Evidence map›Paper›PMID 18325486›Full record

ReviewCellular immunology

Regulation of IGF-I function by proinflammatory cytokines: at the interface of immunology and endocrinology.

Jason C O'Connor, Robert H McCusker, Klemen Strle, Rodney W Johnson, Robert Dantzer, Keith W Kelley

Open access · greenAbstract readReview
In one paragraph

Review in Cellular immunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 1 pooled it
10.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

100 citing papers in PubMed, 1 synthesis or guideline pooled it, 238 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Article
  7. Review
  8. Longitudinal variations of paraspinal muscle fatty infiltration in obese patients after bariatric surgery.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026
    Article
  9. Article
  10. Article
  11. Evaluation of the Effect of IL-1 Antagonists on Pituitary Function.International journal of endocrinology · 2026
    Article
  12. Review
  13. Growth hormone - releasing hormone in the immune system.Reviews in endocrine & metabolic disorders · 2025
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

40 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 2 countries.

Jason C O'ConnorIntegrative Immunology and Behavior Program, Department of Animal Sciences, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.
Robert H McCusker
Klemen Strle
Rodney W Johnson
Robert Dantzer
Keith W Kelley
University of Illinois Urbana-Champaign · US

Funding

REGULATION OF INTERLEUKIN-6 IN THE AGING BRAINR01AG016710 · NIA · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI JOHNSON, RODNEY W · 2000 to 2015
$4.8M
CYTOKINES, BEHAVIOR, AND MENTAL HEALTHR01MH051569 · NIMH · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI KELLEY, KEITH W · 1995 to 2008
$2.6M
Neuroimmune Mechanisms of Depressive-Like Behavior During AgingR01AG029573 · NIA · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI KELLEY, KEITH W · 2007 to 2011
$2.1M
AIDS, Immune Activation and Mental HealthR01MH079829 · NIMH · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI DANTZER, ROBERT · 2006 to 2010
$1.8M
Neuroimmunology of Behavioral and Mood DisordersR01MH071349 · NIMH · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI DANTZER, ROBERT · 2004 to 2008
$1.6M
Neuroimmune Control of Biobahavioral ProcessesR01AG023580 · NIA · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI JOHNSON, RODNEY W · 2005 to 2009
$1.5M
CYTOKINE AND HORMONE INTERACTIONS IN COMORBIDITY OF AIDSR01AI050442 · NIAID · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI KELLEY, KEITH W. · 2002 to 2005
$1.4M
NIAID NIH HHS AI 50422NIAID NIH HHS R01 AI050442NIA NIH HHS AG 023580NIA NIH HHS AG 029573NIA NIH HHS AG 16710NIA NIH HHS R01 AG016710NIA NIH HHS R01 AG023580NIA NIH HHS R01 AG029573NIMH NIH HHS MH 079829NIMH NIH HHS MH 51569NIMH NIH HHS MH71349NIMH NIH HHS R01 MH051569NIMH NIH HHS R01 MH071349NIMH NIH HHS R01 MH079829
6 · The paper itself

Abstract

During the past decade, the immune and endocrine systems have been discovered to interact in controlling physiologic processes as diverse as cell growth and differentiation, metabolism, and even human and animal behavior. The interaction between these two major physiological systems is a bi-directional process. While it has been well documented that hormones, including prolactin (PRL), growth hormone (GH), insulin-like growth factor-I (IGF-I), and thyroid-stimulating hormone (TSH), regulate a variety of immune events, a great deal of data have accumulated supporting the notion that cytokines from the innate immune system also affect the neuroendocrine system. Communication between these two systems coordinates processes that are necessary to maintain homeostasis. Proinflammatory cytokines often act as negative regulatory signals that temper the action of hormones and growth factors. This system of 'checks and balances' is an active, ongoing process, even in healthy individuals. Dysregulation of this process has been implicated as a potential pathogenic factor in the development of co-morbid conditions associated with several chronic inflammatory diseases, including type 2 diabetes, cardiovascular disease, cerebrovascular disease, inflammatory bowel disease, rheumatoid arthritis, major depression, and even normal aging. Over the past decade, research in our laboratory has focused on the ability of the major proinflammatory cytokines, tumor necrosis factor (TNF)alpha and interleukin (IL)-1beta, to induce a state of IGF resistance. This review will highlight these and other new findings by explaining how proinflammatory cytokines induce resistance to the major growth factor, insulin-like growth factor-I (IGF-I). We also highlight that IGF-I can induce resistance or reduce sensitivity to brain TNFalpha and discuss how TNFalpha, IL-1beta, and IGF-I interact to regulate several aspects of behavior and cognition.

Indexed as

AnimalsBrainHumansInsulin-Like Growth Factor IInterleukin-1betaMiceTumor Necrosis Factor-alphaInsulin-Like Growth Factor IInterleukin-1betaTumor Necrosis Factor-alpha

Identifiers

PMID18325486
PMCPMC2615236
OpenAlexW2006585084

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.