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Meningeal vascular damage accompanies mild traumatic brain injury. McGavern and colleagues report that distinct myeloid cell subsets are temporally recruited to the lesion and are critical for meningeal re-vascularization after such injury.
Mice are generally the ‘go-to’ organism for modeling of the human immune system, but this often leads to inaccurate interpretations. Ernst and Carvunis argue in this Comment that taking into account the evolutionary and environmental context can generate better models of disease.
The activating natural killer cell receptor NKG2C can specifically recognize peptides derived from the cytomegalovirus protein UL40 in the context of HLA-E. This drives the expansion of a population of adaptive NKG2C+ natural killer cells.
γδ T cells accumulate with age in adipose tissue and produce the cytokine IL-17, which controls the homeostasis of regulatory T cells and adaptive thermogenesis. Thus, maintenance of core body temperature unexpectedly relies on these adipose tissue–resident γδ17 T cells.
The role of the transcription factor c-Maf varies in different CD4+ T cell subsets and can be associated with either pro-inflammatory activity or anti-inflammatory activity, depending on the cell context.
Myeloid cells exhibit different inflammatory phenotypes after brain injury, yet the relative mechanistic roles for these diverse cell types in post-traumatic tissue damage and repair remain controversial.
Evasion of the immune system and global activation of the immune system are hallmarks of human immunodeficiency virus (HIV) infection. Studies reveal that macrophages might be responsible for HIV-associated pathogenesis via resistance to killing and induction of chronic inflammation.
Harris and colleagues show that the cytokine TGF-β is required for colonization of the microglial niche and maintenance of central nervous system integrity. Acute loss of TGF-β leads to proinflammatory responses and fatal demyelinating disease.
Meningeal vascular damage accompanies mild traumatic brain injury, which persists in a fraction of patients. McGavern and colleagues report that distinct myeloid cell subsets are temporally recruited to the wound site during tissue repair; however, re-injury at early time points impairs recovery.
NK cells constrain infection by cytomegalovirus. Romagnani and colleagues show that human NKG2C+ NK cells recognize distinct HCMV UL40 viral peptides, which can vary among viral isolates. NKG2C+ NK cells thereby demonstrate adaptive-like recognition that can discriminate between closely related viral strains.
Lynch, Brenner and colleagues find that tissue-resident γδ T cells reside in adipose tissues in both mice and humans. These cells play essential roles in regulating thermogenesis and supporting age-dependent increases in adipose-tissue regulatory T cell populations.
Macrophages can be an important niche for chronic viral infection. Walker and colleagues demonstrate that macrophages are intrinsically resistant to CTL-mediated killing and can thereby contribute to the maintenance of HIV reservoirs and chronic inflammation.
Higher-order TCRs have been postulated to maintain high antigen sensitivity and trigger signaling. Huppa and colleagues use various investigative techniques and find exclusively monomeric TCR–CD3 complexes that drive the recognition of antigenic pMHC.
The transcription factor c-Maf controls IL-10 production in T cells. O’Garra and colleagues use systems and in vivo functional analysis of T cell subsets to reveal distinct context-specific roles for c-Maf.