1887

Abstract

Trehalose 6,6′-dimycolate (TDM), an immunomodu- lator, potentiates non-specific resistance in mice to influenza virus infection. When mice were injected intravenously with TDM, the striking proliferation of a minority of T-lymphocytes bearing gamma/delta T-cell receptors ( T-cells) that accumulated in granulomatous lungs was thought to be associated with the maintenance of acquired resistance to lethal influenza virus infection. To clarify the cellular basis of the defence against influenza virus, mice were depleted of T-cells, alpha/beta (ap) T-cells, or natural killer (NK) cells by administration of corresponding antibodies prior to influenza virus infection. The depletion of T-cells significantly abrogated the augmented resistance of TDM- treated mice to infection, as did depletion of either α T-cells or NK cells. To gain insight into the functional ability of T-cells, we evaluated the cytotoxic activity ofthisT-cell subset againsta panel of target cell lines that were stably transfected with the influenza virus haemagglutinin (HA) gene from A/PR/8/34(H1N1) and A/Aichi/2/68(H3N2) strains. The T-cells from TDM-treated mice showed profound cytotoxicity against the target cells expressing HA of either the H1 or H3 subtype, in a non-major histocompatibility complex-restricted manner. Taken together, these results indicate that T-cells play a non-specific role, in conjunction with α T-cells and NK cells, in protecting mice against influenza virus infection, and that the recognition and destruction of HA-expressing target cells by the activated T-cells is one of the steps involved in this anti-influenza virus immuno- surveillance.

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1997-07-01
2022-05-23
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