NDLI: Activation signals leading to proliferation of normal and leukemic CD3+ large granular lymphocytes

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Activation signals leading to proliferation of normal and leukemic CD3+ large granular lymphocytes

Content Provider	Scilit
Author	Aprile, Ja Russo, M. Pepe, Ms Loughran, Tp Jr
Copyright Year	1991
Description	The activation signals leading to proliferation of normal and leukemic CD3+ large granular lymphocytes (LGL) were studied in vitro. Anti-CD3 monoclonal antibody (MoAb) alone (P less than .01) and recombinant interleukin-2 (IL-2) alone (P less than .01) caused significant stimulation of peripheral blood mononuclear cells (PBMC) from four CD3+ LGL leukemia patients, as measured in a 3H-thymidine incorporation assay. Recombinant interleukin-4 (IL-4) alone had no effect (P = .11). The combination signals of anti-CD3 MoAb and either IL-2 or IL-4 produced a proliferative response greater than anti-CD3 MoAb alone (P less than .01) or lymphokine alone (P less than .01). Leukemic LGL, purified by two-color sorting, were subsequently activated by anti-CD3 MoAb and IL-2 and assessed for DNA content by viable Hoechst No. 33342 (HO) staining. Results of these studies demonstrated that leukemic LGL were stimulated directly by anti-CD3 MoAb and IL-2, with the percentage of cells in cell cycle (S + G2/M) ranging from 16% to 72%. Normal CD3+ LGL were also stimulated to enter the cell cycle by anti-CD3 and IL-2. These results show that leukemic LGL proliferate in vitro after activation through the T-cell receptor and/or lymphokine.
Related Links	https://ashpublications.org/blood/article-pdf/78/5/1282/606364/1282.pdf
Ending Page	1285
Page Count	4
Starting Page	1282
DOI	10.1182/blood.v78.5.1282.1282
Journal	Blood
Issue Number	5
Volume Number	78
Language	English
Publisher	American Society of Hematology
Publisher Date	1991-09-01
Access Restriction	Open
Subject Keyword	Hematology Research and Experimental Medicine Antibody Lymphocytes Signals Lgl Recombinant Granular Viable Anti Cd3 Leukemic Journal: Blood (Vol- 82, Issue- 5)
Content Type	Text
Resource Type	Article

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