Lactate dehydrogenase-release assay: a reliable, nonradioactive technique for analysis of cytotoxic lymphocyte-mediated lytic activity against blasts from acute myelocytic leukemia - PubMed (original) (raw)
Lactate dehydrogenase-release assay: a reliable, nonradioactive technique for analysis of cytotoxic lymphocyte-mediated lytic activity against blasts from acute myelocytic leukemia
E Weidmann et al. Ann Hematol. 1995 Mar.
Abstract
Treatment of patients in remission of acute myelocytic leukemia using immunotherapy with interleukin 2 is a new approach to prolonging remission duration in this disease. As an important mechanism for the pathophysiology of eradication of residual myelocytic blast populations, activation of cytotoxic effector lymphocytes has frequently been discussed. However, the associated immunological research has been complicated to some extent, because in conventional chromium 51-release assays, blast cells frequently fail to incorporate sufficient amounts of 51Cr and/or spontaneously release high amounts of 51Cr. Recently, we established a culture system which promotes the outgrowth of cytotoxic T lymphocytes in bone marrow-derived mononuclear cells cultured in IL-2. To study cytotoxicity and the responsible mechanisms of the obtained T-cell lines and clones, we modified a previously described cytotoxicity assay, based on the release of lactate dehydrogenase (LDH-release assay) for use in cryopreserved blasts obtained from the bone marrow of patients with acute myelocytic leukemia. Using this assay, we were able to detect cytotoxicity of IL-2-activated peripheral blood lymphocytes from three healthy controls against a number of blast samples obtained from the bone marrow of patients with AML (up to more than 40% lysis at an effector target cell ratio of 20:1). However, a minority of AML blasts seem to be resistant to lysis by IL-2-activated lymphocytes. In bone marrow-derived T-cell lines from patients with AML we detected lytic activity against autologous blasts in three of seven cases tested by LDH release, ranging from 29 to 63% at an effector target ratio of 10:1. Additionally, T-cell clones with different phenotypes were established which were able to mediate cytotoxicity against autologous blast cells. Thus, cytotoxicity against freshly isolated blasts from patients with acute myelocytic leukemia can be analyzed reliably, reproducibly, and without the use of isotopes by the LDH-release assay.
Similar articles
- Bone marrow-derived T-cell clones obtained from untreated acute myelocytic leukemia exhibit blast directed autologous cytotoxicity.
Jahn B, Bergmann L, Weidmann E, Brieger J, Fenchel K, Schwulera U, Hoelzer D, Mitrou PS. Jahn B, et al. Leuk Res. 1995 Feb;19(2):73-82. doi: 10.1016/0145-2126(94)00119-u. Leuk Res. 1995. PMID: 7869744 - Culture of normal and leukemic bone marrow in interleukin-2: analysis of cell activation, cell proliferation, and cytokine production.
Klingemann HG, Neerunjun J, Schwulera U, Ziltener HJ. Klingemann HG, et al. Leukemia. 1993 Sep;7(9):1389-93. Leukemia. 1993. PMID: 8371589 - A novel nonradioactive CFDA assay to monitor the cellular immune response in myeloid leukemia.
Yang T, Chen ZZ, Kolb HJ, Buhmann R. Yang T, et al. Immunobiology. 2013 Apr;218(4):548-53. doi: 10.1016/j.imbio.2012.06.014. Epub 2012 Jul 2. Immunobiology. 2013. PMID: 22883564 Clinical Trial. - Activation of lymphocyte anti-tumour responses in man: effector heterogeneity and the search for immunomodulators.
Vose BM. Vose BM. Cancer Metastasis Rev. 1987;5(4):299-312. doi: 10.1007/BF00055375. Cancer Metastasis Rev. 1987. PMID: 3552279 Review.
Cited by
- Induction of anti B-cell malignance CTL response by subfamily-shared peptides derived from variable domain of immunoglobulin heavy chain.
Xiaoling G, Ying L, Jing L, Huifang L, Xia Z, Qingqing F, Ping Z. Xiaoling G, et al. Cancer Immunol Immunother. 2005 Nov;54(11):1106-14. doi: 10.1007/s00262-005-0696-z. Epub 2005 May 12. Cancer Immunol Immunother. 2005. PMID: 15889252 Free PMC article. - Feline adipose-derived mesenchymal stem cells induce effector phenotype and enhance cytolytic function of CD8+ T cells.
Taechangam N, Walker NJ, Borjesson DL. Taechangam N, et al. Stem Cell Res Ther. 2021 Sep 6;12(1):495. doi: 10.1186/s13287-021-02558-5. Stem Cell Res Ther. 2021. PMID: 34488876 Free PMC article. - Jadomycin breast cancer cytotoxicity is mediated by a copper-dependent, reactive oxygen species-inducing mechanism.
Hall SR, Blundon HL, Ladda MA, Robertson AW, Martinez-Farina CF, Jakeman DL, Goralski KB. Hall SR, et al. Pharmacol Res Perspect. 2015 Mar;3(2):e00110. doi: 10.1002/prp2.110. Pharmacol Res Perspect. 2015. PMID: 25729577 Free PMC article. - The preparation of HL-60 cells vaccine expressing BCG heat shock protein 70 and detection of its immunogenicity in vitro.
Li XL, Zhao YX, Sun LR, Yang J, Xu HJ. Li XL, et al. Hum Vaccin Immunother. 2012 Oct;8(10):1376-81. doi: 10.4161/hv.21321. Epub 2012 Aug 16. Hum Vaccin Immunother. 2012. PMID: 22894947 Free PMC article. - CD1d-expressing breast cancer cells modulate NKT cell-mediated antitumor immunity in a murine model of breast cancer metastasis.
Hix LM, Shi YH, Brutkiewicz RR, Stein PL, Wang CR, Zhang M. Hix LM, et al. PLoS One. 2011;6(6):e20702. doi: 10.1371/journal.pone.0020702. Epub 2011 Jun 13. PLoS One. 2011. PMID: 21695190 Free PMC article.
References
- Cancer Res. 1991 Nov 15;51(22):6153-62 - PubMed
- J Immunother (1991). 1992 Aug;12(2):123-31 - PubMed
- Cancer Res. 1991 Feb 1;51(3):964-8 - PubMed
- J Clin Immunol. 1981 Jan;1(1):51-63 - PubMed
- Leuk Res. 1995 Feb;19(2):73-82 - PubMed
MeSH terms
Substances
LinkOut - more resources
Other Literature Sources
Medical
Research Materials