Issues

No CSR or affinity maturation was observed in AID^S38A/S38AMSH2^−/− and AID^S38A/S38AUNG^−/− mice.

AID phosphorylated at serine 38 regulates BER- and MMR-dependent CSR and SHM.

The mesentery and omentum in mice contain various forms of lymphoid tissues.

FLAgs represent a partially compartmentalized form of lymphoid aggregate.

FLAgs efficiently bind B cells and high-grade B cell lymphoma.

Th1 cells rolling on selectins trigger DAP12-dependent activation of integrin αLβ2.

DAP12 signaling in Th1 cells facilitates slow rolling, arrest, and migration.

DOCK2-deficient CD8⁺ T cells spontaneously convert into virtual memory cells.

Dock2^−/− CD8⁺ T cells exhibit enhanced responsiveness to weak agonists.

The tetraspanin CD53 is required for normal B cell development.

CD53 promotes B cell development by maintaining IL-7R signaling.

CD53 functions cell autonomously during B lymphopoiesis.

ELGAN/ELBW neonates are lymphopenic and their T cells have altered homing capacity.

ELGAN/ELBW infants with chorioamnionitis have an altered Treg population.

Two successive inversional V-to-DJ rearrangements can occur on one Tcrb allele.

Both Vβ usage and Vβ selection are abnormal for inversional rearrangements.

RPM and BM-DCs, not cDC1, cross-prime CTL via the MR-dependent cytosolic pathway.

RPM and cDC1 cross-prime at different phases after infection/immunization.

RPM produce distinct early effector CTL that limit early viral spread.

PLY induces PMN migration across pulmonary epithelial cells.

PLY-dependent PMN migration requires pore formation and epithelial 12-LOX activity.

Diverse pore-forming toxins induce PMN migration.

Clonal stability is a feature of memory inflation.

Stochastic expansions maintain clonal stability during memory inflation.

Persistent clonotypes are often public in the context of memory inflation.

Platelets modulate IFN-γ production by PBMCs in response to C. albicans.

The effect required direct contact between platelets and monocytes.

Platelet modulation of the Th1 response was dependent on PGE₂.

Mice deficient in Sema3E are more resistant to LPS-induced acute inflammation.

Sema3E regulates macrophage phenotype and function in response to LPS.

Dgkζ deficiency protects from the induction of inflammatory arthritis.

Dgkζ deficiency limits activation of proinflammatory macrophages.

Dgkζ deficiency reduces phosphorylation of STAT1 and STAT3 in activated macrophages.

pXela-UAAg is the first structure of an amphibian classical MHC-I molecule.

The A pocket is the largest and the C–F pockets are positively charged in pXela-UAAg.

The AB loop of pXela-UAAg reveals a unique shape for binding β2m in nonmammals.

KDM6 demethylases are upregulated in inflammatory DC following RSV infection.

KDM6 during RSV infection alters APC function of DC.

KDM6 increases proinflammatory responses and RSV-driven immunopathology.

IL-23/17/17R signaling is upregulated in P. aeruginosa keratitis.

IL-17 suppresses TH2 response, upregulates osteoprotegerin, and worsens keratitis.

IL-17 could be a therapeutic target for treating P. aeruginosa keratitis.

Frequencies of CD38⁺PD-1⁺ TCR Vδ1 and Vδx cells increase after malaria infection.

CD38⁺PD1⁺ TCR Vδ1 cells are oligoclonal, as shown by single-cell CDR3δ analysis.

TCR Vδ1 cells show long-term phenotypic alterations after blood-stage parasitemia.

NK cell functioning is impaired in E2-deficient (E2^−/−) mice.

E2^−/− mice exhibit increased melanoma metastatic burden in lungs.

E2^−/− NK cells display reduced Ly49D and increased NKG2A/CD94 expression.

Pembrolizumab reduces the differentiation of human FOXP3⁺ iTregs.

FOXP3 downregulation by pembrolizumab was mediated by activation of mTOR.

PD-1 blockade shifts iTreg polarization in favor of Th1 and Th17 subsets.

Hyperexpression of GM-CSF in tumor cells promotes M-MDSC immunosuppression.

Efferocytosis enhances immunosuppression of Ly6C^high myeloid cells.

Chemoresistance decreases the sensitivity to CTL-induced cytotoxicity.