- Antibody-secreting plasma cells persist for decades in human intestine
This study provides a definite answer to the long-standing question concerning the longevity of the secretory antibody response. Landsverk et al. show that antigenic attrition affects a minor plasma cell subset and that distinct plasma cells are likely maintained for life in the human small intestine.
- The epidermal polarity protein Par3 is a non–cell autonomous suppressor of malignant melanoma
Mescher et al. uncover a novel tissue-born tumor suppression mechanism, engaging polarity proteins in the epithelial microenvironment that prevent malignant outgrowth of neighboring cell types through control of heterologous cell–cell contacts. Moreover, their data support an emerging role of P-cadherin, which is frequently amplified in human carcinoma, as a protumorigenic and proinvasive adhesion molecule, thus placing it as a promising druggable target to disrupt tumor–microenvironment interactions for anticancer therapy.
- Class II MHC–independent suppressive adhesion of dendritic cells by regulatory T cells in vivo
Yan et al. demonstrate that in vivo T reg cells can form prolonged contacts with dendritic cells (DCs) in an MHC-independent manner and suppress the ability of the same DCs to contemporaneously engage in stable interactions with and activate conventional T cells.
- Strong adhesion by regulatory T cells induces dendritic cell cytoskeletal polarization and contact-dependent lethargy
Chen et al. show that regulatory T cells adhere to dendritic cells (DCs) with high binding forces. This strong binding causes cytoskeletal polarization in the latter, which limits DCs’s ability to form productive engagement with other antigen-specific T cells.
- Defective ATG16L1-mediated removal of IRE1α drives Crohn’s disease–like ileitis
Tschurtschenthaler et al. report a Crohn’s disease–like ileitis mediated by IRE1α that develops in mice with intestinal-epithelial Atg16l1 deletion when they age. The authors propose a selective autophagy process involved in the removal of IRE1α clusters during ER stress.
- IKKα controls ATG16L1 degradation to prevent ER stress during inflammation
Decreased ATG16L1 stabilization is associated with increased susceptibility to develop inflammatory bowel diseases. Diamanti et al. identify IKKα as a central upstream kinase of ATG16L1, providing evidence that ATG16L1 stabilization is controlled by phosphorylation downstream of TNF and NOD activation.