upon activation in vitro or in vivo in a proliferation-dependent fashion. Our data suggest that the majority of CD11cloB220+ “IKDC-like” cells represent activated NK cells.

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19

Katchar, Kia, Elise E. Drouin, and Allen C. Steere. "Natural killer cells and natural killer T cells in Lyme arthritis." Arthritis Research & Therapy 15, no. 6 (2013): R183. http://dx.doi.org/10.1186/ar4373.

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20

Vivier, Eric, Sophie Ugolini, Didier Blaise, Christian Chabannon, and Laurent Brossay. "Targeting natural killer cells and natural killer T cells in cancer." Nature Reviews Immunology 12, no. 4 (March 22, 2012): 239–52. http://dx.doi.org/10.1038/nri3174.

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21

Sarneva, Mariana, Nikola L. Vujanovic, M. R. M. van den Brink, Ronald B. Herberman, and John C. Hiserodt. "Lymphokine-activated killer cells in rats: Generation of natural killer cells and lymphokine-activated killer cells from bone marrow progenitor cells." Cellular Immunology 118, no. 2 (February 1989): 448–57. http://dx.doi.org/10.1016/0008-8749(89)90392-4.

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22

Drake, B. L., and J. R. Head. "Murine trophoblast can be killed by lymphokine-activated killer cells." Journal of Immunology 143, no. 1 (July 1, 1989): 9–14. http://dx.doi.org/10.4049/jimmunol.143.1.9.

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Abstract The ability of fetal trophoblast cells in the placenta to resist cell-mediated lysis may be important for successful pregnancy. Previous studies in this laboratory demonstrated that cultured midterm mouse trophoblast cells are not susceptible to allospecific CTL generated by standard in vitro protocols, to antibody-dependent cell-mediated cytotoxicity, or to naive or IFN-activated NK cells, despite expressing the requisite target structures. However, we now report that murine trophoblast can be killed, in a non-MHC-specific manner, by LAK cells. Normal mouse spleen cells cultured for 4 days in IL-2-containing lymphokine preparations characteristically killed both NK-sensitive (YAC-1) and NK-resistant (EL4, P815) target cells, and mediated significant lysis of both cultured and freshly isolated trophoblast cells (35 to 55%, E/T 100/1). Pretreatment of the LAK cells with anti-ASGM1 antibody and C markedly reduced the lysis of trophoblast and YAC-1 targets, suggesting that the responsible cells belonged to the NK lineage. The ability of IL-2-activated NK cells to kill midterm murine trophoblast cells was confirmed using a population of highly lytic NK cells generated by culturing spleen cells from severe combined immunodeficiency mice in 500 U/ml rIL-2 for 5 days. These effector cells killed YAC-1, EL4 and P815 target cells at much lower E/T ratios than was achieved with the normal splenic LAK cells, and mediated significant lysis of both freshly isolated (45 to 50%, E/T 20/1) and cultured trophoblast cells (68 to 76%, E/T 20/1). The susceptibility of trophoblast to LAK cells and IL-2-activated NK cells supports the need for suppressor mechanisms regulating IL-2 activity at the maternal-fetal interface.

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23

Da Silva, Kevin. "Restraining natural killer cells." Nature Medicine 19, no. 6 (June 2013): 683. http://dx.doi.org/10.1038/nm.3241.

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24

Ugolini, Sophie, and Eric Vivier. "Natural killer cells remember." Nature 457, no. 7229 (January 2009): 544–45. http://dx.doi.org/10.1038/457544a.

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25

GRIMM, ELIZABETH A., LAURIE B. OWEN-SCHAUB, WILLIAM G. LOUDON, and MASATO YAGITA. "Lymphokine-Activated Killer Cells." Annals of the New York Academy of Sciences 532, no. 1 Cytotoxic T C (August 1988): 380–86. http://dx.doi.org/10.1111/j.1749-6632.1988.tb36355.x.

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26

Lanier, Lewis L. "Natural killer cells: roundup." Immunological Reviews 214, no. 1 (December 2006): 5–8. http://dx.doi.org/10.1111/j.1600-065x.2006.00464.x.

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27

Bennett, Michael. "Killer cells protect themselves." Blood 104, no. 8 (October 15, 2004): 2214. http://dx.doi.org/10.1182/blood-2004-07-2840.

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28

Boysen, Preben, and Anne K. Storset. "Bovine natural killer cells." Veterinary Immunology and Immunopathology 130, no. 3-4 (August 2009): 163–77. http://dx.doi.org/10.1016/j.vetimm.2009.02.017.

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29

Caligiuri, Michael A. "Human natural killer cells." Blood 112, no. 3 (August 1, 2008): 461–69. http://dx.doi.org/10.1182/blood-2007-09-077438.

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Abstract Natural killer (NK) cells were discovered more than 30 years ago. NK cells are large granular lymphocytes that belong to the innate immune system because unlike T or B lymphocytes of the adaptive or antigen-specific immune system, NK cells do not rearrange T-cell receptor or immunoglobulin genes from their germline configuration. During the past 2 decades there has been a substantial gain in our understanding of what and how NK-cells “see,” lending important insights into their functions and purpose in normal immune surveillance. The most recent discoveries in NK-cell receptor biology have fueled translational research that has led to remarkable results in treating human malignancy.

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30

van der Vliet, Hans JJ, Herbert M. Pinedo, B. Mary E. von Blomberg, Alfons JM van den Eertwegh, Rik J. Scheper, and Giuseppe Giaccone. "Natural Killer T cells." Lancet Oncology 3, no. 9 (September 2002): 574. http://dx.doi.org/10.1016/s1470-2045(02)00850-1.

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31

Viganò, Paola, Paolo Vercellini, Anna Maria Di Blasio, Alberto Colombo, Giovanni Battista Candiani, and Mario Vignali. "“Killer Cells” and Endometriosis." Fertility and Sterility 60, no. 5 (November 1993): 928. http://dx.doi.org/10.1016/s0015-0282(16)56301-8.

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32

Lindemann, A., F. Herrmann, W. Oster, and R. Mertelsmann. "Lymphokine activated killer cells." Blut 59, no. 4 (October 1989): 375–84. http://dx.doi.org/10.1007/bf00321208.

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33

Kyaw, Tin, Peter Tipping, Ban-Hock Toh, and Alex Bobik. "Killer cells in atherosclerosis." European Journal of Pharmacology 816 (December 2017): 67–75. http://dx.doi.org/10.1016/j.ejphar.2017.05.009.

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34

Crinier, Adeline, Emilie Narni-Mancinelli, Sophie Ugolini, and Eric Vivier. "SnapShot: Natural Killer Cells." Cell 180, no. 6 (March 2020): 1280–1280. http://dx.doi.org/10.1016/j.cell.2020.02.029.

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35

Foley, J. F. "Unleashing natural killer cells." Science 351, no. 6275 (February 18, 2016): 827–29. http://dx.doi.org/10.1126/science.351.6275.827-p.

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36

Klingemann, H. "Improving natural killer cells." Cytotherapy 10, no. 3 (2008): 225–26. http://dx.doi.org/10.1080/14653240802028376.

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37

Ding-E Young, John, and Zanvil A. Cohn. "How Killer Cells Kill." Scientific American 258, no. 1 (January 1988): 38–44. http://dx.doi.org/10.1038/scientificamerican0188-38.

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38

Manara, Gian Carlo, Corrado Ferrari, and Giuseppe De Panfilis. "Natural Killer Cells Immunophenotype." American Journal of Dermatopathology 10, no. 3 (June 1988): 278–79. http://dx.doi.org/10.1097/00000372-198806000-00016.

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39

McMillan, Euan M. "Natural Killer Cells Immunophenotype." American Journal of Dermatopathology 10, no. 3 (June 1988): 278–79. http://dx.doi.org/10.1097/00000372-198806000-00017.

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40

Kanellopoulos, Jean. "Natural killer T cells." Biomedical Journal 38, no. 6 (December 2015): 469. http://dx.doi.org/10.1016/j.bj.2016.01.007.

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41

Lee, Jae Hee, Ji Sung Kim, Hong Kyung Lee, Ki Hun Kim, Jeong Eun Choi, A. Young Ji, Jin Tae Hong, Youngsoo Kim, and Sang-Bae Han. "Comparison of cytotoxic dynamics between cytokine-induced killer cells and natural killer cells at the single cell level." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 198.12. http://dx.doi.org/10.4049/jimmunol.198.supp.198.12.

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Abstract Although much has been learned about the cytotoxic mechanisms of cytokine-induced killer (CIK) and natural killer (NK) cells, little is known about how they kill cancer cells at the single-cell level. In the present study, we examined the contact dynamics of CIK and NK cells at the single-cell level by using time-lapse imaging. CIK cells killed MHC-I-negative and -positive cancer cells, but NK cells destroyed MHC-I-negative cells only. Moreover, CIK cells moved in all directions and showed longer tracks than did NK cells. CIK cells showed higher displacement and straightness scores than did NK cells, which indicates long-distance random migration of CIK cells. CIK and NK cells moved at 6.7 mm/min and 4.5 mm/min on average, respectively. These data suggest that CIK cells are likely moving more actively than NK cells. The average threshold number of CIK cells required to kill an individual cancer cell was 6.7 for MHC-I-negative cells and 6.9 for MHC-I-positive cells. That of NK cells was 2.4 for MHC-I-negative cells. Likely due to the higher threshold numbers, killing by CIK cells was delayed in comparison with NK cells: 40% of MHC-negative target cells were killed after 5 h when co-cultured with CIK cells and after 2 h with NK cells. Our data have implications for the rational design of CIK or NK cell–based immunotherapy of cancer patients

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42

Andoniou, Christopher E., Daniel M. Andrews, and Mariapia A. Degli-Esposti. "Natural killer cells in viral infection: more than just killers." Immunological Reviews 214, no. 1 (December 2006): 239–50. http://dx.doi.org/10.1111/j.1600-065x.2006.00465.x.

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43

Guo, Qingming, Danni Zhu, Xiaocui Bu, Xiaofang Wei, Changyou Li, Daiqing Gao, Xiaoqiang Wei, Xuezhen Ma, and Peng Zhao. "Efficient killing of radioresistant breast cancer cells by cytokine-induced killer cells." Tumor Biology 39, no. 3 (March 2017): 101042831769596. http://dx.doi.org/10.1177/1010428317695961.

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Recurrence of breast cancer after radiotherapy may be partly explained by the presence of radioresistant cells. Thus, it would be desirable to develop an effective therapy against radioresistant cells. In this study, we demonstrated the intense antitumor activity of cytokine-induced killer cells against MCF-7 and radioresistant MCF-7 cells, as revealed by cytokine-induced killer–mediated cytotoxicity, tumor cell proliferation, and tumor invasion. Radioresistant MCF-7 cells were more susceptible to cytokine-induced killer cell killing. The stronger cytotoxicity of cytokine-induced killer cells against radioresistant MCF-7 cells was dependent on the expression of major histocompatibility complex class I polypeptide–related sequence A/B on radioresistant MCF-7 cells after exposure of cytokine-induced killer cells to sensitized targets. In addition, we demonstrated that cytokine-induced killer cell treatment sensitized breast cancer cells to chemotherapy via the downregulation of TK1, TYMS, and MDR1. These results indicate that cytokine-induced killer cell treatment in combination with radiotherapy and/or chemotherapy may induce synergistic antitumor activities and represent a novel strategy for breast cancer.

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44

Cameron, A., B. Kirby, W. Fei, and C. Griffiths. "Natural killer and natural killer-T cells in psoriasis." Archives of Dermatological Research 294, no. 8 (November 2002): 363–69. http://dx.doi.org/10.1007/s00403-002-0349-4.

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45

Vremec, David, Meredith O'Keeffe, Hubertus Hochrein, Martina Fuchsberger, Irina Caminschi, Mireille Lahoud, and Ken Shortman. "Production of interferons by dendritic cells, plasmacytoid cells, natural killer cells, and interferon-producing killer dendritic cells." Blood 109, no. 3 (October 12, 2006): 1165–73. http://dx.doi.org/10.1182/blood-2006-05-015354.

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Abstract The capacity of mouse spleen conventional dendritic cells (cDCs) and plasmacytoid dendritic cells (pDCs) to produce interferon-γ (IFN-γ) or IFN-α was assessed, and compared with that of natural killer (NK) cells and the recently identified interferon-producing killer dendritic cells (IKDCs), both of which are frequent contaminants in DC preparations. Fully developed cDCs or pDCs, if free of NK cells or IKDCs, showed little capacity for IFN-γ production. However, an early developmental form of the CD4−8+ cDC subtype, and the Ly6C− Ly49Q− pDC subtype, both were able to produce moderate amounts of IFN-γ, although less than IKDCs. In response to toll-like receptor 9 stimuli, both the Ly6C+ Ly49Q+ and the Ly6C− Ly49Q− pDC subtypes were effective producers of IFN-α. However, IKDCs, which efficiently produced IFN-γ and showed immediate cytotoxicity on NK target cells, did not produce IFN-α un-der these conditions.

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46

Schott, Eckart, Roberto Bonasio, and Hidde L. Ploegh. "Elimination In Vivo of Developing T Cells by Natural Killer Cells." Journal of Experimental Medicine 198, no. 8 (October 20, 2003): 1213–24. http://dx.doi.org/10.1084/jem.20030918.

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Natural killer cells gauge the absence of self class I MHC on susceptible target cells by means of inhibitory receptors such as members of the Ly49 family. To initiate killing by natural killer cells, a lack of inhibitory signals must be accompanied by the presence of activating ligands on the target cell. Although natural killer cell–mediated rejection of class I MHC–deficient bone marrow (BM) grafts is a matter of record, little is known about the targeting in vivo of specific cellular subsets by natural killer cells. We show here that development of class I MHC–negative thymocytes is delayed as a result of natural killer cell toxicity after grafting of a class I MHC–positive host with class I MHC–negative BM. Double positive thymocytes that persist in the presence of natural killer cells display an unusual T cell receptor–deficient phenotype, yet nevertheless give rise to single positive thymocytes and yield mature class I MHC–deficient lymphocytes that accumulate in the class I MHC–positive host. The resulting class I MHC–deficient CD8 T cells are functional and upon activation remain susceptible to natural killer cell toxicity in vivo. Reconstitution of class I MHC–deficient BM precursors with H2-Kb by retroviral transduction fully restores normal thymic development.

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47

Young, JD-E., and ZA Cohn. "Molecular Basis of Lymphocyte-Mediated Destruction of Traget Cells." Physiology 3, no. 5 (October 1, 1988): 211–16. http://dx.doi.org/10.1152/physiologyonline.1988.3.5.211.

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Subsets of lymphocytes, known as cytotoxic T lymphocytes or natural killer cells, are potent killers of target cells. These immune cells have large granules in their cytoplasm containing cytotoxic peptides and other factors. Several of these molecules have been isolated and their functions elucidated.

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48

&NA;. "Lymphokine activated killer cells see Interleukin 2/interferon alpha/lymphokine activated killer cells." Reactions Weekly &NA;, no. 375 (November 1991): 10. http://dx.doi.org/10.2165/00128415-199103750-00053.

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49

Uchida, Takahiro, Seigo Ito, Hiroo Kumagai, Takashi Oda, Hiroyuki Nakashima, and Shuhji Seki. "Roles of Natural Killer T Cells and Natural Killer Cells in Kidney Injury." International Journal of Molecular Sciences 20, no. 10 (May 20, 2019): 2487. http://dx.doi.org/10.3390/ijms20102487.

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Mouse natural killer T (NKT) cells and natural killer (NK) cells are innate immune cells that are highly abundant in the liver. In addition to their already-known antitumor and antimicrobial functions, their pathophysiological roles in the kidney have recently become evident. Under normal circumstances, the proportion of activated NKT cells in the kidney increases with age. Administration of a synthetic sphingoglycolipid ligand (alpha-galactosylceramide) further activates NKT cells, resulting in injury to renal vascular endothelial cells via the perforin-mediated pathway and tubular epithelial cells via the TNF-α/Fas ligand pathway, causing acute kidney injury (AKI) with hematuria. Activation of NKT cells by common bacterial DNA (CpG-ODN) also causes AKI. In addition, NKT cells together with B cells play significant roles in experimental lupus nephritis in NZB/NZW F1 mice through their Th2 immune responses. Mouse NK cells are also assumed to be involved in various renal diseases, and there may be complementary roles shared between NKT and NK cells. Human CD56+ T cells, a functional counterpart of mouse NKT cells, also damage renal cells through a mechanism similar to that of mice. A subpopulation of human CD56+ NK cells also exert strong cytotoxicity against renal cells and contribute to the progression of renal fibrosis.

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Merluzzzi, Vincent J., Mark D. Smith, and Kathleen Last-Barney. "Similarities and distinctions between murine natural killer cells and lymphokine-activated killer cells." Cellular Immunology 100, no. 2 (July 1986): 563–69. http://dx.doi.org/10.1016/0008-8749(86)90054-7.

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