necrosis factor alpha. Pregnancy presents a unique immune challenge for the maternal host. Systemically, significant gestation-dependent immune adaptions arise throughout pregnancy and characterisation of these is a major focus of materno-fetal immunology
J A Tamblyn, M Hewison, C L Wagner, J N Bulmer, and M D Kilby
Rene F Chun, John S Adams, and Martin Hewison
-for-profit sector. References Adams JS Hewison M 2008 Unexpected actions of vitamin D: new perspectives on the regulation of innate and adaptive immunity . Nature Clinical Practice. Endocrinology and Metabolism 4 80 – 90 . Adams JS Chen H Chun RF
Jacob H Hollis, Stafford L Lightman, and Christopher A Lowry
Introduction The changes in neuroendocrine activity in response to peripheral immune system activation are an important adaptive response. Neuroendocrine responses to immune activation include increases in plasma concentrations of
D S Boeldt and I M Bird
developing fetus. In basic terms, we can describe the gross changes, which permit a healthy maternal vasculature in pregnancy, but our understanding is more limited in terms of how the body coordinates the necessary adaptive processes from the molecular level
Nicolás Gigena, Vanina A Alamino, María del Mar Montesinos, Magalí Nazar, Ruy A Louzada, Simone M Wajner, Ana L Maia, Ana M Masini-Repiso, Denise P Carvalho, Graciela A Cremaschi, and Claudia G Pellizas
reported ( De Vito et al . 2011 , 2012 , Cremaschi et al . 2016 ). However, studies on the impact of THs on the initiation of adaptive immunity at the level of antigen-presenting cells (APCs) are just emerging. We provided the first evidence of the
Joan Villarroya, Rubén Cereijo, Aleix Gavaldà-Navarro, Marion Peyrou, Marta Giralt, and Francesc Villarroya
others restrict the use of the term to proteins released by the brown adipocyte ‘cell type’. This is a biologically relevant distinction, considering the presence of non-brown adipocyte cells in the BAT (e.g. macrophages and other immune cells, vascular
Bruce S McEwen, Jason D Gray, and Carla Nasca
laboratories, that redefined neuroendocrinology as a field that also studies two-way brain body communication via the neuroendocrine, autonomic, immune and metabolic systems. This research has uncovered the remodeling of brain architecture mediated by hormones
JA Baugh and SC Donnelly
The diverse actions of macrophage migration inhibitory factor (MIF) within the immuno-neuroendocrine system are yet to be fully understood, but it is clear that MIF plays a pivotal role in the regulation of both the innate and adaptive immune response. An emerging body of data presently indicates that MIF's position within the cytokine cascade is to act in concert with glucocorticoids to control the 'set point' and magnitude of the immune and inflammatory response. In this article we will review the actions of MIF within the immune system and discuss the overlapping and contrasting aspects of MIF and glucocorticoid biology. In particular we will focus on the role of MIF within the immuno-neuroendocrine interface and suggest molecular mechanisms by which MIF may counter-regulate glucocorticoid function. Finally we will discuss emerging evidence that functional MIF gene-promoter polymorphisms render one susceptible to elevated MIF expression, and the development of an exaggerated immune/inflammatory response that potentiates the progression to chronic inflammatory disease.
F. A. Antoni, J. Hoyland, M. D. Woods, and W. T. Mason
Stress provokes a cohort of homeostatic reflexes by the central nervous, the immune as well as the metabolic control systems of the body. These powerful adaptive responses, which can cause a collapse of body homeostasis in the absence of feedback inhibition, are suppressed by adrenal glucocorticoid hormones. A prominent and physiologically significant early action of glucocorticoids that requires the induction of newly synthesized messenger RNA and protein is the suppression of ACTH release by anterior pituitary corticotroph cells. It is demonstrated here that glucocorticoids inhibit stimulated ACTH secretion in pituitary corticotroph tumour (AtT-20) cells by reducing stimulus-evoked intracellular free calcium transients. Thus, the data show for the first time that intracellular calcium signals may be modified by rapidly induced proteins. It is proposed that this is a general mechanism that underlies the early inhibitory effects of glucocorticoids during stress in various types of cell.
RP Donn and DW Ray
The immunological and neuroendocrine properties of macrophage migration inhibitory factor (MIF) are diverse. In this article we review the known cellular, molecular and genetic properties of MIF that place it as a key regulatory cytokine, acting within both the innate and adaptive immune responses.The unexpected and paradoxical induction of MIF secretion by low concentrations of glucocorticoids is explored. The role of MIF as a locally acting modulator of glucocorticoid sensitivity within foci of inflammation is also discussed. MIF has no homology with any other pro-inflammatory cytokine and until recently lacked a recognised transmembrane receptor. MIF has also been shown to be directly taken up into target cells and to interact with intracellular signalling molecules, including the Jun activation domain-binding protein Jab-1.Comprehensive analysis of the MIF gene has identified important functional polymorphisms and a series of genetic studies has revealed both association and linkage of MIF with inflammatory diseases. Altered MIF regulation may therefore be pivotal to acquiring chronic inflammation following an innate immune response.