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Human T Lymphocyte Clones: Influence of Culture Conditions and Optimization of Proliferative Assays
Author(s) -
LUNDIN K. E. A.,
BOSNES V.,
GAUDERNACK G.
Publication year - 1989
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1989.tb01191.x
Subject(s) - biology , lymphokine , immunology , interleukin 2 , transfection , autocrine signalling , antigen , peripheral blood mononuclear cell , cell culture , lymphocyte , lymphoblast , t lymphocyte , microbiology and biotechnology , cytokine , in vitro , genetics
Many CD4 + human T lymphocyte clones (TLC) are found not to proliferate against appropriate stimulating cells, and many lose this capacity during culture. This may be due, not to a defect in the recognition of the antigen, but to an inability to produce sufficient amounts of interleukin 2 (IL‐2) for autocrine growth, since specific HLA‐restricted proliferative responses could be induced in ‘non‐proliferative’ clones by the addition of exogenous IL‐2 or phorbol myristate acetate (PMA). Of various factors tested during expansion procedures of the clones, the proliferative capacity could only be restored by changing the stimulatory cells from B lymphoblastoid cell lines (B‐LCL) to peripheral blood mononuclear cells (PBM). The cytotoxicity of the TLC was found to be independent of its proliferative capacity. After restoration of the proliferative capacity, a mouse B lymphoma cell line transfected with the appropriate HLA DQA and DQB genes was still not able to induce proliferation in the absence of exogenous IL‐2. We conclude that (1) ‘non‐proliferative’ TLC may recognize their targets, but fail to proliferate due to temporary lack of IL‐2 production, and (2) even ‘proliferative’ T cells may fail to respond to certain target cells carrying the specific antigen, such as a murine transfectant, in the absence of exogenous IL‐2.