Issues

Mild COVID-19 cases have increased memory B cells 1 mo after symptom onset.

BCR repertoires of mild COVID-19 cases are clonally diverse and mutated.

The activation of mast cells via IgE signaling induces the early phase of PFAS.

IL-33 and TSLP involve the pathogenesis of PFAS.

Our murine model might provide a useful therapeutic platform for PFAS.

miR-21 has context-dependent effects on AFC and GC responses.

miR-21 promotes TLR7-driven autoimmunity with activation of multiple B cell pathways.

miR-21 is required for optimal B cell responses to T-dependent foreign Ag.

CDCP1 is detectable on DCs and its expression is upregulated by CAWS stimulation.

Absence of CDCP1 attenuates cardiac vasculitis in a mouse model of Kawasaki disease.

IL-7 and IL-15 levels reflect the degree of T cell depletion early after HSCT.

Elevated IL-7 and IL-15 are associated with expansion of memory T cells.

Low IL-7 and IL-15 levels are associated with aGvHD in children treated with ATG.

Human UCB B cells express a variable, interindividually conserved Ig repertoire.

UCB B cells respond efficiently to stimulation, favoring IgA plasma cell fate.

UCB B cells are similar but not identical to murine B-1 cells.

HSV-2 gD inhibits TNF-α–mediated NF-κB activation.

HSV-2 gD interacts with p65 to inhibit p65 nuclear translocation.

Novel anti–CD37CAR-T cells were developed to target another B cell Ag.

Shorter spacer length CAR mediated the attenuated signaling rather than longer spacer CAR.

Optimizing the spacer length minimized fratricide to maintain the antitumor effect.

TCR affinity determines the speed and magnitude of the CD4⁺ T cell response.

IL-12 rather than TCR affinity controls Th1 effector function acquisition.

TCR affinity calibrates cell division to time IL-12Rβ2 upregulation.

ADA administration prevents host tissue damage and bacterial burden.

ADA differentially inhibits AURKA–WNT signaling with activation of the HIPPO pathway.

HIPPO signaling positively regulates anti-inflammatory genes and resolvins.

T cells are increasingly activated and apoptotic during acute COVID-19.

Acutely ill COVID-19 patients display mitochondrial metabolic defects in T cells.

These T cells show impaired metabolic reprogramming upon activation in vitro.

PEDV M protein inhibits type I IFN production.

PEDV M protein interacts with the ID of IRF7 to suppress IRF7 activation.

The 1-55 region of M protein is essential for disruption of IRF7 function.

CX3CR1⁺PD-1⁺ CD8 T cells contain a quiescent subset with progenitor-like features.

TIM3⁻CX3CR1⁺ cells are intermediates during a transition of TPEX to CX3CR1⁺ cells.

TCF-1⁺TOX^lo memory-like cells are derived from CX3CR1⁺ exhausted CD8 T cells.

Human and mouse CVT CD8 T cells share matching phenotypes.

CVT memory CD8 T cells decay faster than their circulating and gut counterparts.

This numerical decline in the CVT is associated with impaired early viral control.

NF90 and NF110 isoforms of ILF3 restrain monocyte-derived DC maturation.

ILF3 dampens sensing of HIV-1 and other innate immune agonists of TLR7/8 and cGAS.

NF110–ILF3 regulates genes associated with DC maturation and cholesterol homeostasis.

Knockout of Mkp-1 exacerbates cytokine storms during E. coli–induced sepsis.

Mkp-1 restrains IFN-β expression in macrophages by controlling p38 activity.

Blocking type I IFN signaling during E. coli infection exacerbates disease severity.

IRAK-M deficiency skews the expansion of low-grade inflammatory Ly6C⁺⁺ monocytes.

Inflammatory monocytes due to IRAK-M deletion express elevated CD40 and CD11a.

IRAK-M suppresses monocyte inflammatory polarization through inhibiting TRAM.

Epithelial IL-33 secretion involves IL-33 signaling via its ST2 receptor.

IL-33–dependent signaling activates Src kinase and EGFR.

Epithelial IL-33 signaling involves activation of the NADPH oxidase DUOX1.

SARS-CoV-2 surface proteins in isolation activate inflammatory responses.

Lung inflammation depends on alveolar epithelial cell type I IFN signaling.

LPS induces PDE10A upregulation in macrophages in vitro and in lung tissues.

PDE10A regulates MCP-1 production in macrophages.

PDE10A inhibition reduces lung inflammation in mouse models of LPS exposure.

Low pHe increases mitochondrial biogenesis and function in macrophages.

Low pHe induces M2-like polarization, reducing immune responsiveness.

These changes are reversible when normal pH is restored.

Complement receptor 3 forms a high-affinity complex with iC3b.

In solution, iC3b appears to have a preferred location of the thioester domain.

The CR3 headpiece molecule is valuable for analysis of receptor–ligand interactions.

Gut bacteria induce a unique subset of ILC3s expressing granzyme B.

Gut bacteria induce IL-15, which stimulates granzyme B expression in ILC3s.

ILC3s respond to IL-15 via cis and trans presentation during bacteria exposure.

Systemic infusion of SHED-EVs ameliorates SLE-like phenotypes in MRL/lpr mice.

SHED-EVs improve hematopoiesis and immunoregulation of recipient BMMSCs.

SHED-EV–impacted BMMSC functions are dependent on rescuing the telomerase activity.

KIR Cen B is associated with protection from relapse following HCT.

KIR Cen B02 provides stronger protection against relapse.

Protection from relapse associates with presence of less inhibitory KIR.

ChipCytometry was used for multiplex immunophenotyping of human tonsils.

It is viable for high-content profiling of cell suspensions and tissue sections.

ChipCytometry can identify and localize cell populations and rare cell types.