Modulation of superantigen‐induced T‐cell deletion by antibody anti‐Pgp‐1 (CD44)

• Published in: Immunology 1996-02, Vol.87 (2), p.191-197
• Main Authors: AYROLDI, E., CANNARILE, L., RICCARDI, C.
• Format: Article
• Language: English
• Subjects: Animals; Antibodies, Monoclonal - immunology; Apoptosis - immunology; CD2 Antigens - immunology; CD3 Complex - immunology; Cell Culture Techniques; Enterotoxins - immunology; Flow Cytometry; Hyaluronan Receptors - immunology; Lymphocyte Activation; Mice; Mice, Inbred C3H; Precipitin Tests; Solubility; Superantigens - immunology; T-Lymphocyte Subsets - immunology; T-Lymphocyte Subsets - physiology
• ISSN: 0019-2805; 1365-2567
• DOI: 10.1046/j.1365-2567.1996.466540.x

We examined the effects of anti‐Pgp‐1 (CD44) antibody on the in vitro deletion of murine CD4 and CD8 single positive T cells induced by Staphylococcal enterotoxin B (SEB). Soluble anti‐Pgp‐1 antibody enhanced the apoptosis and decreased the proliferation of SEB‐responding T cells. In contrast, cross‐linked anti‐Pgp‐1 antibody provided costimulatory signals for the T‐cell activation induced by anti‐CD3 antibody. Hyaluronic acid (HA), a ligand of Pgp‐1, did not affect proliferation and deletion induced by SEB, whereas it mimicked the effects of the cross‐linked antibody in anti‐CD3‐driven proliferation. T‐cell Pgp‐1 surface expression after 48 hr incubation with SEB was unchanged as compared to unstimulated cells. However, when the memory T cells were established, some Vβ8+ (SEB‐specific) T cells Pgp‐1low became Pgp‐1high, displaying a bimodal character. Moreover, the Pgp‐1 increased expression correlated with an increase of Pgp‐1 soluble form in the supernatant. These findings suggested that signals following the triggering of the Pgp‐1 molecule are important in controlling T‐cell survival.