Issues

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.

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

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

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

PI3Kδ is essential for protective humoral immune responses against trypanosomes.

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

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.

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.

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.

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.

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.

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

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

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.

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.