Interleukin-2 production in Brown-Norway rats with HgCl2-induced autoimmune disease: paradoxical in vivo versus in vitro findings.
In autoimmune diseases, mitogen-induced IL-2 production in vitro is generally considered to be diminished despite evidence of lymphoid hyperactivity in vivo. HgCl2 is known to cause T-dependent polyclonal B cell activation in Brown-Norway (BN) rats, resulting in autoimmune disease. We show here that the IL-2 producing capacity of cells from HgCl2-treated BN rats is low, but that HgCl2 treatment in vitro (10(-7) M) enhances IL-2 production of normal BN splenocytes. Lewis (LEW) rats are resistant to HgCl2-induced autoimmune disease. HgCl2 treatment of these rats in vivo does not significantly decrease the IL-2 production of their splenocytes. However, HgCl2 treatment of normal LEW splenocytes in vitro enhances their IL-2 production but this requires an HgCl2 concentration ten times greater (10(-6) M) in LEW than in BN rats. These findings are discussed in an attempt to resolve the paradox between the in vivo immune hyperactivity seen in HgCl2-treated BN rats, and the apparently low IL-2 production of their splenocytes in vitro.
Baran
D
D
Inserm U28-Hôpital Broussais, Paris, France.
Lantz
O
O
Dosquet
P
P
Sfaksi
A
A
Druet
P
P
D000818:Animals; D001327:Autoimmune Diseases / Q000139:chemically induced / Q000276:immunology*; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D003208:Concanavalin A / Q000494:pharmacology; D007376:Interleukin-2 / Q000096:biosynthesis*; D007700:Kinetics; D008213:Lymphocyte Activation / Q000187:drug effects; D008214:Lymphocytes / Q000276:immunology; D008297:Male; D008627:Mercuric Chloride / Q000494:pharmacology; D051381:Rats; D011914:Rats, Inbred BN; D011917:Rats, Inbred Lew; D013154:Spleen / Q000276:immunology
D007376:Interleukin-2; D003208:Concanavalin A; D008627:Mercuric Chloride