Gene editing to generate precisely matched primary human T cell populations demonstrates that the common autoimmune risk allele in the tyrosine phosphatase, PTPN22, promotes signaling in cells expressing a low-avidity, self-reactive TCR specific for a diabetes-associated self-antigen.

Phosphorylation of the phosphatase SHP-1 by PKC-θ in natural killer (NK) cells induces SHP-1 inhibition, revealing a novel molecular pathway that sustains NK cell activation threshold.

HpBARI is a protein secreted by a parasitic helminth, which binds to and blocks the IL-33 receptor, suppressing IL-33-dependent type 2 immune responses.

Similar to T cell exhaustion, natural killer cell dysfunction in chronic hepatitis B patients results from deregulated calcium pathway.

Under conditions where the force of HIV infection per cell is high, partial attenuation of infection with inhibitors can increase the number of live infected cells and may paradoxically be beneficial for viral spread.

A novel antibody recognizing receptor-binding region of MARV glycoprotein was developed and displays broad-spectrum neutralizing activity to filovirus species when NPC2 was fused to the N-terminus of the mAb.

NAD⁺ exhibits profound therapeutic effects in experimental septic shock models by dampening the systemic inflammatory response and leading to improved survival.

A novel reporter model system serves as a valuable tool for studying latent HIV-1 infection and identifies potent latency reversing agent.

IL-27 exerts differential activation of STAT1 and STAT3 via IL-27Ra and GP130, respectively, leading to a kinetic decoupling of its gene expression program, which contributes to tune its immuno-modulatory activities.

Genetic variants located in DNA repair genes and a reduced burden of somatic mutations protect the oldest living persons from age-related diseases, allowing an healthy aging phenotype.