Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Absence of IL-4 facilitates the development of chronic autoimmune myasthenia gravis in C57BL/6 mice.

Journal of immunology (Baltimore, Md. : 1950) - 1 Jan 2003

Ostlie Norma, Milani Monica, Wang Wei, Okita David, Conti-Fine Bianca M

Abstract excerpt

Myasthenia gravis (MG) is a T cell-dependent, Ab-mediated autoimmune disease. Ab against muscle acetylcholine receptor (AChR) cause the muscular weakness that characterizes MG and its animal model, experimental MG (EMG). EMG is induced in C57BL6 (B6) mice by three injections of Torpedo AChR (TAChR) in adjuvant. B6 mice develop anti-TAChR Ab that cross-react with mouse muscle AChR, but their CD4+ T cells do not...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to B7-1 Antigen
Share to CD40 Antigens
Share to Epitopes, T-Lymphocyte

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Immunization

Share to Injections, Subcutaneous

Share to Interleukin-4

Share to Receptors, Cholinergic

Share to Torpedo

Source

Identifiers

PMID: 12496449
DOI: 10.4049/jimmunol.170.1.604

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Absence of IL-4 facilitates the development of chronic autoimmune myasthenia gravis in C57BL/6 mice.PMID 12496449Read ↗

Transgenic expression of IL-10 in T cells facilitates development of experimental myasthenia gravis.Semantic proximity Read ↗

Absence of IFN-gamma or IL-12 has different effects on experimental myasthenia gravis in C57BL/6 mice.Semantic proximity Read ↗

C57BL/6 mice genetically deficient in IL-12/IL-23 and IFN-gamma are susceptible to experimental autoimmune myasthenia gravis, suggesting a pathogenic role of non-Th1 cells.Semantic proximity Read ↗

The susceptibility to experimental myasthenia gravis of STAT6-/- and STAT4-/- BALB/c mice suggests a pathogenic role of Th1 cells.Semantic proximity Read ↗

Mice with IFN-gamma receptor deficiency are less susceptible to experimental autoimmune myasthenia gravis.Semantic proximity Read ↗

Major histocompatibility complex class II gene disruption prevents experimental autoimmune myasthenia gravis.Semantic proximity Read ↗

Experimental myasthenia gravis in Aire-deficient mice: a link between Aire and regulatory T cells.Semantic proximity Read ↗

Inhibitory IgG receptor FcgammaRIIB fails to inhibit experimental autoimmune myasthenia gravis pathogenesis.Semantic proximity Read ↗

Genetic deficiency of estrogen receptor alpha fails to influence experimental autoimmune myasthenia gravis pathogenesis.Semantic proximity Read ↗

Fatigue and muscle atrophy in a mouse model of myasthenia gravis is paralleled by loss of sarcolemmal nNOS.Semantic proximity Read ↗

Immunization of mice with LRP4 induces myasthenia similar to MuSK-associated myasthenia gravisSemantic proximity Read ↗

Ek alpha transgene in B10 mice suppresses the development of myasthenia gravis.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.