How T cells go rogue in the absence of Roquins.

  title={How T cells go rogue in the absence of Roquins.},
  author={Abdalla Akef and S. Muljo},
  journal={Non-coding RNA investigation},
Roquin-1 and Roquin-2 are RNA-binding proteins essential for modulating T cell activity. Indeed, Roquin dysfunction has been linked to autoimmunity in mice. Essig and colleagues (2017) determine their functions in Foxp3+ T regulatory cells and uncover novel mechanisms of Roquin-mediated regulation of its target mRNAs (1). 
2 Citations
Deiminated proteins in extracellular vesicles and serum of llama (Lama glama)—Novel insights into camelid immunity
This is the first report of deiminated proteins in serum and EVs of a camelid species, highlighting a hitherto unrecognized post-translational modification in key immune and metabolic proteins in camelids, which may be translatable to and inform a range of human metabolic and inflammatory pathologies. Expand
How T cells go rogue in the absence of Roquins.
Roquin-1 and Roquin-2 are RNA-binding proteins essential for modulating T cell activity and their functions in Foxp3+ T regulatory cells are determined and novel mechanisms of Roquinmediated regulation of its target mRNAs are uncovered. Expand


Loss of Roquin induces early death and immune deregulation but not autoimmunity
Deletion of Roquin in T or B cells, or in the entire hematopoietic system of mice, alters immune homeostasis but does not result in autoimmunity.
Roquin-2 shares functions with its paralog Roquin-1 in the repression of mRNAs controlling T follicular helper cells and systemic inflammation.
The Roquin family emerges as a posttranscriptional brake in the adaptive and innate phases of antibody responses, ameliorating autoantibody-induced arthritis. Expand
Roquin represses autoimmunity by limiting inducible T-cell co-stimulator messenger RNA
A newly discovered pathway that prevents autoimmunity by limiting the levels on T lymphocytes of a co-stimulatory receptor, the inducible T-cell co- Stimulator (ICOS), is defined and the therapeutic potential of partially antagonising the ICOS pathway is highlighted. Expand
Roquin paralogs 1 and 2 redundantly repress the Icos and Ox40 costimulator mRNAs and control follicular helper T cell differentiation.
Roquin-1 and Roquin-2 proteins redundantly repressed the mRNA of inducible costimulator (Icos) and identified the Ox40 costimulatory receptor as another shared mRNA target and combined acute deletion increased Ox40 signaling, as well as Irf4 expression, and imposed Tfh differentiation on CD4(+) T cells. Expand
Structural basis for RNA recognition in roquin-mediated post-transcriptional gene regulation
It is shown that the N-terminal ROQ domain from mouse roquin adopts an extended winged-helix fold, which is sufficient for binding to the constitutive decay element (CDE) in the Tnf 3′ UTR. Expand
Attenuation of AMPK signaling by ROQUIN promotes T follicular helper cell formation
It is reported that ROQUIN has a paradoxical function on Tfh differentiation mediated by its RING domain: mice with a T cell-specific deletion of the ROQ domain have unchanged Th1, Th2, Th17, and Tregs during a T-dependent response but show a profoundly defective antigen-specific T fh compartment. Expand
Roquin recognizes a non-canonical hexaloop structure in the 3′-UTR of Ox40
Crystal structures and NMR data show that the Roquin-1 ROQ domain recognizes hexaloops in the SELEX-derived ADE and in an ADE-like variant present in the Ox40 3′-UTR with identical binding modes. Expand
Roquin binds microRNA-146a and Argonaute2 to regulate microRNA homeostasis
It is shown that Roquin enhances Dicer-mediated processing of pre-miR-146a, a microRNA that targets Icos mRNA, and emerges as a protein that can bind Ago2, miRNAs and target mRNAs, to control homeostasis of both RNA species. Expand
Roquin binds inducible costimulator mRNA and effectors of mRNA decay to induce microRNA-independent post-transcriptional repression
In helper T cells, roquin localized to processing (P) bodies and downregulated ICOS expression, and showed an intrinsic preference for a previously unrecognized sequence in the 3′ untranslated region (3′ UTR). Expand
Roquin Suppresses the PI3K‐mTOR Signaling Pathway to Inhibit T Helper Cell Differentiation and Conversion of Treg to Tfr Cells
Roquin proteins preclude spontaneous T cell activation and aberrant differentiation of T follicular helper (Tfh) or T helper 17 (Th17) cells, and Roquin‐mediated control of PI3K‐mTOR signaling prevents autoimmunity by restraining activation and differentiation of conventional T cells and specialization of Treg cells. Expand