Annales de l'Institut Pasteur. Immunology最新文献

The influences of prostaglandin E2 (PGE2), 15-hydroxyeicosatetraenoic acid (15-HETE) and leukotrienes (LT) on the proliferative response of mature (PNA⁻) and immature (PNA⁺) mouse thymocytes was investigated. Both PNA⁺ and PNA⁻ thymocytes proliferated when cultured with concanavalin A plus interleukin-2. PGE2 in concentrations of 10⁻⁶ to 10⁻⁹ M caused significant inhibition of proliferation of both PNA⁺ and PNA⁻ thymocytes in these cultures. In contrast, the lipoxygenase products 15-HETE, LTB4, LTC4 and LTD4 caused marked increases in proliferation of PNA⁺ thymocytes while having no effect on PNA⁻ cells. Therefore, the effect of leukotrienes on thymocyte proliferation depends upon the level of cell maturation and mainly affects immature PNA⁺ thymocytes.

Two different BALB/c IgMk polyspecific monoclonal natural autoantibodies E7 and D23 were administered to neonatal BALB/c mice. When adults, these mice were immunized and challenged with calf myosin, BALB/c actin, human transferrin, calf thymus DNA or TNP-coupled bovine serum albumin (TNP/BSA), in complete Freund's adjuvant. The levels of serum antibody were evaluated by enzyme immunoassay.

No differences in anti-actin, anti-transferrin and anti-DNA antibody titres were noted between control and antibody-treated mice. However, anti-myosin antibody titres significantly increased in mice treated with either the E7 or D23 antibody, and anti-TNP antibody titres significantly decreased in mice treated with E7 but not with D23. These differences persisted after antigenic challenge and involved only the IgG response of treated mice. These results suggest that polyspecific natural autoantibodies may be involved in the regulation of the humoral immune response.

An anti-Klebsiella pneumoniae K5a capsular polysaccharide vaccine was evaluated as a preventive approach for protecting squirrel monkeys, Saimiri sciureus, in our breeding colony. Based on an 8-month vaccination schedule over a period of more than two years, this vaccine, regardless of the animal's age, resulted in a reduction of this particular bacterial infection and its generally associated fatal outcome. IgG antibody responses in naive and vaccinated animals were monitored over an extended period by radioimmunoassay and showed a marked increase above the initial naturally occurring antibody titres. No side-effects were observed after repeated vaccination of several hundred animals during a two-year period.

In this study, we used preparations highly enriched in human natural killer (NK) cells to further characterize the mechanism of taget-cell-induced NK inactivation. Highly enriched populations of NK cells were obtained by a newly developed, single-step sheep red blood cell rosette assay. This method, which did not require any incubation steps to facilitate cell contact, permitted a rapid and efficient isolation if NK cells from adherent-cell-depleted peripheral blood lymphocytes. The non-rosetted cells had high NK activity, possessed large granular lymphocyte (LGL) morphology and expressed the NK-associated antigens Leu-11a, Leu-7, OKM1 and NKH-1. In contrast, the rosetted cells had significantly lower NK activity, possessed typical lymphocyte morphology and expressed the T-cell-associated marker OKT3.

Next, we examined the ability of these NK-enriched effector cells (EC_c) to become inactivated by K562. Functional studies revealed that EC_c lost $\text{≥95\%}$ of their lytic capacity following incubation with K562 at a ratio of 2/1 for 6 h. However, to achieve this level of inactivation, it was essential that the cell suspension be gently mixed every 90–120 min. Inactivation was not due to cell death and did not reflect changes in the percentages of cells bearing the Leu-11a, Leu-7, OKM1 and NKH-1 antigens, but was associated with an increase in cell surface concentration of OKM1. As judged by gross morphology, the percentages of LGL in EC_c before and after treatment with K562 were essentially the same. Finally, K562-treated EC_c also lost their ability to mediate antibody-dependent cellular cytotoxicity (ADCC), suggesting that both NK-cell-mediated cytotoxicity and ADCC may involve a common lytic pathway.