Ceramide-independent CD28 and TCR signaling but reduced IL-2 secretion in T cells of acid sphingomyelinase-deficient mice
| Autor: | Petra Bauer, Karl Deres, Wilhelm Stoffel, B. Stoffel, Michael Nix |
|---|---|
| Rok vydání: | 1998 |
| Předmět: |
Ceramide
T cell T-Lymphocytes Immunology Receptors Antigen T-Cell Ceramides Lymphocyte Activation chemistry.chemical_compound Mice CD28 Antigens medicine Superantigen Immunology and Allergy Animals Secretion Cells Cultured biology CD28 Receptors Interleukin-2 Molecular biology Mice Mutant Strains Mice Inbred C57BL medicine.anatomical_structure Sphingomyelin Phosphodiesterase chemistry Concanavalin A biology.protein Interleukin-2 Acid sphingomyelinase Signal transduction Lysosomes Spleen medicine.drug Signal Transduction |
| Zdroj: | European journal of immunology. 28(3) |
| ISSN: | 0014-2980 |
| Popis: | Ceramide generated by lysosomal acid sphingomyelinase (aSMase) has been proposed to contribute to CD28 co-stimulatory signaling pathways. We used an aSMase-deficient mouse line ( asmase − / − ) to elucidate the role of the aSMase in splenocytes stimulated with either a combination of anti-CD3 and anti-CD28 antibodies, the lectin concanavalin A (Con A) or the superantigen staphylococcal enterotoxin B. All stimuli were shown to induce IL-2 expression, Con A additionally triggered the expression of high-affinity IL-2 receptor. However, in asmase − / − mice secretion of IL-2 was significantly reduced, whereas the intracellular IL-2 levels were elevated. Proliferation of anti-CD3/anti-CD28 or Con A-stimulated aSMase-deficient splenocytes was reduced up to 50 % after 72 h in comparison to wild-type cells. We conclude that ceramide generated by aSMase is not involved in CD28 signal transduction, but rather a perturbation of the secretory system is responsible for the impaired proliferation of aSMase-deficient splenocytes. |
| Databáze: | OpenAIRE |
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