Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Autoimmune Disorders01:29

Autoimmune Disorders

Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
Concept and Mechanism of Autoimmune Diseases
The immune system...
Type I Diabetes I: Introduction01:12

Type I Diabetes I: Introduction

Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1 diabetes is an...
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia Gravis ll: Pathophysiology

The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Local and global microstructural and functional thalamomotor connectivity alterations in Parkinson's disease following motor learning.

NPJ Parkinson's disease·2026
Same author

Neural correlates of Parkinson's improvements after combined digital-levodopa therapy: a pilot study.

Brain communications·2026
Same author

The genetic and clinical characteristics of oculopharyngeal muscular dystrophy patients in Israel.

Orphanet journal of rare diseases·2026
Same author

Early Clinical Swallow Evaluation Is Associated with Lower Malnutrition Prevalence at Discharge in Neurogeriatric Rehabilitation Patients: A Prospective Study.

Nutrients·2026
Same author

Heterogeneous response to efgartigimod in real-world experience with myasthenia gravis: Predictors and treatment strategies.

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics·2026
Same author

Urinary dysfunction in myasthenia Gravis: a cross-sectional case-control study.

Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology·2026
Same journal

Decoding gut microbiome alterations in celiac disease: Implications for pathogenesis and treatment.

Autoimmunity reviews·2026
Same journal

Rethinking immunosuppression in limited cutaneous systemic sclerosis. The lcSSc conundrum; pros and cons for a timely immunosuppressive treatment.

Autoimmunity reviews·2026
Same journal

Kidney failure in patients with ANCA-associated vasculitis: A systematic review of outcomes.

Autoimmunity reviews·2026
Same journal

The role of antimicrobial peptides in rheumatoid arthritis: From mucosal predisposition to chronic synovitis.

Autoimmunity reviews·2026
Same journal

The role of short-chain fatty acids as key mediators of gut microbiota - host crosstalk in thyroid diseases.

Autoimmunity reviews·2026
Same journal

Intermittent hydrarthrosis (periodic synoviosis): A narrative review.

Autoimmunity reviews·2026
See all related articles

Related Experiment Video

Updated: May 26, 2026

Induction of Experimental Autoimmune Hypophysitis in SJL Mice
10:38

Induction of Experimental Autoimmune Hypophysitis in SJL Mice

Published on: December 17, 2010

Prolactin and autoimmunity.

Shahar Shelly1, Mona Boaz, Hedi Orbach

  • 1Department of Medicine B, Wolfson Medical Center, Holon, Israel.

Autoimmunity Reviews
|December 14, 2011
PubMed
Summary
This summary is machine-generated.

Prolactin (PRL) and estrogen significantly influence the immune system, with elevated prolactin levels (hyperprolactinemia) potentially promoting autoimmunity and various autoimmune diseases.

More Related Videos

Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis
10:52

Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis

Published on: December 17, 2010

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Related Experiment Videos

Last Updated: May 26, 2026

Induction of Experimental Autoimmune Hypophysitis in SJL Mice
10:38

Induction of Experimental Autoimmune Hypophysitis in SJL Mice

Published on: December 17, 2010

Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis
10:52

Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis

Published on: December 17, 2010

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Area of Science:

  • Immunology
  • Endocrinology
  • Autoimmunity

Background:

  • Sex hormones, particularly estrogen and prolactin (PRL), play a crucial role in immune response modulation.
  • Prolactin is secreted by the pituitary gland and lymphocytes, exerting immune-stimulatory effects and promoting autoimmunity.
  • Hyperprolactinemia (HPRL) is linked to clinical symptoms like galactorrhea and menstrual irregularities.

Purpose of the Study:

  • To explore the association between hyperprolactinemia and a wide range of autoimmune diseases.
  • To investigate the immune-stimulatory mechanisms of prolactin, including its effects on B cell tolerance and autoantibody production.
  • To examine the correlation between prolactin levels and disease activity in specific autoimmune conditions.

Main Methods:

  • Review of existing literature on prolactin, autoimmunity, and associated diseases.
  • Analysis of clinical manifestations and immunological parameters in patients with hyperprolactinemia.
  • Exploration of the role of genetic factors and prolactin isoforms in disease pathogenesis.

Main Results:

  • Hyperprolactinemia is associated with numerous autoimmune diseases, including SLE, RA, Hashimoto's thyroiditis, and MS.
  • PRL enhances B cell responses, reduces tolerance induction, and increases autoantibody production.
  • A correlation exists between prolactin levels and disease activity in certain autoimmune conditions.
  • PRL isoforms exhibit varying bioactivity, influencing prolactin receptor interactions.

Conclusions:

  • Elevated prolactin levels are implicated in the development and progression of multiple autoimmune diseases.
  • Understanding the immune-modulatory role of prolactin and its isoforms is critical for managing autoimmune conditions.
  • Further research into genetic factors and PRL isoforms may reveal novel therapeutic targets for autoimmune diseases.