This article discusses mucosal-associated invariant T-cell prophylactic and therapeutic vaccination schemes tested by Sakai et al. in mouse models of Mycobacterium tuberculosis infection together with the outcomes and observations.

Ng et al. have identified NKG7 as a regulator of inflammation in response to diverse immunological challenges. While NKG7 was required for the degranulation of cytotoxic cells, additional defects including reduced expansion and trafficking of CD8 T cells, and altered antigen presentation, were noted in NKG7-deficient mice. The precise mechanism by which NKG7 mediates its effects has not been resolved but may involve regulation of endosomal vesicle trafficking.

In this study, we showed that induction of inflammation in the peritoneal cavity by Toll-like receptor 2 (TLR2) agonists induces chemokine production with very high levels of the CCR2 ligands CCL2 and CCL7. Natural killer (NK) cells are recruited to the peritoneum after TLR2-induced inflammation in a CCR2-dependent manner, but do not acquire an activated phenotype. Recruited NK cells can be activated by interleukin (IL)-12 and IL-18 to express CD69 and interferonγ.

Human visceral and subcutaneous white adipose tissues seem to limit inflammation during obesity by differentially altering their macrophage subset composition. In the obese visceral tissue the inflammatory CLEC5A⁺ macrophage subset diminishes its counts, whereas a CD11c⁺ with a mixed M1/M2 phenotype is expanded. Subcutaneous adipose tissue expansion is dominated by a subset of M2-like macrophages, with a minor contribution of an M1-like subpopulation.

The intact human mammary tissue, termed patient-derived explant (PDE), can be used to investigate cellular responses to a wide variety external stimuli in situ. For this study, we examined the impact of cytokines or environmental chemicals on macrophage phenotypes. We demonstrate that we can polarize macrophages within human breast tissue PDEs toward M1 or M2 and the endocrine-disrupting chemical, benzophenone-3, also affects macrophage polarization.