Neuroendocrine regulation of immunity.
By J. I. Webster, L. Tonelli, Esther M. Sternberg. Annual Review of Immunology, 2003
941 citations recorded by the source corpus.
Subfields: Behavioral Neuroscience, Endocrinology, Diabetes and Metabolism, Immunology
View Paper: https://www.semanticscholar.org/paper/8008bf40d1daa1a885d8f81e8832cf2a50d426b4
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Behavioral Neuroscience
- Gregory E. Miller
- Steve W. Cole
- E. Chen
- Sheldon Cohen
- Denise Janicki-Deverts
- Robin Nusslock
- S. Adamo
- Kevin J. Tracey
In Endocrinology, Diabetes and Metabolism
In Immunology
- Kevin J. Tracey
- Gregory E. Miller
- W. Vanden Berghe
- Steve W. Cole
- S. Adamo
- G. Haegeman
- K. De Bosscher
- E. Chen
Citations in the corpus
- Low early-life social class leaves a biological residue manifested by decreased glucocorticoid and increased proinflammatory signaling (2009, background): “For example, NF- B is a key proinflammatory transcription factor that is subject to potent counterregulation by GR (17).”
- Molecular and cellular endocrinology (2000, neutral): “…metabolic syndromes, - + - + - + 0.0 0.5 1.0 Control HFD HFD+Mt * * p-IRS-1/IRS-1 - + - + - + 0.0 0.5 1.0 1.5 2.0 Control HFD HFD+Mt ** * pAKT/AKT A B - + - + - + 0.0 0.5 1.0 1.5 2.0 2.5 Control HFD HFD+Mt * ** C p-IRS/IRS-1 - + - + - + 0.00 0.25 0.50 0.75 1.00 1.25 Control HFD HFD+Mt * ** D”
- Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk (2012, background): “Moreover, although the focus here has been on GCR in circulating leukocytes and neutrophils, stress could also be associated with illness expression through its effect on the glucocorticoid sensitivity of other cells involved in immune defenses (26).”
- The inflammatory reflex (2002, background): “Functional deficiencies in the release of corticotropin-releasing factor (CRF) predispose Lewis rats to developing experimental arthritis induced by streptococcal antigens because of an insufficient glucocorticoid respons”
- Splenectomy inactivates the cholinergic antiinflammatory pathway during lethal endotoxemia and polymicrobial sepsis (2006, background): “Vagus nerve modulation of the spleen may represent the functionally, hard-wired counterpart to humoral antiinfl ammatory responses, such as the hypothalamic–pituitary– adrenal axis (26).”
- The interplay between the glucocorticoid receptor and nuclear factor-kappaB or activator protein-1: molecular mechanisms for gene repression. (2003, background): “This includes signal transduction cascades elicited by different cell-cell contacts, systemic signals, GR metabolism, and neuroendocrine effects (178, 203, 316, 317).”
- Early-Life Adversity and Physical and Emotional Health across the Lifespan: A Neuro-Immune Network Hypothesis (2015, background): “SNS fibers descend from the brain into organs where leukocytes mature, including bone marrow, the spleen, and thymus, and into organs where pathogen-leukocyte interactions transpire, like the lymph nodes, gut, and lungs (63).”
- Temperature extremes and butterfly fitness: conflicting evidence from life history and immune function (2011, background): “Note in this context that in mammals two mediators of the response to acute stress, norepinephrine and glucocorticoids, are known to be immunosuppressive thus decreasing disease resistance (e.g. Webster et al., 2002; Cao et al., 2003; Sternberg, 2006; Emeny et al., 2007).”
- Norepinephrine and octopamine: linking stress and immune function across phyla (2008, background): “…A Adamo Department of Psychology Dalhousie University Halifax, NS, B3H 4J1, Canada E-mail: sadamo@dal.ca because immune cells in vertebrates (e.g. Webster et al., 2002; Madden, 2003), molluscs (Lacoste et al., 2001b) and insects (Gole et al., 1982; Orr et al., 1985) have receptors for NE or OA.”