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J Immunol (2019) 203 (6): 1407–1408.


J Immunol (2019) 203 (6): 1411–1416.

  • MASP-1 is required for physiological LP activation.

  • MASP-3 circulates predominantly in an active form regardless of the role of MASP-1.

  • MASP-3 is pivotal for physiological AP activation via activation of FD.


J Immunol (2019) 203 (6): 1417–1427.

  • α4 integrins are dispensable for cDCs and pDCs to populate the CNS in steady-state.

  • Itga4−/− moDCs have a competitive disadvantage to accumulate in the inflamed CNS.

  • Accumulation of CD11b+CD103+ DCs in gut lamina propria is dependent on α4 integrins.

J Immunol (2019) 203 (6): 1428–1435.

  • Vitamin D concentrations in COPD patients were lower than concentrations in controls.

  • TGF-β/Smad signaling and EMT were increased in COPD patients compared with controls.

  • Vitamin D status was inversely correlated with EMT in COPD patients.


J Immunol (2019) 203 (6): 1436–1446.

  • Intracellular cAMP regulates CD39-dependent adenosine production in Tregs.

  • Extracellular cAMP directly participates in Treg-derived adenosine production.

  • Increasing the intracellular cAMP level improves the therapeutic efficacy of iTregs.

J Immunol (2019) 203 (6): 1447–1456.

  • TRAF5 deficiency accelerates wound healing by promoting activation of pDCs.

  • TRAF5 controls proinflammatory cytokine production by pDCs via IRF5.


J Immunol (2019) 203 (6): 1457–1467.

  • IL-33 is expressed during early B cell development in both mice and humans.

  • Deficiency of IL-33 promotes B cell fitness via a cell-endogenous mechanism.

  • IL-33 expression is modulated in B cell malignancies.

J Immunol (2019) 203 (6): 1468–1479.

  • Fetal and adult blood Vγ9Vδ2 T cells express a different CDR3 repertoire.

  • The postnatal thymus produces a small number of Vγ9Vδ2 thymocytes.

  • Adult blood Vγ9Vδ2 T cells are derived from postnatal Vγ9Vδ2 thymocytes.


J Immunol (2019) 203 (6): 1480–1492.

  • Trout have limited IgM and IgT repertoire diversity in NALT.

  • Intranasal vaccination in trout triggers systemic and mucosal Ig response.

  • IgM and IgT respond to i.p. and intranasal bacterin vaccination.

J Immunol (2019) 203 (6): 1493–1501.

  • HR supports germinal center B cell survival and Ab affinity maturation.

  • HR is active at the hypermutating Ig locus and influences the SHM mutation pattern.

  • The magnitude of A:T mutagenesis during SHM of the Ig V region increases over time.


J Immunol (2019) 203 (6): 1502–1508.

  • Human CD4 T cells have limited cross-reactive memory to avian H7 proteins.

  • CD4 T cell help can be provided to B cells with novel H7/H3 chimeric vaccines.


J Immunol (2019) 203 (6): 1509–1520.

  • IL-6R signaling on T cells is essential for controlling chronic viral infection.

  • IL-6R signaling on T cells is required for optimal Ab development.

  • IL-6 signaling on T cells regulates ICOS expression on Tfh cells.


J Immunol (2019) 203 (6): 1521–1531.

  • Inflammatory agent exposure causes c-Abl to interact with and phosphorylate PARP1.

  • Tyrosine phosphorylation of PARP1 is crucial for NF-κB activation and gene expression.

J Immunol (2019) 203 (6): 1532–1547.

  • BACH1 and myeloid HMOX1 are required for complete muscle regeneration upon acute injury.

  • BACH1–HMOX1 axis is required for coordinated in situ MF phenotype switch.

  • BACH1 regulates inflammatory and repair gene modules in MFs during tissue injury.

J Immunol (2019) 203 (6): 1548–1559.

  • The transcription of IL-7–AS is dependent on the NF-κB/MAPK pathway.

  • IL-7–AS promotes the expression of CCL2, CCL5, CCL7, and IL6.

  • IL-7–AS interacts with p300 and SWI/SNF complex.

J Immunol (2019) 203 (6): 1560–1570.

  • YIPF5 positively regulates STING-mediated IFN production signaling.

  • YIPF5 is essential for antiviral response against DNA viruses.

  • YIPF5 facilitates STING trafficking by recruiting STING to COPII-coated vesicles.

J Immunol (2019) 203 (6): 1571–1578.

  • Heme induces complement-dependent thromboinflammation in human whole blood.

  • Heme-induced proinflammatory cytokines and tissue factor are C5 dependent.

  • Combined inhibition of C5 and CD14 attenuate prothrombin cleavage.

J Immunol (2019) 203 (6): 1579–1588.

  • A negative feedback loop, integrin–PI3K–ARAP3–integrin, controls integrin inactivation.

  • Integrin inactivation promotes neutrophil transendothelial migration and recruitment.

J Immunol (2019) 203 (6): 1589–1597.

  • Retinoids enhance cathelicidin antimicrobial peptide expression during adipogenesis.

  • The action of retinoids is dependent on hypoxia-inducible factor 1-α.

  • The capacity to induce cathelicidin may explain some therapeutic effects of retinoids.

J Immunol (2019) 203 (6): 1598–1608.

  • NAD+ depletion attenuates TLR4 signal transduction in primary human monocytes.

  • The mechanism involves inhibition of protein phosphorylation in the signal cascade.

  • The proteins in the signal pathway are not quantitatively changed by NAD+ depletion.

J Immunol (2019) 203 (6): 1609–1618.

  • Influenza vaccination primes myeloid cells for enhanced cytokine secretion.

  • Vaccine-enhanced myeloid cytokines boost NK cell responses to influenza virus.


J Immunol (2019) 203 (6): 1619–1628.

  • Peptides with β-amino acids can bind tightly to MHC-II and activate TCR signaling.

  • Incorporation of β-amino acids enhances resistance to degradation by protease(s).

  • A selected β-amino acid–containing peptide stimulated T cells in mice.

J Immunol (2019) 203 (6): 1629–1635.

  • KIR3DL1 allotypes impact the development of Behçet disease.

  • This association appears to be independent of the effect of HLA-B*51.

  • Different KIR3DL1 allotypes are associated with mucocutaneous and ophthalmic disease.


J Immunol (2019) 203 (6): 1636–1649.

  • TRIM58 interacts with TLR2, negatively regulating its expression in myeloid cells.

  • Myeloid cell Trim58 deficiency increases susceptibility to acute colitis via Tlr2.

  • Mucosal expression of human TRIM58 is reduced in active ulcerative colitis.


J Immunol (2019) 203 (6): 1650–1664.

  • DN B cells are abnormally elevated in MS patients but have the same origin as in HC.

  • DN B cells resemble CSM B cells but appear to be at an earlier maturation state.

  • DN and CSM B cells undergo unique differentiation pathways.


J Immunol (2019) 203 (6): 1665–1674.

  • EBV latency III B cells display an immunosuppressive profile similar to Bregs.

  • They repress proliferation of T cells and promote expansion of cTregs and uTregs.

  • Expansion of Tregs depends on PD-L1 whose expression depends on the EBV oncogene LMP1.


J Immunol (2019) 203 (6): 1675.
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