Arachnoid granulations are poorly investigated. We show that they harbor immune cells and communicate with perisinus spaces, suggesting that granulations subserve neuroimmune roles and function as transarachnoidal passageways. These data raise new theories regarding glymphatic–lymphatic coupling and mechanisms of diseases.

How an anomaly in a TCR signaling molecule leads to spontaneous autoimmunity over immunodeficiency is unclear. Qualitative/quantitative reduction of ZAP-70 to a critical range produces autoimmune T cells and impairs Treg function, together eliciting autoimmune arthritis and colitis in mice.

The study identifies a unique role for early T-bet expression in promoting the proliferation of antigen-specific CD8⁺ T cells following vaccination. Early T-bet expression is necessary for optimal LFA1 expression for appropriate cellular interactions and enables optimal expansion and differentiation of effector and memory CD8⁺ T cells.

Nielsen and Zhang et al. show that well-established, Notch4-induced brain arteriovenous malformations are normalized, following deletion of the Notch signaling mediator, Rbpj. Upon complete regression, virtually no AVM relapses in adults, even when the causal factor is reintroduced.

ITLN1, whose expression is regulated by the unfolded protein response, coats a subset of microorganisms, including Akkermansia muciniphila, allows them to thin the inner mucus layer, and increases colitis severity. ITLN1 upregulation in UC may drive similar outcomes.

We report a new mechanism of immune evasion by SARS-CoV-2 based on direct disabling CTLs to form immune synapses through Spike protein binding to ACE2. This mechanism could contribute to the failure of the immune system to control SARS-CoV-2 infection.

The authors identify a tumor-suppressing angiocrine function of CCL2 which is inhibited by tumor-derived adrenomedullin acting via its receptor on endothelial cells. Disinhibition of endothelial CCL2 results in reduced tumor progression through inhibition of adrenomedullin formation by tumor cells.