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J Immunol (2021) 207 (6): 1495.


J Immunol (2021) 207 (6): 1497–1505.


J Immunol (2021) 207 (6): 1507–1512.

  • CD36 selectively binds to avirulent T. gondii and mediates macrophage tropism.

  • CD36 is not required for Th1 immune resistance but is vital for tissue tolerance.

  • The ROP-18 virulence factor negatively regulates CD36 binding to Toxoplasma gondii.


J Immunol (2021) 207 (6): 1513–1521.

  • CCR6 is upregulated on CNS-resident B cells but is not required for CNS entry.

  • B cell expression of CCR6 increases nonspecific plasma cell output following MOG immunization.

  • B cell expression of CCR6 is not required for induction of B cell–dependent EAE.


J Immunol (2021) 207 (6): 1522–1529.

  • AD has been associated with NK cell dysfunction.

  • Individuals with KIR2DS1, KIR2DL5, and KIR2DS5 are more likely to have AD.

  • These KIR genes and KIR-associated HLA epitopes increased the risk of AD.


J Immunol (2021) 207 (6): 1530–1544.

  • LNSC MHC-II drives conversion of CD8 T cells to CD4 CI-Treg cells.

  • LNSC coculture helps generate and expand CI-Treg cells in vitro.

  • CI-Treg cells expanded in stromal cell coculture suppress colitis in mice.

J Immunol (2021) 207 (6): 1545–1554.

  • Fc galactosylation enhances complement activity of WT IgG1, but not hexameric IgG.

  • Fc galactosylation improves hexamerization potential of IgG1.

J Immunol (2021) 207 (6): 1555–1565.

  • P2Y6 deficiency enhances the maturation and functions of NK cells.

  • P2Y6 deficiency promotes the expression of T-bet in NK cells.

  • P2Y6 deficiency increases the antitumor activities of NK cells.


J Immunol (2021) 207 (6): 1566–1577.

  • Exposure of P5 at the surface of NTHi positively correlates with C4BP binding.

  • C4BP bound to the bacterial surface retains its complement inhibitory capacity.

  • C4BP binding to P5 is important for NTHi serum resistance.

J Immunol (2021) 207 (6): 1578–1590.

  • Malaria-specific T cells can enter the brain parenchyma near the onset of ECM.

  • Infiltration of T cells into the brain parenchyma contributes to cerebral pathology.

  • Memory T cells can form within the brain parenchyma after malaria infection.

J Immunol (2021) 207 (6): 1591–1598.

  • T cells from COVID-19 patients display less complex N-glycans at diagnosis.

  • IL-2 is a putative driver of glycan switch in COVID-19 patients.

  • DC-SIGN expression in monocytes at diagnosis predicts poor disease course.


J Immunol (2021) 207 (6): 1599–1615.

  • Mice expressing a mutated form of GFI1 show signs of inflammation.

  • Mutated GFI1 can still occupy genes, leading to a specific histone mark landscape.

J Immunol (2021) 207 (6): 1616–1626.

  • The PP4 complex modulates the IMD-NF-κB–dependent immune response in Drosophila.

  • Loss of PP4 leads to exacerbated IMD-NF-κB signaling and a reduced lifespan.

  • Genetic and coimmunoprecipitation data propose an interaction between PP4 and the IKK complex.

J Immunol (2021) 207 (6): 1627–1640.

  • Crystalline silica induces an immunometabolic response in RAW 264.7 macrophages.

  • Silica induces macrophages activation without requiring LPS priming.

  • Mitochondrial complex II is crucial for macrophage response and survival to silica.

J Immunol (2021) 207 (6): 1641–1651.

  • Anticoagulation by GPRP allows thrombin generation in human whole blood.

  • Thrombin does not cleave plasma C5 in its native form.

  • pH-induced C5 conformational change allows thrombin-mediated cleavage of C5.

J Immunol (2021) 207 (6): 1652–1661.

  • A 15 aa IKIP peptide (46–60 aa of IKIP) inhibits IKK activation.

  • IKIP peptide inhibits IKK activation via disruption of NEMO binding to IKKα/β.

  • Administration of IKIP peptide attenuates inflammatory responses in vivo.


J Immunol (2021) 207 (6): 1662–1671.

  • PEP-619WW mice have superior control of immunogenic tumors.

  • PEP-619WW mice had increased tumor-infiltrating lymphocytes.

  • Tumor-infiltrating lymphocytes have a more activated phenotype in PEP-619WW mice.

J Immunol (2021) 207 (6): 1672–1682.

  • ILC1s are enriched in the bone marrow of patients with AML and leukemic mice.

  • AML promotes ILC1s in part via AHR-mediated skewing of ILC precursor development.


J Immunol (2021) 207 (6): 1683–1693.

  • GM-CSF, TGF-β, and rosiglitazone induced the generation of AM-like cells.

  • AM-like cells serve as a tool for studies of AM differentiation and function.

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