Hyperreactive B cells instruct their elimination by T cells to curb autoinflammation and lymphomagenesis.

B cell immunity carries the inherent risk of deviating into autoimmunity and malignancy, which are both strongly associated with genetic variants or alterations that increase immune signaling. Here, we investigated the interplay of autoimmunity and lymphoma risk factors centered around the archetypal negative immune regulator TNFAIP3/A20 in mice. Counterintuitively, B cells with moderately elevated sensitivity to stimulation caused fatal autoimmune pathology, while those with high sensitivity did not.

Reduction in Renal Heme Oxygenase-1 Is Associated with an Aggravation of Kidney Injury in Shiga Toxin-Induced Murine Hemolytic-Uremic Syndrome.

Hemolytic-uremic syndrome (HUS) is a systemic complication of an infection with Shiga toxin (Stx)-producing enterohemorrhagic , primarily leading to acute kidney injury (AKI) and microangiopathic hemolytic anemia. Although free heme has been found to aggravate renal damage in hemolytic diseases, the relevance of the heme-degrading enzyme heme oxygenase-1 (HO-1, encoded by ) in HUS has not yet been investigated. We hypothesized that HO-1 also important in acute phase responses in damage and inflammation, contributes to renal pathogenesis in HUS.

Protease-activated receptor 2 deficient mice develop less angiotensin II induced left ventricular hypertrophy but more cardiac fibrosis.

Aims: Activation of Protease Activated Receptor 2 (PAR2) has been shown to be involved in regulation of injury-related processes including inflammation, fibrosis and hypertrophy. In this study we will investigate the role of PAR2 in cardiac injury in a mouse model of hypertension using continuous infusion with angiotensin II.

Methods: Hypertension was induced in 12 weeks old wildtype (wt, n = 8) and PAR2 deficient mice (n = 9) by continuous infusion with angiotensin II for 4 weeks using osmotic minipumps.

Diet and Immune Effects Trial (DIET)- a randomized, double-blinded dietary intervention study in patients with melanoma receiving immunotherapy.

Background: Gut microbiome modulation is a promising strategy for enhancing the response to immune checkpoint blockade (ICB). Fecal microbiota transplant studies have shown positive signals of improved outcomes in both ICB-naïve and refractory melanoma patients; however, this strategy is challenging to scale. Diet is a key determinant of the gut microbiota, and we have previously shown that (a) habitual high dietary fiber intake is associated with an improved response to ICB and (b) fiber manipulation in mice impacts antitumor immunity.