Issues

Intestinal IL-17RA signaling mediates systemic glucose and lipid metabolism.

Hepatic IL-17RA signaling does not regulate systemic glucose metabolism.

IL-17RA–driven microbiota changes influence systemic glucose metabolism.

Multiple CD4 T cell Ags are identified by screening a Theileria parva peptide library.

Ags have diverse properties and include polymorphic and conserved proteins.

Parasite infection and viral vector–delivered Ag induce similar CD4 responses.

B cell–intrinsic PD-1 expression inhibits TI-2 B_mem formation and reactivation.

PDL2 expressed by TI-2 B_mem contributes to self-suppression of reactivation.

Adjuvant enables robust IgG boosting to PPS in the context of PD-1 deficiency.

Functionally distinct subsets of CD8 T cells infiltrate islets in type 1 diabetes.

Self-renewing islet CD44^highTCF1⁺ CD8 T cells maintain the autoreactive response.

IL-27 modulates the differentiation of islet-infiltrating CD8 T cell subsets.

IgG-V^N-Glyc sequence motif frequency is elevated in the MG BCR repertoire.

The fraction of total IgG-V^N-Glyc in MG serum is elevated.

The presence of IgG-V^N-Glyc did not alter binding of several MG patient-derived mAbs.

Laboring decidua secretes proinflammatory cytokines, chemokines, and growth factors.

Nonlaboring myometrium secretes multiple chemokines for leukocyte infiltration.

Broad-spectrum chemokine inhibitor prevents activation of maternal leukocytes.

In the absence of RORγt, colonic Tregs lose Foxp3 expression and suppressor function.

RORγt promotes Foxp3 expression by antagonizing effector fate of colonic Tregs.

RORγt represses T-bet to control the suppressor function of Tregs.

TEC-intrinsic ablation of Tsc1 predominantly impairs mTEC with lesser impact on cTEC.

Tsc1 is essential for TEC survival by inhibiting lysosomal-mediated apoptosis.

Lipophilic modification of CD4⁺ peptide enhances Ag presentation.

Lipo-peptide induces Ag-specific immune tolerance.

Lipo-peptide mixture delays progression to end-stage diabetes in NOD mice.

Anti-CD40 Ab fused to CD40L potentiates efficacy for B cell and DC activation.

Anti-CD40–CD40L stabilizes off-rate and drives CD40 clustering and internalization.

An anti-OX40 Ab–OX40L fusion is also a superagonist.

CMV-responsive CD4 and CD8 T cell clonality is stable up to 1 y posttransplant.

The CD8 repertoire becomes more clonal in the first 3 mo after transplant.

Common CDR3 TCRβ motifs were detected among subjects with matched HLA type.

CMV-responsive CD8 T cells are clonally expanded and polyfunctional after transplant.

Clonally expanding cells become more polyfunctional from pre- to posttransplant.

Function and differentiation state are maintained from 3 to 12 mo posttransplant.

iNOS is required for host’s survival in C. deneoformans disseminated infection.

iNOS promotes control of fungal growth in the kidneys but not in other organs.

iNOS^−/− mice infected kidneys show increased inflammation and M2 macrophage bias.

OPN induction potentiates type 2 immune response during C. neoformans infection.

Macrophage-derived OPN promotes C. neoformans growth and proliferation.

OPN is essential for C. neoformans–induced M2 polarization.

CXCL2 on macrophage EVs recruited neutrophils.

CXCL2 EVs activated the CXCR2/PKC/NOX4 pathway.

Targeting EVs CXCL2 is a viable strategy for sepsis treatment.

We have established a bath immersion model of S. epidermidis infection in zebrafish.

Macrophage activation and NF-κB-driven inflammation characterize the host response.

IL-6 signaling is protective against S. epidermidis infection.

α-syn monomers and oligomers efficiently activated the NLRP3 inflammasome via TLR2.

Activation of the NLRP3 inflammasome compromised the α-syn clearance capacity.

NLRP3 inhibition improved the overall clearance of α-syn oligomers.

HSV-1 infection causes the mitochondrial leakage of C1QBP.

Leaked C1QBP inhibits cGAS enzymatic activity.

Leaked C1QBP suppresses IFN production and facilitates viral infection.

A structure and peptide binding motif of a marsupial MHC I molecule is described.

Similar amino acid insertion features of MHC I exist in lower mammals and bats.

Insertions may have implications for specific antiviral immunity in lower mammals.

LGG could promote early B cell development in the JLP of piglets.

LGG might contribute to promote IgA production by secreting p40 protein.

p40 could interact with the potential membrane receptors ARF4 or DIF3 of IPEC-J2.