No abstract

Infliximab is lost into stools of patients with UC. High fecal concentrations of infliximab in the first days after therapy begins are associated with primary nonresponse. Additional studies are needed to determine how therapeutic antibodies are lost through the intestinal mucosa and how this process affects treatment response. Clinical trial ID: NL41310.018.12.

SUMMARY BackgroundFormation of antibodies to infliximab (ATI) inversely correlates with functional drug levels and clinical outcome. Comparison of drug levels and anti-drug antibody monitoring is hampered by lack of standardisation.

Adalimumab trough levels in a range of 5-8 μg/mL are sufficient to reach adequate clinical response. These levels are influenced substantially by concomitant MTX use.

Schistosome infections are characterized by prominent T cell hyporesponsiveness during the chronic stage of infection. We found that schistosome-specific phosphatidylserine (PS) activated TLR2 and affected dendritic cells such that mature dendritic cells gained the ability to induce the development of IL-10-producing regulatory T cells. Using mass spectrometry, schistosomal lysophosphatidylserine (lyso-PS) was identified as the TLR2-activating molecule. This activity appears to be a unique property of schistosomal lyso-PS, containing specific acyl chains, because neither a synthetic lyso-PS (16:0) nor PS isolated from the mammalian host activates TLR2. Taken together, these findings provide evidence for a novel host-parasite interaction that may be central to long term survival of the parasite and limited host pathology with implications beyond parasitology.