Issues

Loss of DNA repair genes Atm and Msh2 produces, to our knowledge, a novel synthetic lethality in mice.

Deletion of Atm and Msh2 in B cells reduces Ig CSR and inhibits blunt joins in NHEJ.

The differentiation of lupus autoantigen-specific B cells relies on glycolysis.

These B cells are more glycolytic under Ag-specific than TLR7 stimulation.

The activation of chromatin-specific CD4 T cells does not require glycolysis.

sSIRL-1 is increased in patients characterized by neutrophilic inflammation.

In vitro activated neutrophils release sSIRL-1 by proteolytic cleavage.

SIRL-1 shedding is prevented by proteinase 3 inhibition.

Galectin-8^−/− mice are resistant to P. aeruginosa keratitis.

Galectin-8 downmodulates the innate immune response.

Treatment with galectin-8 inhibitor markedly reduces the severity of P. aeruginosa keratitis.

Arginase-1 is induced within alveolar macrophages during C. neoformans infection.

Macrophage-derived arginase promotes C. neoformans growth and proliferation.

Macrophage arginase activity is required for cryptococcal brain invasion.

Mucin-derived epitope (MUCKb25) elicits immunodominant T cell response.

MUCKb25 T cell response is nonprotective and not required for parasite control.

Detection of T. cruzi–infected cells by MUCKb25 T cells is limited.

AIM induces foamy macrophages in M. avium infection.

AIM immortalizes M. avium–infected macrophages and makes the disease chronic.

ASFV E184L protein inhibits type I IFN production.

ASFV E184L protein interacts with STING to block STING-mediated immune signaling.

E184L-deficient ASFV induces higher levels of IFNs in pigs than its parental virus.

Leptospires do not induce macrophage death, but trigger mild IL-1β secretion.

LPS from pathogenic leptospires inhibits caspase 11–induced pyroptosis.

Concealing IL-1β inside macrophages limits inflammation.

PEDV inhibits FcRn expression.

PEDV nsp13 causes aberrant methylation.

IL-12Rβ2 on recipient nonhematopoietic cells contributes to aGVHD development.

Targeting IL-12Rβ2 may be a potential strategy in the treatment of aGVHD.

Androgen deprivation therapy results in increased recent thymic emigrants (RTEs).

RTEs traffic to prostate tumors.

RTEs become activated and produce effector cytokines in the tumor microenvironment.

D2HG is a normal lymphocyte metabolite modestly increased by stereoselective uptake.

D2HG binds calcineurin and inhibits its phosphatase activity.

External D2HG abolishes NF-AT–driven transcription and IL-2 synthesis.