Heather M. Ren

TL;DR: High-affinity CXCR5hi PD-1hi CD4 T cells in the brain produce IL-21, which drives CD8 bTRM differentiation in response to a persistent viral infection.

TL;DR: Genetic disruption and intracerebroventricular blockade of PD-1 signaling resulted in an increase in number of MuPyV-specific CD8 bTRM and the fraction of these cells expressing CD103, the αE integrin commonly used to define tissue-resident T cells, however, PD-L1−/− mice persistently infected with Mu PyV showed impaired virus control upon i.c. re-infection withMuPyV.

TL;DR: Using the mouse polyomavirus encephalitis model, it is demonstrated that CD4 T cells regulate development of functional antiviral brain-resident CD8 T cells (bTRM) and renders their maintenance refractory to systemicCD8 T cell depletion.

TL;DR: In this paper, the authors assess the current knowledge regarding CD4 T cell-derived IL-21 and IL21R signaling within CD8 T cells and evaluate what implications it has within several autoimmune diseases including systemic lupus erythematous, rheumatoid arthritis, juvenile idiopathic arthritis, type 1 diabetes mellitus, psoriasis, Sjogren's syndrome, vitiligo, antiphospholipid syndrome, pemphigus and giant cell arteritis.

TL;DR: The residency and maintenance requirements for CD8 bTRM are explored and their roles in controlling viral infections of the brain are discussed, which demonstrates that the infiltration of CD8 T cells into the brain can also be pathogenic.