1). Its role in atherosclerosis is essentially unaddressed to date. MDSCs and their monocyte components often increase in numbers in humans and mice that have cancer
Fulvestrant order or other chronic inflammatory conditions 45–47. The tumor-induced mechanisms that drive this expansion need further investigation, yet interesting studies already indicate that growth factors produced by tumor cells are important. As discussed in What can cardiovascular disease teach us about cancer?, experimental atherosclerosis also leads to great proliferation of Ly6Chigh monocytes in the host 21 and leukocytosis is a risk factor for cardiovascular disease in humans 48. These findings indicate that both diseases trigger systemic monocyte responses, but they also prompt a number of questions. Does atherosclerosis elicit PI3K inhibitor the production
of bona fide MDSCs? Which factors drive the Ly6Chigh monocyte/MDSC response in atherosclerosis and do these factors overlap with those involved in cancer? How do Ly6Chigh monocytes/MDSCs produced in cancer and atherosclerosis compare qualitatively? We propose that investigations of MDSC-like responses at the cellular and molecular levels in atherosclerosis will be valuable. The growth of a tumor and an atherosclerotic lesion are two phenomena where monocyte accumulation and chronic inflammation converge. In this Viewpoint, we have focused on the recent observations in atherosclerosis and cancer. These observations, together with others not discussed here, such as the role of genetics, may serve as useful think tanks for defining future experimental research and for understanding the two diseases better. Conflict of interest: The authors declare no fonancial or commercial conflict of interest. See accompanying Viewpoints: http://dx.doi.org/10.1002/eji.201141719http://dx.doi.org/10.1002/eji.201141894 The complete Macrophage Viewpoint series is available at: http://onlinelibrary.wiley.com/doi/10.1002/eji.v41.9/issuetoc “
“The impact of gestation and fetal–maternal interactions on Methamphetamine pre-existent autoimmune beta cell destruction is
widely unknown. The aim of this study was to investigate the influence of gestation per se and fetal mismatching on the onset of autoimmune diabetes in female non-obese diabetic (NOD) mice. We examined cumulative diabetes frequencies of NOD dams mated to syngeneic NOD, haploidentical CByB6F1/J and fully mismatched C57BL/6J male mice. Pregnancy from NOD males neither increased nor accelerated the diabetes onset of NOD dams (71% by age 28 weeks) compared to unmated female NOD mice (81% by age 28 weeks; P = 0·38). In contrast, delayed diabetes onset was observed when NOD dams were mated at 10 weeks of age with major histocompatibility complex (MHC) haploidentical CByB6F1/J male mice (38% at age 28 weeks; P = 0·01).