Volume 207, Issue 1, July 2021

Three key H2-Oβ Ig domain residues control H2-O function.

MHCII presentation and antiviral Ab responses are diverse in B6J and B6N mice.

Two non-MHC loci mediate the difference in MHCII presentation in B6J and B6N mice.

HIV-infected H9 cells induce type I IFN production by pDC.

Type I IFN induces IFN-γ but not granzyme B intracellular production in CD8⁺ T cells.

Type I IFN potentiates IFN-γ secretion only upon cognate cross-presentation by pDC.

USP19 suppresses the pathogenic potential of Th17 cells.

USP19 removes the K63-linked ubiquitin chain from RORγt lysine 313.

Ubiquitination of RORγt at lysine 313 is essential for recruiting SRC3.

mIL-2/CD25 induces Treg expansion and upregulates CD25 expression in mice.

mIL-2/CD25 shows efficacy in inhibiting lupus nephritis in NZB × NZW and MRL/lpr mice.

Leptomeningeal B cell accumulation is a prominent feature of GME.

Meningeal B cell infiltrates correlate with cortical demyelination as observed in MS.

GME is a natural model to study compartmentalized neuroinflammation as seen in MS.

CD4⁺ T cells from psoriasis patients exhibit decreased PD-1 expression.

The transcription factor CREMα trans-represses PDCD1 and mediates DNA methylation.

Reduced expression of PD-1 is linked to low IL-2 and high IL-17A production.

CSE induces lysosomal damages with LMP.

TRIM16 is responsible for regulating lysophagy during CSE exposure.

Reduction of TRIM16-mediated lysophagy enhances CSE-induced cellular senescence.

Human CD40–B cells are flexible and can be polarized toward distinct functions.

IL-21–CD40–B cells differentiate into Ab-secreting cells.

Combo-CD40–B cells are highly proliferative cells with potent APC functions.

TBI triggers autoantibody production..

Alterations in autoantibody repertoire persist for years postinjury.

GPR65-intronic SNP rs8005161 is associated with the risk of atopic dermatitis.

GPR65-deficient mice developed exacerbated atopic dermatitis in an animal model.

pH and GPR65 signaling regulate neutrophil migration and TNF-α production by T cells.

Alveolar macrophages (AMs) inherently express PD-L1.

PD-L1/CD80 cis-interaction on AMs promotes AM phagocytosis.

Trans-interaction of PD-L1 on AMs with PD-1 on CTLs represses CTL activity.

Innate immune signaling through TLRs affects stress granule assembly.

TLR signaling promotes disassembly of stress granules that are already formed.

Stress granule inhibition is dependent on the kinase activity of the IKK complex.

Bcl6 affects expression of certain cDC markers, such as CD11c and CD8α.

Zbtb46⁺ DC1s develop in Bcl6^cKO mice.

Bcl6^cKO DC1s are functional with respect to tumor rejection.

AR STAT1 deficiency underly bacterial and viral infections.

Complete STAT1 deficiency is more severe disease than partial STAT1 deficiency.

HSCT is the only curative treatment for AR complete STAT1 deficiency.

Adenosine and cytokine synergistically augment γδ T cell activation and Th17 responses.

Blockade of the synergism suppress Th17 responses.

Serum cytokine levels predict pro- or anti-inflammatory effect of adenosine.

S and N SARS-CoV-2 proteins induce an endotoxin tolerance status in vitro.

S and N proteins are associated with a reduced T cell proliferation in patients with COVID-19.

High levels of S and N proteins increase the proportion of secondary infections.

SIV infection reduces CD4/CD8 ratios prior to and during SIV/M. tuberculosis coinfection.

More PD-1/TIGIT-positive CD4⁺ T cells are in granulomas from coinfected macaques.

CD4⁺ T cells in granulomas from SIV/M. tuberculosis macaques produce less TNF.

SVV 3C^pro directly cleaves pGSDMD to induce pyroptosis.

SVV 3C^pro cleaves GSDMD in pigs, but not in humans or mice.

Recognition of fungi by T. xiaojinensis βGRP1 is vital for proPO activation.

A surface layer prevents O. sinensis from βGRP1 detection.

IML8 binds to βGRP1 in the presence of C. militaris and promotes encapsulation.

Neutrophil IRE1α–CASPASE-2 axis is activated during MRSA infection.

IRE1α–CASPASE-2 signaling promotes neutrophil antimicrobial function.

Neutrophil IRE1α controls Ca²⁺ flux, histone citrullination, and NET formation.

Macrophage galactose-type lectin-1 (MGL-1 or CLEC10A) is activated by M. tuberculosis.

MGL-1 plays an important role in controlling mycobacterial proliferation in lung.

Loss of MGL-1 promotes proinflammatory cytokines and lipid accumulation in TB.

TARM-1 was highly expressed on monocytes of active TB patients.

TARM-1 promoted bacterial clearance in macrophage via ROS.

Blocking TARM-1 signal suppressed Th1 polarization and increased TB progression.

Zebrafish otud6b negatively regulates antiviral responses.

Zebrafish otud6b suppresses irf3 and irf7 activation.

Otud6b inhibits K63-linked polyubiquitination of irf3 and irf7.

Gut microbiota is involved in innate immune cell regulation.

IL-33 plays an important role in nILC2 migration.

nILC2 and ILC2 migrate to respond to infection and microbial dysbiosis.

SGK1 promotes alternative, while suppressing inflammatory, macrophage polarization.

SGK1 inversely regulates FoxO1 and STAT3 to control macrophage phenotypes.

SGK1 protects against P. gingivalis–induced periodontal bone loss in a mouse model.

MxG targets and degrades both IPS-1 and STING to impair antiviral immunity.

GTPase and GED domains of MxG contribute to the negative regulatory function.

A variety of viruses achieve the immune evasion through MxG.

Neddylation is activated in mice and macrophages after MRSA infection.

Neddylation facilitates bactericidal ability via increasing macrophage ROS production.

We describe a MHC class I structure of a shark, the most primitive species with MHC.

Many features of binding between the heavy chain, β₂-m, and peptide are archaic.

β₂-m residues Y10, D53, F56, and W60 are critical to form the archaic pMHC-I complex.

TRAF3 is recruited to the TCR/CD28 complex and interacts with LAT.

TRAF3 enhances TCR/CD28 signaling and restrains the negative LAT regulator Dok1.

TCR-induced kinase activation in TRAF3^−/− T cells is enhanced by inhibiting PTP1B.

Retargeting IL-2 delivery to CTLs improves immunotherapy.

Regulatory lymphocytes hinder ex vivo expansion of CTLs.

Tumor-infiltrating NK cells and γδ T cells facilitate adoptive transfer immunotherapy.

We developed a rapid proximity-based assay for neutralizing antibodies to SARS-CoV-2.

The assay measures binding to the spike that blocks ACE2 recognition.

Unlike pseudovirus assays, the method is insensitive to HIV antiretroviral drugs.