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J Immunol (2021) 207 (5): 1223–1224.


J Immunol (2021) 207 (5): 1225–1227.


J Immunol (2021) 207 (5): 1229–1238.

  • Humans with severe viral pneumonia have excessive cytokines in the lower airways.

  • This inflammation is associated with influxes of monocytes and activated lymphocytes.

  • Blood IP-10 concentration correlates with lung inflammation and severe disease.

J Immunol (2021) 207 (5): 1239–1249.

  • IL-22 responses to mycobacterial Ags contributed ∼50% of the total response.

  • Mycobacterial Th22 responses were significantly lower in HIV-infected individuals.


J Immunol (2021) 207 (5): 1250–1264.

  • High macrophage cell density upregulates PDCD4 expression.

  • Secreted GSN is a quorum-sensing autoinducer of macrophages.

  • miR-21–GSN-PDCD4 regulatory network regulates the macrophage inflammatory response.

J Immunol (2021) 207 (5): 1265–1274.

  • Human Th9 cells exhibit a STAT5-mediated gene suppression signature.

  • IL-2/STAT5 suppresses a STAT3-independent Th17-like phenotype in Th9 cells.

  • IL-17 production by IL-2–deprived Th9 cells requires Rorγt and BATF.

J Immunol (2021) 207 (5): 1275–1287.

  • ATP and UTP stimulate P2Y2 receptors to induce PGE2 via CRAC channels and cPLA2.

  • ATP activates P2X receptors to induce IL-6 via CRAC channels and NFAT signaling.

  • P2Y2 and P2X receptors and CRAC channels are attractive targets for airway diseases.

J Immunol (2021) 207 (5): 1288–1297.

  • Nrp-1 expression is induced on a subset of CD4+Foxp3 T cells upon stimulation.

  • Stimulation-induced iNrp-1+CD4+Foxp3 T cells exhibit a highly activated phenotype.

  • Pre-existing nNrp-1+CD4+Foxp3 T cells from naive mice are dysfunctional.


J Immunol (2021) 207 (5): 1298–1309.

  • ISIM reduces PMN-MDSCs and CX3CR1+ M-MDSCs in the tumor.

  • ISIM upregulates PD-L1 in intratumoral MDSCs and synergizes with anti–PD-L1 therapy.

  • Deletion of IRF8 in myeloid cells increases PMN-MDSCs and causes poor outcome.

J Immunol (2021) 207 (5): 1310–1321.

  • A trimeric HA-Fc protein is characterized by its binding with HA mAbs or FcRn.

  • FcRn-targeted nasal immunization with HA-Fc induces mucosal and systemic immunity.

  • FcRn-mediated nasal delivery of HA-Fc confers protection from influenza infection.


J Immunol (2021) 207 (5): 1322–1332.

  • miR-21 is upregulated in myeloid cells and organs during L. donovani infection.

  • Lack of miR-21 enhances IL-12 production and Th1 response during L. donovani infection.

  • miR-21−/− hosts are more resistant to VL caused by L. donovani.

J Immunol (2021) 207 (5): 1333–1343.

  • NK cells from ZIKV-infected patients produced high levels of IFN-γ and TNF-α.

  • Overproduction of IFN-γ by NK cells is correlated with STAT-5 activation.

  • Cytokine production is mediated by MIC molecules expressed by ZIKV+ cells.

J Immunol (2021) 207 (5): 1344–1356.

  • Longitudinal CyTOF analysis of tetramer+ SARS-CoV-2–specific CD8+ T cells was performed.

  • Nucleocapsid-specific T and Ab responses are coordinated.

  • Self-renewing potential and polyfunctionality of tetramer+ cells change over convalescence.

J Immunol (2021) 207 (5): 1357–1370.

  • ZIP8 is upregulated in macrophages and DCs after bacterial stimulation.

  • ZIP8 loss augments lung inflammation, bacterial dissemination, and mortality.

  • ZIP8 loss increases NF-κB signaling and alters T cell priming.

J Immunol (2021) 207 (5): 1371–1376.

  • IFN-γ drives lethal lung inflammation during postinfluenza MRSA pneumonia.

  • IFN-γ promotes inflammatory cytokine storm during postinfluenza MRSA pneumonia.

  • TNF-α hyperproduction exacerbates inflammatory lung damage.

J Immunol (2021) 207 (5): 1377–1387.

  • Usp1 is expressed in activated T cells and interacts with Id2 and Id3.

  • Usp1 loss affects CD8+ T cells responding to secondary but not primary infection.

  • Usp1-deficient memory CD8+ T cells have diminished Id2 protein and proliferation.

J Immunol (2021) 207 (5): 1388–1400.

  • Protein immunization induces lineage-nonpolarized effector CD4 T cells.

  • Nonpolarized memory cells become Th1 cells during the recall response to infection.

  • Viral infection restricts GC Tfh cell formation compared with protein immunization.

J Immunol (2021) 207 (5): 1401–1410.

  • PI3Kδ is essential for protective humoral immune responses against trypanosomes.

  • PI3Kδ promotes IL-10 responses that antagonize early control of parasite growth.


J Immunol (2021) 207 (5): 1411–1418.

  • Myeloid RACK1 deficiency renders mice resistant to viral infection.

  • Virus infection enhances RACK1 T50 phosphorylation via AMPK activation.

  • RACK1 T50 phosphorylation promotes the binding and consequent inhibition of IRF3/7.

J Immunol (2021) 207 (5): 1419–1427.

  • SIRPα controls TLR agonist– and IFN-γ–induced macrophage proinflammatory activation.

  • SIRPα deficiency exacerbates type I diabetes and peritonitis in mice.

  • SFK(s), but not Lyn, phosphorylate SIRPα to recruit SHP-1 in proinflammatory states.

J Immunol (2021) 207 (5): 1428–1436.

  • Transcription factor TCF4 in DCs protects against autoimmune neuroinflammation.

  • TCF4 regulates p38 MAPK activation and proinflammatory cytokine expression in DCs.

  • TCF4 activation in DCs limits pathological effector T cell differentiation.

J Immunol (2021) 207 (5): 1437–1447.

  • Keap1 moderates cytokine induction upon virus infection by binding to chromatin.

  • Keap1 is required for NF-κB p50 and G9a-GLP recruitment, which represses transcription.

  • Keap1 forms complexes with NF-κB p50 and NF-κB p65 that bind chromatin in living cells.

J Immunol (2021) 207 (5): 1448–1455.

  • Lack of individual TLRs had moderate or no effect on anti–S. aureus host defenses.

  • Simultaneous absence of TLR7, 9, and 13 results in hypersusceptibility to S. aureus.

  • Immune recognition of S. aureus is mediated by the concerted action of TLR7/9/13.


J Immunol (2021) 207 (5): 1456–1467.

  • IL-33 stimulates DCs to express Sema4A and exerts antitumor immunity.

  • Sema4A expression on DCs activates CTLs via Sema4A–Plexin B2 axis.


J Immunol (2021) 207 (5): 1468–1477.

  • In this study, we convert an anti-CD4 Ab into an scFv-based immuno-PET tracer.

  • This short-lived PEGylated probe can noninvasively monitor CD4+ T cells in mice.

  • This approach should be applicable to any clinically useful Ig.

J Immunol (2021) 207 (5): 1478–1492.

  • A Bach2 transgene enables unlimited growth of B cells cultured with CD154 and IL-21.

  • Bach2-transgenic cell lines have stable BCRs and transduce signals upon BCR ligation.

  • B cells secrete large quantities of Ig after the Bach2 transgene is silenced.

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