Effective T-cell immune responses in the absence of the serine/threonine kinase RIP2
| Autor: | Chiara Nembrini, Manfred Kopf, Benjamin J. Marsland, Regina Reissmann |
|---|---|
| Rok vydání: | 2008 |
| Předmět: |
Cellular differentiation
medicine.medical_treatment T cell Immunology Receptors Antigen T-Cell CD8-Positive T-Lymphocytes Lymphocytic Choriomeningitis Biology Lymphocyte Activation Microbiology Interferon-gamma Mice Th2 Cells Immune system Receptor-Interacting Protein Serine-Threonine Kinase 2 medicine Animals Lymphocytic choriomeningitis virus Listeriosis Cell Proliferation Serine/threonine-specific protein kinase Mice Inbred BALB C T-cell receptor Cell Differentiation Th1 Cells Flow Cytometry Adoptive Transfer Coculture Techniques Cell biology Mice Inbred C57BL Infectious Diseases Cytokine medicine.anatomical_structure Receptor-Interacting Protein Serine-Threonine Kinases Cell activation CD8 Signal Transduction |
| Zdroj: | Microbes and Infection. 10:522-530 |
| ISSN: | 1286-4579 |
| DOI: | 10.1016/j.micinf.2008.01.016 |
| Popis: | The serine/threonine kinase RIP2 has been reported to be essential for Nod1 and Nod2 mediated cell activation, and has been suggested to play a role in the signaling cascade downstream of the T-cell receptor. We sought to ascertain the exact role of RIP2 in T-helper cell differentiation and CD8+ T-cell effector function in vivo and in vitro. In contrast to previous reports, we found that RIP2-deficient T cells did not exhibit impaired proliferation upon TCR engagement in vitro, and differentiation to cytokine producing Th1 or Th2 cells was normal in the absence of RIP2. These results were confirmed in vivo, as wild-type and RIP2-deficient virus-specific CD8+ T cells expanded comparably in mice after LCMV infection. Wild-type and RIP2-deficient CD4+ and CD8+ T cells from infected mice also showed similar proliferation and cytokine production when restimulated with full or partial agonist peptides ex vivo. Furthermore, no significant difference in adaptive T-cell responses could be observed between wild-type and RIP2-deficient mice after Listeria monocytogenes infection. Thus contrary to early reports, our data show that RIP2 is not an essential component of the TCR signaling machinery. |
| Databáze: | OpenAIRE |
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