PILLARS OF IMMUNOLOGY
ANTIGEN RECOGNITION AND RESPONSES
Self-Antigens Displayed on Liposomal Nanoparticles above a Threshold of Epitope Density Elicit Class-Switched Autoreactive Antibodies Independent of T Cell Help
A threshold of epitope density for a self-antigen elicits IgG1, IgG2b, and IgG3.
The class-switched autoreactive Abs were induced in the absence of T cell help.
TREX1 catalytic inactivity causes self-DNA sensing and IFN-I–dependent autoimmunity.
TREX1-deficient T cells exhibit evidence of DNA sensing and IFN-α expression.
Activated TREX1–deficient T cells spontaneously produce IFN-α protein.
Overexpression of SH2-Containing Inositol Phosphatase Contributes to Chronic Lymphocytic Leukemia Survival
B cell–specific deletion of Ship2 phosphatase reduces CLL formation in a mouse model.
Ship2 inhibition reduces Akt/mTORC1/S6 signaling in murine and human CLL cells.
Ship2 supports survival of CLL cells via the key antiapoptotic protein Mcl-1.
IMMUNOTHERAPY AND VACCINES
A Computationally Optimized Broadly Reactive Antigen Subtype–Specific Influenza Vaccine Strategy Elicits Unique Potent Broadly Neutralizing Antibodies against Hemagglutinin
Immunization with COBRA P1 elicits broadly HA-binding ASC.
P1 HA-elicited mAbs have different binding and functional activities.
The P1-elicited 1F8 mAb exhibits broad H1N1 binding and functional activity.
INFECTIOUS DISEASE AND HOST RESPONSE
Dendritic cells recognize and mount an immune response against B. miyamotoi.
Recognition of B. miyamotoi is partially mediated by TLR2.
Dendritic cells stimulated with B. miyamotoi induce proliferation of T cells.
Porcine Reproductive and Respiratory Syndrome Virus Enhances Self-Replication via AP-1–Dependent Induction of SOCS1
PRRSV infection induces SOCS1 upregulation.
PRRSV N protein upregulates SOCS1, and NLS-2 is essential for this function.
AP-1 signaling pathways are indispensable for PRRSV-induced SOCS1 expression.
INNATE IMMUNITY AND INFLAMMATION
An Early Neutrophil Recruitment into the Infectious Site Is Critical for Bacterial Lipoprotein Tolerance–Afforded Protection against Microbial Sepsis
BLP tolerization promotes an early PMN recruitment in the infectious site.
This early PMN influx occurs via the CXCL2-formed concentration gradient.
Blockage of PMN influx eliminates BLP tolerance–afforded protection against sepsis.
IKIP Negatively Regulates NF-κB Activation and Inflammation through Inhibition of IKKα/β Phosphorylation
IKIP inhibits NF-κB activation.
IKIP inhibits IKKα/β phosphorylation.
IKIP protects mice against LPS-induced septic shock and DSS-induced colitis.
Annotated lncRNA 1810058I24Rik encodes a conserved mitochondrial micropeptide.
Macrophages fail to activate the Nlrp3 inflammasome in the absence of Mm47.
Genetic deletion of Mm47 in macrophages affects only Nlrp3 and not Aim2 or Nlrc4.
Fibrinogen is a specific trigger for cytolytic eosinophil degranulation.
Eosinophils adhere to and degrade fibrinogen substrates in a CD11b-dependent manner.
Fibrinogen-interacting eosinophils are more metabolically active than collagen.
MOLECULAR AND STRUCTURAL IMMUNOLOGY
LSD1 suppresses PD-1 expression following acute infection or ex vivo induction.
Blimp-1 binding to the Pdcd1 locus is required to recruit LSD1.
LSD1 is required to fully remethylate the Pdcd1 proximal promoter region.
Elevated Choline Kinase α–Mediated Choline Metabolism Supports the Prolonged Survival of TRAF3-Deficient B Lymphocytes
Chkα and choline metabolism are upregulated in mouse TRAF3–deficient B cells.
Reconstitution of TRAF3 in human malignant B cells inhibits choline metabolism.
Inhibition of Chkα reverses the survival phenotype of TRAF3-deficient B cells.
Correction: Deficiency of the AIM2–ASC Signal Uncovers the STING-Driven Overreactive Response of Type I IFN and Reciprocal Depression of Protective IFN-γ Immunity in Mycobacterial Infection
On the cover: Three-dimensional reconstruction of confocal images of a macrophage (green) closely associated with a bundle of peripheral nerve fibers (blue; semitransparent) in mouse skin. F4/80 (red) marks interstitial dermal macrophages.
Photo credit: Philipp Henneke.
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