Histone deacetylase 1 controls CD4⁺ T cell trafficking in autoinflammatory diseases.
Hamminger P, et al … and Ellmeier W. (2021). J Autoimmun. 119:102610. doi: 10.1016/j.jaut.2021.102610 PubMed link
CD4⁺ T cell trafficking is a fundamental property of adaptive immunity. In this study, we uncover a novel role for HDAC1 in controlling effector CD4⁺ T cell migration, thereby providing mechanistic insight into why a T cell-specific deletion of HDAC1 protects against experimental autoimmune encephalomyelitis (EAE).

The histone deacetylases 1 and 2 restrain CD4⁺ cytotoxic T lymphocyte differentiation.
Preglej T, et al … and Ellmeier W. (2020). JCI Insight. 5(4):e133393. doi: 10.1172/jci.insight.133393. PubMed link
Some effector CD4⁺ T cell subsets display cytotoxic activity, thus breaking the functional dichotomy of CD4⁺ helper and CD8⁺ cytotoxic T lymphocytes. Here we show that levels of histone deacetylases 1 and 2 (HDAC1-HDAC2) are key determinants of CD4⁺ CTL differentiation.

The transcription factor MAZR/PATZ1 regulates the development of FOXP3⁺ regulatory T cells.
Andersen L et al … and Ellmeier, W (2019). Cell Rep. 29(13):4447-4459.e6. doi: 10.1016/j.celrep.2019.11.089 PubMed link
FOXP3⁺ Treg cells are essential for maintaining tolerance and immune homeostasis. Here we reveal that MAZR and its expression levels play a key role in controlling Treg cell development and differentiation.

A T cell-specific deletion of HDAC1 protects against experimental autoimmune encephalomyelitis.
Göschl L, et al … and Ellmeier W. (2017). Journal of Autoimmunity, pii: S0896-8411(17)30595-4. doi: 10.1016/j.jaut.2017.09.008. PubMed link
Here were report that HDAC1 function in T cells is important for the development of experimental autoimmune encephalomyelitis. These data suggest that selective inhibition of HDAC1 might be a novel treatment strategy for multiple sclerosis.

CD4 T cell lineage integrity is controlled by the histone deacetylases HDAC1 and HDAC2.
Boucheron, N, Tschismarov, R, et al … and Ellmeier, W.* (2014). Nature Immunology, 15(5):439-48. PubMed link
Here we revealed am unexpected plasticity of CD4+ T cells towards the cytotoxic lineage. We demonstrate that HDAC1 and HDAC2 are essential to maintain the integrity of CD4⁺ T cells by repressing repressing Runx-CBFβ complexes that otherwise induce a CD8⁺ effector T cell-like program in CD4⁺ T cells.

The zinc-finger protein MAZR is part of the transcription factor network that controls the CD4 versus CD8 lineage fate of double-positive thymocytes.
Sakaguchi S, et al … and Ellmeier, W. (2010). Nature Immunology, 11:442-8 (selected in News & Views section – Nat Immunol 11, pages 370–371 (2010); see picture at the right). PubMed link
Here we identified that MAZR regulates CD8 lineage differentiation by repressing ThPOK in MHC class I-signaled DP thymocytes.