In:
European Journal of Immunology, Wiley, Vol. 26, No. 12 ( 1996-12), p. 3066-3073
Abstract:
γδ T cell populations are known to expand in response to intracellular bacterial infectious agents regardless of previous priming. We have shown previously that soluble factor(s) produced by Mycobacterium ‐stimulated monocytes activate cord blood γδ T cells to proliferate. In this study, we investigated whether cytokines produced by monocytes are responsible for γδ T cell activation in vitro : interleukin (IL)‐1β, IL‐6, IL‐8, IL‐12, tumor necrosis factor (TNF)‐α and granulocyte/macrophage colony‐stimulating factor were examined. Recombinant human IL‐12 stimulated γδ T cells, but not αβ T cells in peripheral blood mononuclear cells, to express CD25 on their surfaces, and to expand in number in vitro . IL‐12‐primed γδ T cell numbers increased to a greater extent in the culture to which exogenous IL‐2 (5 U/ml) was added. Anti‐TNF‐α monoclonal antibody inhibited IL‐12‐induced up‐regulation of CD25 on γδ T cells, suggesting that endogenous TNF‐α may play a role in IL‐12‐induced activation of γδ T cells. Recombinant TNF‐α synergistically augmented IL‐12‐induced activation of γδ T cells. Furthermore, IL‐12 up‐regulated TNF receptors on γδ T cells in vitro : TNF‐α binding to its receptor induced CD25 expression on the γδ T cells in an autocrine or paracrine fashion, or perhaps both. It also became evident that both IL‐12 and TNF‐α were produced by mycobacterial lysate‐stimulated monocytes. Taken together, these results suggest that upon confrontation with mycobacterial organisms, γδ T cells can be quickly and antigen‐nonspecifically activated by soluble factors including IL‐12 and TNF‐α, both of which are produced by mononuclear phagocytes in response to mycobacterial organisms.
Type of Medium:
Online Resource
ISSN:
0014-2980
,
1521-4141
DOI:
10.1002/eji.1830261237
Language:
English
Publisher:
Wiley
Publication Date:
1996
detail.hit.zdb_id:
1491907-2
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