| Literature DB >> 6241599 |
Abstract
Accessory cells are required for the activation of helper T cells. We have examined two characteristics of accessory cells, their expression of I-A, and their ability to release IL1. We provide evidence that these two properties are related, and postulate that membrane I-A molecules participate in the pathway leading to IL1-release. Experimental results are described relating I-A to IL1-release as follows: 1. In vitro-educated Ly1 T cells stimulate IL1-release from M phi; this process is H-2-restricted and blocked by anti-I-A antibodies. 2. H-2-restriction between T cells and M phi is overcome in the presence of ConA, but this unrestricted interaction is also blocked by anti-I-A. 3. LPS stimulation of IL1-release is blocked by anti-I-A. These findings suggested an active role for I-A molecules on IL1-producing cells. We next describe a series of experiments designed to assess the requirements for I-A versus IL1 during T cell activation. In a number of experimental systems, T cells demonstrated a requirement for I-A-recognition, but none that could not also be satisfied by IL1: 1. Generation of helper T cells in allogeneic chimeras. 2. Proliferation of KLH-primed lymph node cells. 3. Proliferation of KLH-primed lymph node cells from chronically anti-I-A-suppressed mice. 4. Proliferation of GAT-primed lymph node cells from nonresponder mice. These findings suggest that for many kinds of T cells (not necessarily all) the apparent requirement for I-A-recognition is primarily involved in stimulating IL1-release from accessory cells.Entities:
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Year: 1984 PMID: 6241599 DOI: 10.1016/S0171-2985(84)80112-6
Source DB: PubMed Journal: Immunobiology ISSN: 0171-2985 Impact factor: 3.144