Results 31 to 40 of about 161,044 (231)

Cellular and humoral responses after second and third SARS-CoV-2 vaccinations in patients with autoimmune diseases treated with rituximab: specific T cell immunity remains longer and plays a protective role against SARS-CoV-2 reinfections

open access: yesFrontiers in Immunology, 2023
BackgroundHumoral and cellular immune responses are known to be crucial for patients to recover from COVID-19 and to protect them against SARS-CoV-2 reinfection once infected or vaccinated.ObjectivesThis study aimed to investigate humoral and T cell ...
Natalia Egri   +9 more
doaj   +1 more source

A case report of a novel compound heterozygous mutation in a Brazilian patient with deficiency of Interleukin-1 receptor antagonist (DIRA)

open access: yesPediatric Rheumatology Online Journal, 2020
Background Deficiency of the natural antagonist of interleukin-1 was first described in 2009 and so far 20 patients has been reported. In Brazil just two cases have been reported both carrying the same homozygous 15 bp deletion.
Leonardo Oliveira Mendonça   +9 more
doaj   +1 more source

Autoinflammatory Diseases: a Rapidly Advancing Field

open access: yes, 2022
Autoinflammatory diseases (AIDs) are a group of genetic disorders characterized by generalized inflammatory responses and multiorgan involvement primarily caused by dysregulated innate immunity.
SONG Hongmei, GAO Sihao
core   +1 more source

Childhood versus adulthood-onset autoinflammatory disorders: myths and truths intertwined

open access: yesReumatismo, 2013
Autoinflammatory disorders are characterized by spontaneous episodes of systemic inflammation deriving from inherited defects of the innate immune system.
L. Cantarini   +9 more
doaj   +1 more source

Autoinflammatory keratinization diseases [PDF]

open access: yesJournal of Allergy and Clinical Immunology, 2017
Inflammation caused by the hyperactivation of innate immunity due to genetic factors occasionally leads to inflammatory cutaneous keratinization diseases. Such inflammatory keratinization diseases with genetic autoinflammatory mechanisms are called “autoinflammatory keratinization diseases” (AiKDs). We proposed a four-part definition of AiKDs.
Akiyama, Masashi   +3 more
openaire   +3 more sources

MicroRNAs in Juvenile Idiopathic Arthritis: State of the Art and Future Perspectives

open access: yesBiology, 2023
Juvenile Idiopathic Arthritis (JIA) represents the most common chronic pediatric arthritis in Western countries and a leading cause of disability in children.
Simone Pelassa   +3 more
doaj   +1 more source

Spectrum of Genetic Autoinflammatory Diseases Presenting with Cutaneous Symptoms

open access: yesActa Dermato-Venereologica, 2020
Autoinflammatory diseases comprise a group of chronic disabling entities characterized by inflammation without the presence of infectious agents, auto-antibodies or antigen-specific T-cells. Many autoinflammatory diseases are caused by monogenic defects,
Hanna Bonnekoh   +5 more
doaj   +1 more source

Monogenic autoinflammatory diseases [PDF]

open access: yesRheumatology, 2014
During the past 15 years, a growing number of monogenic inflammatory diseases have been described and their respective responsible genes identified. The proteins encoded by these genes are involved in the regulatory pathways of inflammation and are mostly expressed in cells of the innate immune system.
Ricardo A G, Russo, Paul A, Brogan
openaire   +2 more sources

An international registry on autoinflammatory diseases: the Eurofever experience [PDF]

open access: yes, 2012
Item does not contain fulltextOBJECTIVE: To report on the demographic data from the first 18 months of enrollment to an international registry on autoinflammatory diseases in the context of the Eurofever project.
Hentgen, V.   +74 more
core   +1 more source

The Interactions Between Autoinflammation and Type 2 Immunity: From Mechanistic Studies to Epidemiologic Associations

open access: yesFrontiers in Immunology, 2022
Autoinflammatory diseases are a group of clinical syndromes characterized by constitutive overactivation of innate immune pathways. This results in increased production of or responses to monocyte- and neutrophil-derived cytokines such as interleukin-1β (
McKella Sylvester   +2 more
doaj   +1 more source

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