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B E Torbett

Publications and source records attributed to B E Torbett.

40 records · Page 3Linked to original sources
PubMed1988

Cloned cytotoxic T lymphocytes as target cells. II. Polarity of lysis revisited.

The original polarity of lysis experiments suggested that CTL are themselves sensitive to whatever mechanism it is that CTL use to lyse their targets. This concept has placed certain limitations on possible mechanisms of lysis by CTL. Recently, we found in studies with cloned CTL as targets that cloned CTL are in fact highly resistant to lysis by other CTL, as well as to their cytotoxic granule proteins. We show here that although cloned CTL are extremely resistant to lysis by primary and cloned CTL, they are readily inactivated functionally by all primary CTL and by at least one CTL clone. Moreover, cloned CTL are also functionally inactivated by cytotoxic granule proteins. The activation of CTL, which we call inhibitin, is Ca2+ insensitive and distinct from hemolytic activity, and is, thus, unlikely to be perforin. These experiments suggest a possible alternative interpretation of the original polarity of lysis experiments.

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PubMed1988

The role of accessory molecules in T-helper activation induced by antigen, lectin, or CD3 antibodies.

We examined the role of L3T4 and LFA-1 molecules in T-helper-cell activation, under conditions where the physical stability of T helper-accessory cell interactions was not an issue. T-helper hybridomas were activated by accessory cells coated either with concanavalin A (Con A) or with CD3 antibodies. Activation of the T helper cells was measured by microtubule-organizing center (MTOC) reorientation as an early activation event, and by interleukin-2 (IL-2) production as an indication of a fully matured response. Both parameters were strongly blocked by L3T4 and LFA-1 antibodies in the case of Con A activation. In the case of stimulation with accessory cell-bound CD3 antibody, activation was blocked by LFA-1 but not L3T4 antibody. These results support the notion that L3T4 and LFA-1 molecules play more than a simple adhesion role in T-cell activation. The differential effect of L3T4 antibody in the case of Con A activation vs CD3 activation is consistent with the possibility that L3T4 and the alpha/beta portions of the T-cell receptor must interact during antigen- and lectin-stimulated T-cell activation.

Animals↗
PubMed1986

Multiple pathways for antigen-independent activation of a T helper hybridoma.

An important question in mitogen activation of T cells is whether the T cell must interact with a major histocompatibility complex product during the activation process. The T helper hybridoma AODH 7.1 is specific for human gamma globulin in the context of IEd, and when activated secretes interleukin 2. The mitogen concanavalin A (Con A) can activate AODH 7.1 cells directly, but two other standard T cell mitogens, phytohemagglutinin (PHA) and neuraminidase-galactose oxidase, cannot. However, Con A, PHA and neuraminidase-galactose oxidase could all activate AODH 7.1 when presented on various cloned class II+ cell lines. There was an absolute requirement for the presentor cell to be class II+, and the activation signal on mitogen-treated class II+ presentor could be blocked by monoclonal antibody to the class II antigens. To determine if class II molecules were absolutely required for the presentation of a mitogen activation signal we used class II- LtK- L cells and two LtK- cell class II gene transformants as presentor cells. Only the class II+ transformants, but not the class II- LtK- cells, could present either Con A or PHA. The class II requirement cannot be bypassed through provision of soluble factors. However, when Con A was used to activate AODH 7.1 cells directly, it appeared to be acting in a transmembrane fashion. It was not the case that AODH 7.1 cells were responding to Con A on a neighboring AODH 7.1 cell, and no class II antigens were involved. These results are consistent with the idea that different routes of activation exist for T cells, at least at the level of signal recognition.

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