Interleukin-12 alone can not enhance the expression of the cutaneous lymphocyte associated antigen (CLA) by superantigen-stimulated T lymphocytes.
It has been reported that bacterial superantigens induce interleukin (IL)-12 dependent expression of the cutaneous lymphocyte associated antigen (CLA) and that this may be relevant to the association between certain skin diseases and infections including psoriasis and streptococcal tonsillitis. We have confirmed that the streptococcal pyrogenic superantigen C (SpeC) increases CLA expression by both CD4+ and CD8+ T cells when PBMCs are incubated in medium enriched with fetal calf serum (FCS). However, such an increase could not be induced in medium enriched with human serum (HS) even when recombinant IL-12 was added to the PBMCs cultures. Strikingly, CD4+ T cells incubated with SpeC in HS showed a marked reduction in CLA expression, which was not due to apoptosis. In contrast, SpeC did induce T cell proliferation and expression of CD25, CD54 and CD103 in the presence of HS indicating that the absence of SpeC induced CLA expression in HS was not due to SpeC inhibitors. Although addition of low amounts of lipopolysaccharide endotoxin (LPS) caused a highly significant increase in CLA expression in the absence of SpeC in cultures enriched with HS, a combination of LPS and SpeC did not increase CLA expression beyond that induced by LPS alone. The superantigen-induced CLA expression in FCS was partially inhibited by anti-IL-12 but not by anti-IL-18 or antibodies to transforming growth factor (TGF)-beta. It is concluded that IL-12 alone can not increase CLA expression but requires the help of other factor(s) present in FCS but not in HS. Although LPS can induce CLA expression it does not seem to be the factor that interacts with IL-12 to induce superantigen-mediated CLA expression in cultures enriched with FCS.
Sigmundsdóttir
H
H
Department of Immunology, Landspitali University Hospital, Reykjavik, Iceland.
Gudjónsson
J E
JE
Valdimarsson
H
H
D015703:Antigens, CD / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte; D000951:Antigens, Neoplasm; D001426:Bacterial Proteins; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D002455:Cell Division / Q000276:immunology; D002478:Cells, Cultured; D005098:Exotoxins / Q000276:immunology; D006801:Humans; D039001:Integrin alpha Chains / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D018664:Interleukin-12 / Q000276:immunology*; D008070:Lipopolysaccharides / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology*; D008562:Membrane Glycoproteins / Q000378:metabolism*; D008565:Membrane Proteins; D015375:Receptors, Interleukin-2 / Q000378:metabolism; D016201:Receptors, Lymphocyte Homing / Q000378:metabolism; D012867:Skin / Q000276:immunology; D018089:Superantigens / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*
D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D000951:Antigens, Neoplasm; D001426:Bacterial Proteins; C063419:CTAGE1 protein, human; D005098:Exotoxins; D039001:Integrin alpha Chains; D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D008565:Membrane Proteins; D015375:Receptors, Interleukin-2; D016201:Receptors, Lymphocyte Homing; C117980:SpeA protein, Streptococcus pyogenes; D018089:Superantigens; C091367:alpha E integrins; C027951:erythrogenic toxin; D018799:Intercellular Adhesion Molecule-1; D018664:Interleukin-12