For many years the study of cellular immunology was impeded by the inability to propagate and expand homogeneous populations of antigen-specific lymphocytes in vitro. In the mid-1970's, Kohler and Milstein (1, 2) developed a technique that allowed the immortalization of antigen-specific B cells by fusing them to transformed and spontaneously proliferating myeloma cells, thereby producing B cell hybridomas . Hybridoma technology was subsequently applied to T lymphocytes, providing a convenient source of T cells for in vitro study (3)(4)(5), and the establishment of antigen-specific T cell hybridomas made it possible to analyze the requirements for antigenic stimulation in model systems (6). Murine antigenspecific T cell hybridomas are commonly prepared by using polyethylene glycol to fuse antigen-primed T cell blasts to the spontaneously proliferating AKRderived thymoma, BW5147 . These T cell hybridomas can be tested for their ability to respond to the antigen used to prime the normal lymphocyte fusion partner, and the cells that exhibit the appropriate specificity can be cloned and expanded to large numbers.For normal T lymphocytes, occupancy of the antigen receptor usually results in a complex series of activation events that include expression of new cell surface receptors, production of lymphokines, and entry of the cell into its growth cycle (7) . This last response is not pertinent when using T cell hybridomas, because they are spontaneously proliferating cells. Therefore, the approach that has generally been used to assess the result of antigen receptor occupancy of T cell hybridomas is to quantitate their production of lymphokines, typically IL-2 (6). In recent years it has become evident that the occupancy of a variety of receptors that typically promote growth in normal cells, e.g., occupancy of receptors for epidermal growth factor (8), transforming growth factor ,B (9), and even IL-2 (10, 11), can inhibit the growth of certain transformed cells. We therefore undertook an analysis of the effect of antigen-mediated activation upon the growth of murine T cell hybridomas . We found that stimulation with antigen resulted in a dose-dependent decrease in both [sH]thymidine incorporation and cell growth . This phenomenon displayed the same ligand-specificity as did IL-2 production, as demonstrated by its requirement for a specific allelic form of the la molecule, anticlonotypic (i.e., anti-antigen receptor) antibody blocking exper-
This study describes a male patient with human immunodeficiency virus infection, grade IV-C (oropharyngeal moniliasis and Pneumocystis carinii pneumonia), associated with visceral involvement produced by Leishmania braziliensis which was identified by deoxyribonucleic acid hybridization after the polymerase chain reaction had been performed. The patient was treated with molgramostim in association with meglumine antimonate to enhance macrophage destruction of parasites.
The aim of this study was to develop a model of inflammatory bowel disease (IBD) induced by colonic application of 2,4-dinitrofluorobenzene in previously sensitized BALB-c mice. During the follow-up period of 30 days we observed ulcerations, haemorrhage, necrosis, and mononuclear infiltration in the colonic mucosa of previously sensitized (experimental) and, to a lesser extent, nonsensitized (control) animals. In addition, the animals in the experimental group developed adhesions, thickening of colonic segments, stenosis, and dilatation of the colon, and some animals also developed megacolon. Oedema, mononuclear infiltration, and superficial ulcerations were observed in the ileum of experimental animals and, to a lesser extent, in the control group. In addition, the animals in the experimental group developed extraintestinal changes in the liver and spleen (that is, pericholangitis and lymphofollicular proliferation). We suggest that this model of IBD may have some value for the study of early pathogenetic mechanisms of IBD and for developing new therapeutic modalities for this condition.
Bleomycin alone is not a good starting agent for EKS, whereas ABV seems to be a good choice, because it can produce an acceptable palliation of advanced EKS without major toxicity.
This study estimated the frequency of nine primitive reflexes (PR) and assessed their possible clinical value in a group of patients with acquired immunodeficiency syndrome. We studied 78 patients with human inmunodeficiency type 1 (HIV-1) infection in WHO clinical stage 3 or 4 and 81 matched seronegative controls. All participants were examined using a standardized neurological examination and the Mini-Mental State Examination. Cognitive impairment and PR was found in 36% of patients but in none of the controls (P<0.0001; logistic regression odds ratio: 14.7). Overall, PR were 2-36 times more frequent in patients with HIV-1 infection. This association was stronger for the glabellar, snout, Rossolimo, and digital signs. At least two PR were observed in 92% of patients vs. 8% of controls (P<0.0001; 95% confidence interval: 68%-100%; logistic regression odds ratio: 10.8). These data support the association of PR with cognitive decline in patients with advanced HIV-1 infection without overt neurological disease. Larger follow-up studies with multivariate techniques are needed to identify which PRs are useful as indicators of HIV-1-associated cognitive/motor complex and minor neurocognitive disorders.
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