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W Ptak

Publications and source records attributed to W Ptak.

At least 163 records · Page 9Linked to original sources
PubMedDate not supplied

A role for platelet release of serotonin in the initiation of contact sensitivity.

Finding contact sensitivity (CS) responses that were fairly normal in ear swelling, and in serotonin (5-HT) dependence in mast-cell-deficient mice, led to experiments to determine whether platelets supplemented mast cells as a source of 5-HT in CS. Severe depletion of platelets, and consequently blood 5-HT, with antiplatelet antibody, strongly inhibited CS, especially in mast-cell-deficient mice, suggesting that platelets supplemented mast cells. Furthermore, human platelets sensitized in vitro with anti-(tri-nitro-phenyl) IgE, and transferred intravenously together with isolated late-acting effector T cells, provided CS initiation due to local 5-HT release. Similar, IgE-dependent in vitro release of 5-HT was C dependent. These findings establish the importance of antigen-specific platelet release of 5-HT in CS initiation.

Amphetamine↗
PubMedDate not supplied

Gamma/delta T cells from tolerized alpha/beta-TCR-deficient mice antigen specifically inhibit contact sensitivity in vivo and IFN-gamma production in vitro.

Contact sensitivity (CS) responses to reactive hapten antigens (Ag), such as picryl chloride, are classical examples of T-cell-mediated immune responses in vivo. There is also abundant evidence that T cells exposed in vivo to high intravenous doses of Ag can downregulate CS (high-dose Ag tolerance). To clarify cell types that effect CS and mediate its downregulation, we have studied CS in mice congenitally deficient in alpha/beta T cells (alpha-/- mice). We show that alpha-/- mice cannot mount CS, implicating alpha/beta T cells as critical CS effector cells. However, after high-dose Ag tolerization, these alpha-/- mice can downregulate alpha/beta CS effector cells adoptively transferred to them. The active cells in tolerized alpha-/- mice are gamma/delta TCR+ cells which downregulate CS effector alpha/beta T cells Ag-specifically upon adoptive cell transfer. Moreover, gamma/delta cells can Ag-specifically downregulate IFN-gamma production by CS effector cells in vitro. These findings establish that gamma/delta T cells are not CS effector cells but downregulate CS, in agreement with recent reports that gamma/delta T cells downregulate IgE responses.

Animals↗
PubMedDate not supplied

Positive regulatory gamma delta T cells in contact sensitivity: augmented responses by in vivo treatment with anti-gamma delta monoclonal antibody, or anti-V gamma 5 or V delta 4.

Contact sensitivity (CS) responses, induced by skin painting with reactive haptens like picryl chloride or oxazolone, are classical examples of in vivo immunity mediated by alpha beta T cells. Our previous studies showed that gamma delta T cells were required to assist the alpha beta CS-effector T cells in the successful adoptive cell transfer of CS responses. These spleen and lymph node-derived gamma delta+ CS-assisting regulatory cells were CD3+, CD4-CD8+, non-antigen-specific, and non-MHC-restricted, and preferentially expressed V gamma 5 and V delta 4 variable regions. In the current study we show that systemic treatment of mice in vivo with anti-gamma delta mAb, produced a similar positive influence on CS responses in two different systems: i.e. active sensitization, or adoptive cell transfer. In addition to augmented CS responses produced by treatment with pan anti-gamma delta TCR mAb, anti-gamma delta-V region mAb were examined, and augmentation of CS also was produced by anti-V gamma 5 and anti-V delta 4 mAb, the V regions determined previously to be preferentially expressed on gamma delta CS-assisting cells. We speculate that the positive influence of anti-gamma delta mAb was not caused by quantitative changes in gamma delta T cells, because FACS studies demonstrated a lack of in vivo depletion of peripheral blood and lymphoid gamma delta T cells, and also no depletion of epidermal dendritic gamma delta T cells (DETC), in mice treated with anti-gamma delta TCR mAb. Instead, our data favor the hypothesis that CS-assisting gamma delta T cells can be activated in vivo by anti-gamma delta TCR mAb interacting with their gamma delta TCR, at least with the short term protocols we employed, resulting in augmentation of CS responses perhaps by releasing positively-acting factors, such as certain cytokines.

Adoptive Transfer↗