Macrophages isolated from various tissues manifest differences in cell shape, the expression of surface markers, as well as metabolic and functional activities. However, the heterogeneity of macrophages expressing the same marker in different tissues has not been fully addressed. In the present study, mouse F4/80+ peritoneal exudate macrophages (PEMs) and splenic macrophages (SPMs) appeared similar in most respects. But the percentages of cells expressing CD80, CD40, MHC-II, TLR2, or TLR4, but not CD11c, CD54, or CD23, in freshly isolated F4/80+ SPMs were significantly higher than those in PEMs, whereas the levels of CD86+ cells in F4/80+ SPMs were markedly lower than those in PEMs. After lipopolysaccharide (LPS) stimulation, F4/80+ SPMs expressed significantly higher levels of CD86, CD40, or MHC-II than F4/80+ PEMs, but not CD11c, CD80, CD54, or CD23. F4/80+ SPMs had remarkably lower non-opsonic phagocytotic capacity against chicken RBCs or allo-T cells than PEMs as determined by two-photon microscopes and flow cytometry. SPMs produced markedly more NO than PEMs when cultured with LPS or allo-T cells. Furthermore, SPMs exhibited stronger immunogenicity than PEMs, as determined by the ability to stimulate T cell proliferation, delayed type hypersensitivity, and IFN-gamma production. The data showed the differences between SPMs and PEMs with regard to the phenotypes, phagocytosis, and immunogenicity, which may offer important information for us to better understand the distinguished immune responses of macrophages in spleens and the peritoneal cavity.

The transforming growth factor-beta (TGF-beta) protein family is highly evolutionarily conserved and they have been implicated in many biological processes. Also, TGF-beta can exert pivotal functions in the immune system. It is widely accepted that regulatory T cells (Treg cells) play an important role in the maintenance of the immune homeostasis, but the underlying molecular mechanisms through which they can gain and/or perform suppressive functions in an active way remains to be defined. Though the engagement of TGF-beta in the Treg cells has been discounted for a period of time, an emerging body of data has established a close link between Treg cells and TGF-beta, as TGF-beta has been demonstrated to induce the expression of Foxp3, which acts as a master regulator for the development and function of Treg cells. We will, herein, focus on the crucial role of TGF-beta signaling in Treg cell biology and summarize the current studies regarding TGF-beta in the generation and function of CD4+CD25+Treg cells both in vivo and in vitro.

Grave’s disease (GD) occurs due to an autoimmune dysfunction of thyroid gland cells, leading to manifestations consistent with hyperthyroidism. Various studies have confirmed the link between autoimmune conditions and changes in the composition of intestinal microbial organisms. However, few studies have assessed the relationship between the disease of GD and the changes of intestinal microbiota. Therefore, this study aimed to investigate changes in intestinal flora that may occur in the setting of GD. Thirty-nine patients with GD and 17 healthy controls were enrolled for fecal sample collection. 16S rRNA sequencing was used to analysis the diversity and composition of the intestinal microbiota. High-throughput sequencing of 16S rRNA genes of intestinal flora was performed on Illumina Hiseq2500 platform. Comparing to healthy individuals, the number of Bacilli, Lactobacillales, Prevotella, Megamonas and Veillonella strains were increased, whereas the number of Ruminococcus, Rikenellaceae and Alistipes strains were decreased among patients with GD. Furthermore, patients with GD showed a decrease in intestinal microbial diversity. Therefore, it indicates that the diversity of microbial strains is significantly deduced in GD patients, and patients with GD will undergo significant changes in intestinal microbiota, by comparing the intestinal flora of GD and healthy controls. Theses conclusion are expected to provide a preliminary reference for further researches on the interaction mechanism between intestinal flora and GD.

Our present study showed that the interaction of IL2 and IL2R across species might have defects. Together with the wide physiological functions of IL2, our data indicated that physiological disorders could be caused by the poor function of xenogeneic donor IL2 on host cells in full hematopoietic chimera. Our data suggested an additional potential advantage for the mixed xenogeneic chimeras.