| First Author | Koutník J | Year | 2022 |
| Journal | Cell Commun Signal | Volume | 20 |
| Issue | 1 | Pages | 54 |
| PubMed ID | 35440091 | Mgi Jnum | J:325482 |
| Mgi Id | MGI:7280981 | Doi | 10.1186/s12964-022-00864-w |
| Citation | Koutnik J, et al. (2022) Addressing the role of PKD3 in the T cell compartment with knockout mice. Cell Commun Signal 20(1):54 |
| abstractText | BACKGROUND: The Protein kinase D3 (PKD3) has been implicated in signal transduction downstream of the T cell receptor (TCR). However, its role for the activation of primary T lymphocytes has not been elucidated so far. METHODS: Expression of PKD isoforms in primary murine T cells was determined by RT-PCR and SDS-Page. A germline PKD3-knockout mouse line was analyzed for its immune response to OVA/alum intraperitoneal immunization. Phenotyping of the T cell compartment ex vivo as well as upon stimulation in vitro was performed by flow cytometry. Additionally, cytokine expression was assessed by flow cytometry, RT-PCR and Luminex technology. RESULTS: PKD expression in T cells is modulated by TCR stimulation, leading to a rapid down-regulation on mRNA and on protein level. PKD3-deficient mice respond to immunization with enhanced T follicular helper cell generation. Furthermore, peripheral PKD3-deficient CD4(+) T cells express more interleukin-2 than wild type CD4(+) T cells upon TCR stimulation ex vivo. However, purified naive CD4(+) T cells do not differ in their phenotype upon differentiation in vitro from wild type T cells. Moreover, we observed a shift towards an effector/memory phenotype of splenic T cells at steady state, which might explain the contradictory results obtained with pan-T cells ex vivo and naive-sorted T cells. CONCLUSION: While PKD3-deficiency in vivo in mice leads to a skewing of the T cell compartment towards a more activated phenotype, this kinase seems to be dispensable for naive CD4(+) T cell differentiation in vitro. Video Abstract. |
