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Increased Body Temperature

Increased Body Temperature

A body temperature above 38°C (100.4 °F) is known as fever or pyrexia, and a person with fever is termed 'febrile.' Typically, the hypothalamus, a part of the brain that acts as the body's thermostat, regulates body temperature through a thermoregulatory setpoint. It receives signals from cold and warm thermal receptors throughout the body and adjusts the body's temperature accordingly. Fever occurs when this hypothalamic setpoint is altered, usually in response to an infection or illness.

Types of Fever

Types of Fever

Fever can be triggered by several factors, including infections, nervous system disorders, certain cancers, blood diseases like leukemia, embolism, thrombosis, heatstroke, dehydration, surgical trauma, crushing injuries, and allergic reactions.
Here are the different types of fever:

Factors Affecting the Risk of Infection

Factors Affecting the Risk of Infection

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The integrity and count of the white blood cells help the body resist pathogens and fight infection. When impaired, it reduces the body's resistance to pathogens. The acidic pH levels of the gastrointestinal, genitourinary tracts, and skin create...

Introduction to Innate and Adaptive Immunity

Introduction to Innate and Adaptive Immunity

The human immune system is a complex defense mechanism that protects the body from harmful pathogens and foreign substances. It comprises two crucial components: innate and adaptive immunity.
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NF-κB-dependent Signaling Pathway

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Related Experiment Video

Updated: Jul 2, 2026

Using RNA-interference to Investigate the Innate Immune Response in Mouse Macrophages

Using RNA-interference to Investigate the Innate Immune Response in Mouse Macrophages

Published on: November 3, 2014

Fevers, genes, and innate immunity.

J G Ryan¹, D L Kastner

¹Genetics and Genomics Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, MD 20892, USA.

Current Topics in Microbiology and Immunology

|August 30, 2008

Summary

This summary is machine-generated.

Autoinflammatory syndromes are genetic disorders causing recurrent inflammation. Discovering gene mutations like MEFV and CIAS1 has revealed key pathways in innate immunity and inflammation.

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Area of Science:

Genetics
Immunology
Molecular Biology

Background:

Autoinflammatory syndromes are characterized by recurrent inflammatory episodes, distinct from autoimmune diseases.
Familial Mediterranean fever (FMF) is a prototype, with its causative gene MEFV and protein pyrin identified.
Other autoinflammatory conditions involve mutations in CIAS1 (cryopyrin) and MVK, impacting inflammasome and isoprenoid pathways.

Purpose of the Study:

To review the clinical phenotypes of autoinflammatory syndromes.
To discuss the underlying genetic mutations associated with these syndromes.
To explore current concepts regarding the pathophysiology of autoinflammatory diseases.

Main Methods:

Clinical characterization of patient phenotypes.
Genetic analysis including positional cloning to identify causative genes.
Biochemical pathway analysis to understand disease mechanisms.

Main Results:

Identification of MEFV (pyrin) as the gene mutated in FMF.
Discovery of CIAS1 (cryopyrin) mutations in cryopyrinopathies, leading to inflammasome activation and IL-1beta release.
Linkage of hyperimmunoglobulin D with periodic fever syndrome (HIDS) to MVK mutations in the isoprenoid pathway.
Unanticipated finding of TNFR1 mutations causing a proinflammatory phenotype.

Conclusions:

Distinct clinical phenotypes of autoinflammatory syndromes correlate with specific genetic mutations.
These genetic discoveries have elucidated critical roles of proteins like pyrin and cryopyrin in innate immunity.
Understanding these pathways, including inflammasome and IL-1beta, offers insights into inflammation regulation.