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Titolo:
IL-4-dependent effector phase in autoimmune exocrinopathy as defined by the NOD.IL-4-gene knockout mouse model of Sjogren's syndrome
Autore:
Brayer, JB; Cha, S; Nagashima, H; Yasunari, U; Lindberg, A; Diggs, S; Martinez, J; Goa, J; Humphreys-Beher, MG; Peck, AB;
Indirizzi:
Univ Florida, Coll Dent, Dept Oral Biol, Gainesville, FL 32610 USA Univ Florida Gainesville FL USA 32610 ral Biol, Gainesville, FL 32610 USA Univ Florida, Coll Med, Dept Pathol Immunol & Lab Med, Gainesville, FL 32611 USA Univ Florida Gainesville FL USA 32611 Lab Med, Gainesville, FL 32611 USA Univ Florida, Ctr Orphaned Autoimmune Dis, Gainesville, FL 32610 USA Univ Florida Gainesville FL USA 32610 mune Dis, Gainesville, FL 32610 USA
Titolo Testata:
SCANDINAVIAN JOURNAL OF IMMUNOLOGY
fascicolo: 1-2, volume: 54, anno: 2001,
pagine: 133 - 140
SICI:
0300-9475(200107/08)54:1-2<133:IEPIAE>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
DIABETIC NOD MOUSE; SALIVARY-GLANDS; ANIMAL-MODEL; MICE; AUTOANTIBODIES; ANTIBODIES; MECHANISMS; RECEPTORS; APOPTOSIS; DISEASE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Humphreys-Beher, MG Univ Florida, Coll Dent, Dept Oral Biol, POB 100424, Gainesville, FL 32610USA Univ Florida POB 100424 Gainesville FL USA 32610 10USA
Citazione:
J.B. Brayer et al., "IL-4-dependent effector phase in autoimmune exocrinopathy as defined by the NOD.IL-4-gene knockout mouse model of Sjogren's syndrome", SC J IMMUN, 54(1-2), 2001, pp. 133-140

Abstract

NOD mice manifest many features of autoimmune exocrinopathy (Sjogren's syndrome), a disease generally characterized by a chronic, progressive immunological attack against the exocrine tissues of the salivary and lacrimal glands. Previous studies using the NOD congenic partner strain, NOD.Ig mu (null), defined an important role for B lymphocytes in the development of xerostomia, implicating autoantibodies reactive with the acetylcholine muscarinic receptor (M3R) as the possible effector mechanism. In the present study, we have examined the impact of the cytokine, interleukin (IL)-4, on autoimmune exocrinopathy by using the IL-4 gene knockout (KO) NOD mouse strain, NOD.IL-4(-/-). Despite manifesting the physiological aberrations and marked leukocytic infiltration of the salivary glands characteristic of autoimmune xerostomia in NOD mice, the NOD.IL-4(-/-) mice do not develop xerostomia. However, NOD.IL-4(-/-) mice that received adoptively transferred T lymphocytes derived from NOD.Ig mu (-/-) mice progress to xerostomia, thereby reversing the defect. While progression or lack of progression to xerostomia correlated with the ability of the NOD.IL-4(-/-) mice to express detectable anti-M3R autoantibodies, the precise mechanism of how IL-4 influences the development of autoimmune xerostomia remains speculative.

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Documento generato il 21/09/20 alle ore 16:14:24