Issues

Protective HLA alleles in HIV infection recruit biased T cell repertoires.

The T cell repertoire is highly similar between different rates of HIV progression.

HLA-DR can be engineered to function as a CAR molecule in CD8⁺ T cells.

CD8⁺ T cells expressing HLA-DR1 CAR molecules efficiently lyse CD4⁺ T cells in vivo.

HLA-DR1:CII peptide CAR T cells inhibit the development of autoimmune arthritis.

Phenotypic differences exist between cord and birth peripheral blood CD4 cells.

Synchronous increase of Th17/Treg cells is disrupted by HIV/ART exposure.

Intrauterine HIV exposure was associated with a biomarker for epithelial gut damage.

HuR ablation in CD4⁺ T cells alleviates allergic airway inflammation in the OVA model.

CMLD-2 inhibits Th2 cytokine levels in CD4⁺ T cells from type 2 high asthmatics.

AICAR inhibits cytokine production in CD4⁺ cells in non–type 2 and type 2 high asthmatics.

HLA-H*02:07 encodes a membrane-bound protein.

HLA-H*02:07 inhibits human effector cell activity.

HLA-H*02:07 is of archaic origin.

IL-2 and CD107a expression in HIV-specific T cells is enhanced with IC blockade.

Combinations of two Abs to LAG-3, CTLA-4, or TIGIT showed the greatest activity.

CD8 count and CD4/CD8 ratio correlate with magnitude of response to IC blockade.

OPTN mediates protection from HSV-2 by regulating the intrinsic immune response.

OPTN loss results in hyperproliferation of HSV-2 and reduced CCL5 induction.

OPTN/CCL5 nexus restricts hyperproliferative spread of primary HSV-2 infection.

ORAI1 regulates tonic IFN-I signaling via modulating baseline Ca²⁺ levels.

Deletion of ORAI1 enhances host susceptibility to SARS-CoV-2 infection.

Shed PrP^C derivatives and PrP^C in extracellular vesicles regulate innate immunity.

The macrophage NMDA-R/LRP1 complex mediates the activity of PrP^C released by cells.

The NMDA-R/LRP1 complex functions as an extracellular vesicle receptor in target cells.

PWD and 11.2 DCs have less NO production than B6 DCs.

PWD and 11.2 DCs maintain postactivation mitochondrial respiration.

NO levels between B6 and 11.2 DCs inversely correlate with L. monocytogenes control.

Following MWCNT exposure, eosinophilic inflammation is more severe in female airways.

ILC2s are not required for MWCNT-induced eosinophilia.

Female AMs develop a more exaggerated M2a phenotype than those of males after MWCNT exposure.

Obese Srgn^−/− mice have reduced adipose tissue inflammation and adipocyte size.

Adipose tissue Srgn mRNA is predominantly expressed by resident immune cells.

Patients with obesity have increased SRGN mRNA expression in adipose tissue.

Recombinant and plasma-derived human C5a signal comparatively at C5aR1 and C5aR2.

Recombinant but not plasma-derived human C5a induces IL-6 release in macrophages.

The recombinant C5a-induced cytokine response is independent of C5aR1 or endotoxin.

Ig enhancers (DIVACs) increase RNA Pol II stalling in the SHM target gene.

DIVACs do not operate by increasing antisense transcription.

IL-2 and IL-7 induce S6K^strong and S6K^weak signals, leading to forming T_E and T_M cells.

IL-7–stimulated S6K^weak signaling controls T cell memory via FOXO1 and AMPK pathways.

Active TGF-β is present in many cancer indications.

dnTGFβRII can be coexpressed in T cells with engineered TCRs.

dnTGFβRII–expressing T cells are resistant to inhibition by TGF-β.

The IgNAR region >3.13 Mb was enriched 245.531-fold by CATCH.

Twenty holes of 3508 bp of the IgNAR region were filled using PacBio HiFi reads.

Five potential germline V alleles of IgNAR1 were found.