Lipopolysaccharide‐Induced Mediators Assisting the Proliferative Response of C3H/HeJ Thymocytes to Concanavalin A

Abstract

Abstract3H-Thymidine uptake of thymocytes from LPS-responder

Lpsd/Ran of endotoxin-resistant C3H/HeJ mice is defective in mediating lipopolysaccharide endotoxin responses

“…This defect is expressed in a variety of ways. For example, C3H͞HeJ B cells do not proliferate or differentiate with LPS, their T cells are not stimulated by LPS to enhance polyclonal B cell responses, and thymocyte proliferation in response to Con A is not enhanced by LPS (2,3). Macrophage phagocytosis and cytotoxicity are not stimulated by LPS and the cytokines such as tumor necrosis factor (TNF), interleukin 1 (IL-1), colonystimulating factor (CSF), interferon (IFN), and prostaglandins stimulated by LPS in responder cells are not induced in C3H͞HeJ macrophages (4).…”

Restoration of lipopolysaccharide-mediated B-cell response after expression of a cDNA encoding a GTP-binding protein

“…This defect is specific and expressed in a variety of ways. For example, C3H/HeJ B cells do not proliferate or differentiate when exposed to LPS, and the proliferation of their thymocytes induced by concanavalin A is not enhanced by LPS (11,17,(24)(25)(26)(27)(28)(29). Macrophage phagocytosis and cytotoxicity are not stimulated by LPS, and the cytokines such as tumor necrosis factor, interferon, colony stimulating factor, and interleukin-1 (IL-1) and the prostaglandins stimulated by LPS in responder cells are not induced in C3H/HeJ macrophages (17).…”