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J Immunol (2023) 211 (4): 509.


J Immunol (2023) 211 (4): 511–517.
J Immunol (2023) 211 (4): 518–526.


J Immunol (2023) 211 (4): 527–538.

  • FcεRI-mediated mast cell function is susceptible to isoprenylation inhibitors.

  • K-Ras is a critical component of FcεRI-mediated mast cell activation.

  • Targeting isoprenylation can suppress allergic inflammation in vivo.


J Immunol (2023) 211 (4): 539–550.

  • NK cells from HCMV+ individuals have elevated levels of glycolytic metabolites.

  • NK cells from HCMV+ individuals exhibit very high levels of deoxyribonucleotides.

  • Adaptive NK cells exhibit more robust mTORC1 activation in response to activation.


J Immunol (2023) 211 (4): 551–562.

  • CD103 restrains Treg migration in inflamed skin when E-cadherin is upregulated.

  • CD103 supports interactions of Tregs with CD11c-expressing cells in inflamed skin.

  • CD103 inhibition increases inflammation in contact hypersensitivity.

J Immunol (2023) 211 (4): 563–575.

  • Distinct glutamine inhibition strategies cause unique changes to CD8 T cell function.

  • T cell metabolism compensates according to how glutamine metabolism is targeted.

  • Timing and strategy for use of glutamine-targeting agents modify T cell outcomes.

J Immunol (2023) 211 (4): 576–590.

  • pDCs cooperate with B cells through the production of IFN-I and CXCL10.

  • pDCs enhance the T-independent B response through a p38 MAPK–STAT1 axis.

  • pDCs enhance TLR-stimulated autoantibody production in FO B and MZ B cells.

J Immunol (2023) 211 (4): 591–600.

  • miR-308 targets Tab2 to negatively regulate the immune response.

  • Relish binds the promoter and activates the expression of miR-308.

  • The Relish–miR-308–Tab2 axis is critical for immune homeostasis in the Drosophila Imd pathway.


J Immunol (2023) 211 (4): 601–611.

  • M. tuberculosis induces RARE genes by human monocytes.

  • M. tuberculosis metabolizes serum components and activates RAR pathway.

  • BMS493, a specific pan-RAR inverse agonist, inhibits M. tuberculosis growth in mice.

J Immunol (2023) 211 (4): 612–625.

  • Human dendritic cells present Borrelia-derived peptides on HLA-DR molecules.

  • Borrelia-exposed mo-DCs undergo profound and unique molecular and cellular changes.

  • Borrelia-exposed mo-DCs may have unique immunoregulatory properties.

J Immunol (2023) 211 (4): 626–632.

  • There is a role for Rora in Th2 cell development.

  • Rora CD4-deficient mice expel worms and develop allergic lung inflammation.


J Immunol (2023) 211 (4): 633–647.

  • Granzyme K expression on innate lymphocytes is associated with a memory-like phenotype.

  • Granzyme K+ cells are enriched in nonlymphoid tissues and express CCR5.

  • Granzyme K+ cells are enriched in tumors and produce IFN-γ but not IL-17a.

J Immunol (2023) 211 (4): 648–657.

  • Histones produce acute thromboinflammatory responses in vascular endothelium.

  • Suramin protects small blood vessels from histone-induced damage.

J Immunol (2023) 211 (4): 658–672.

  • CcGSDMEb-1/2 were cleaved only by CcCaspase-1b.

  • CcGSDMEb-1/2 exerted toxicity to cells through its N-terminal domains.

  • CcGSDMEb-1/2 could regulate the secretion of CcIL-1β and the bacterial clearance.


J Immunol (2023) 211 (4): 673–682.

  • Mass cytometry analysis reveals intratumor immune changes caused by anti-CCR8 therapy.

  • CCR8+ Treg depletion alters intratumor CD8+ T cell activation and exhaustion status.

  • CD8+ T cell exhaustion is associated with CCR8+ Treg infiltration in human tumors.

J Immunol (2023) 211 (4): 683–692.

  • GPR56 and granzyme B were significantly coexpressed in circulating T cells.

  • Increased circulating GPR56+ T cells were related to lung cancer progression.

  • Anti-GPR56 stimulation of GPR56+ T cells significantly upregulated granzyme B.

J Immunol (2023) 211 (4): 693–705.

  • IR-induced immunoproteasomes and APM correlate with tumor T cell infiltration.

  • Forcing LMP7 expression in an LMP7-negative tumor generates immune rejection.

  • The irradiation effect on the APM is NF-κB dependent.

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