Cytotoxic T lymphocytes (CTL) are present at high activities in adult patients infected with the human immunodeficiency virus (HIV). In this report, CTL effectors were identified in peripheral blood mononuclear cells (PBMC) of children born to HIV-1-infected mothers. These CTL killed HLA-matched HIV-1-infected H9 target cells or doubly transfected P815-A2-env, gag or nef mouse tumor cells, which expressed the viral antigens in association with HLA-A1/A3 or HLA-A2, respectively. HIV-1-specific CTL were detected early after birth (less than 2 months) and remained present during the asymptomatic phase of the infection. As in HIV-1-infected adults, HIV-specific CTL declined with disease progression. Surprisingly, HIV-1-specific CTL were detected in the PBMC of three children who subsequently became seronegative.

No abstract

Summary. Insulin receptors have been demonstrated in isolated rat intestinal epithelial cells. The specific binding of l:sI-insulin was time -and temperaturedependent, the optimal temperature of study being 15 ~ Dissociation of bound l:sI-insulin by an excess of unlabelled hormone was rapid and attained 66 + 2% in 2 h. When initiated by dilution, the dissociation attained 35 • 4% in 2 h, and 72 _ 1% in 2 h when 10 -7 mol/1 unlabeUed insulin was added. The pH optimum for the binding process was between 7.5 and 8, and the binding increased proportionally to cell protein concentration up to 1.5 mg/ml. Under standard conditions (2 h at 15 ~ the degradation of the labelled hormone in the medium accounted for 20-50% of total tracer, depending on the concentration of cells. At apparent equilibrium (2 h at 15~ unlabelled insulin in the range of 10-10 to 10 -7 mol/1 inhibited competitively the binding of 4.3-7 • 10 -11 mol/l ~:sI-insulin; fifty percent inhibition was obtained with 3 • 10 -9 mol/lnativeinsulin. Scatchard analysis, after correction for degradation, gave curvilinear plots, that may be explained by two orders of binding sites, with 2,000 • 200 sites/cell of high affinity (Ka = 2.2 • 0.2 • 1091/mol) and 39,000 • 3,000 sites/cell of low affinity (Ka = 5.6 • 1.6 • 1071/mol). The potency of proinsulin to compete with ~:sI-insulin for the binding site was 3% that of insulin, unrelated peptides were inactive. Such results give a molecular basis to different reports suggesting that the intestine could be a target-tissue for insulin.

No abstract