Evidence map›Paper›PMID 16514168›Full record

ReviewExperimental biology and medicine (Maywood, N.J.)2006

The immune system as a regulator of thyroid hormone activity.

John R Klein

Open access · greenAbstract readReview
In one paragraph

Review in Experimental biology and medicine (Maywood, N.J.), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

40 citing papers in PubMed, 119 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Local TSH/TSHR signaling promotes CD8Cancer communications (London, England) · 2024
    Article
  6. Article
  7. Article
  8. Review
  9. Article
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  12. Review
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  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
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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

1 author at 1 institution in 1 country.

John R KleinDepartment of Diagnostic Sciences, University of Texas Health Science Center at Houston, Room 3.094F, Dental Branch, 6516 MD Anderson Boulevard, 77030, USA. john.r.klein@uth.tmc.edu
The University of Texas Health Science Center at Houston · US

Funding

GUT-DERIVED IMMUNE EFFECTOR CELLSR01DK035566 · NIDDK · UNIVERSITY OF TULSA · PI KLEIN, JOHN R · 1988 to 2012
$2.9M
GUT-DERIVED IMMUNE EFFECTOR CELLSR23DK035566 · NIDDK · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI KLEIN, JOHN R · 1986 to 1987
–
NIDDK NIH HHS DK 035566NIDDK NIH HHS R01 DK035566
6 · The paper itself

Abstract

It has been known for decades that the neuroendocrine system can both directly and indirectly influence the developmental and functional activity of the immune system. In contrast, far less is known about the extent to which the immune system collaborates in the regulation of endocrine activity. This is particularly true for immune-endocrine interactions of the hypothalamus-pituitary-thyroid axis. Although thyroid-stimulating hormone (TSH) can be produced by many types of extra-pituitary cells--including T cells, B cells, splenic dendritic cells, bone marrow hematopoietic cells, intestinal epithelial cells, and lymphocytes--the functional significance of those TSH pathways remains elusive and historically has been largely ignored from a research perspective. There is now, however, evidence linking cells of the immune system to the regulation of thyroid hormone activity in normal physiological conditions as well as during times of immunological stress. Although the mechanisms behind this are poorly understood, they appear to reflect a process of local intrathyroidal synthesis of TSH mediated by a population of bone marrow cells that traffic to the thyroid. This hitherto undescribed cell population has the potential to microregulate thyroid hormone secretion leading to critical alterations in metabolic activity independent of pituitary TSH output, and it has expansive implications for understanding mechanisms by which the immune system may act to modulate neuroendocrine function during times of host stress. In this article, the basic underpinnings of the hematopoietic-thyroid connection are described, and a model is presented in which the immune system participates in the regulation of thyroid hormone activity during acute infection.

Indexed as

AnimalsBone MarrowBone Marrow CellsBone Marrow TransplantationHematopoietic SystemHumansImmune SystemThyroid GlandThyrotropinThyrotropin

Identifiers

PMID16514168
PMCPMC2768616
OpenAlexW1774685281

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.