The Obese Strain of Chickens: An Animal Model with Spontaneous Autoimmune Thyroiditis

Endothelial cell apoptosis is a primary pathogenetic event underlying skin lesions in avian and human scleroderma.

“…3 C). The healthy NWL and UCD-058 controls as well as OS chickens, an unrelated model for autoimmune Hashimoto thyroiditis (19), were AECA negative (Fig. 3, Tables III and IV.…”

“…The following strains of chickens were used: UCD lines 200 and 206, which spontaneously develop an inherited scleroderma-like disease (7,18), healthy UCD line 058, which have the same MHC haplotype ( B 15 ) as line 206, normal White Leghorn (NWL) chickens as healthy outbred controls, and the obese strain (OS), a chicken model of spontaneous autoimmune thyroiditis (19,20), as a control with an unrelated organ-specific autoimmune disease. NWL chickens were purchased from a local breeder (F. Moser, Polling, Austria).…”

Premature Ovarian Failure and Ovarian Autoimmunity

“…BB rats also show a rapid thymic involution (170). The OS strain of chickens has inborn defects in its suppressor cell system (159). Whether there are similar inborn defects in immunoregulatory cells in the human that lead to an endocrine autoimmune disease needs to be established.…”

A Role for IL-15 in Driving the Onset of Spontaneous Autoimmune Thyroiditis?

“…The onset of mononuclear cell infiltration of the thyroid in OS chicks is from 7 days of age, the first cells forming the multifocal infiltrates in the thyroid gland being activated CD4 ϩ , IL-2R ϩ , TCR-␣␤ 1 ϩ T cells (4). By 1 or 2 mo of age, the thyroid architecture is almost completely destroyed (5,6). OS chickens exhibit general immune system hyperreactivity, believed in part to be due to intrinsic production of cytokines, perhaps IL-2 (7).…”

“…OS chickens exhibit general immune system hyperreactivity, believed in part to be due to intrinsic production of cytokines, perhaps IL-2 (7). Other immunomodulating factors in OS chickens that may contribute to SAT include premature emigration of Th cells from the thymus to the periphery during ontogenesis (8), an imbalance between effector and suppressor cells (9), and a disturbed immune-endocrine system interaction (6). Cytokines, in particular, probably have a role in initiating and perpetuating the disease.…”