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Interaction between oligodendroglia and immune cells: Mitogenic effect of an oligodendrocyte precursor cell line on syngeneic T lymphocytes
Author(s) -
Yamamura T.,
Sun D.,
Aloisi F.,
Klinkert W. E. F.,
Wekerle Hartmut
Publication year - 1992
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490320207
Subject(s) - oligodendrocyte , immune system , microbiology and biotechnology , precursor cell , cell culture , biology , cell , chemistry , immunology , neuroscience , central nervous system , myelin , genetics
We analyzed cellular interactions between T lymphocytes and a recently established immortal glial line, L3 that retains several properties of immature oligo‐dendrocytes (Aloisi et al., J Neurosci Res 27:16–24, 1990). L3 oligodendrocytes (L3‐OL) cannot be induced to express class II antigens, nor do they specifically present antigen to syngeneic specific T lymphocyte. However, L3‐OL strongly enhance the proliferation of freshly activated, interleukin‐2(IL‐2)‐dependent T‐line lymphocytes and concanavalin A (ConA)‐activated lymphoblasts, irrespective of their antigen specificity or surface phenotype (CD4 + or CD8 + ). Resting and some activated T cells were susceptible to the mitogenic effect of L3‐OL only in the presence of exogenous IL‐2, not of other cytokines. The mitogenic effect of L3‐OL did not depend on cell viability. It was observed in paraformaldehyde‐fixed L3‐OL cells and in membrane preparations, but not in culture supernatant. Neither intact L3‐OL cells nor membrane preparations had direct IL‐2 activity. The conclusion that the mitogenic effect of L3‐OL cells is exerted by membrane structures acting as a costimulatory factor(s) of IL‐2 is supported by the finding that it is largely blocked by a monoclonal anti‐IL‐2 receptor antibody. The effect is distinct from membrane‐bound IL‐1, membrane‐bound tumor necrosis factor‐α (TNF‐α), IL‐3, or IL‐6 and cannot be reconstituted by these cytokines. © 1992 Wiley‐Liss, Inc.