Influence of major histocompatibility haplotype on autoimmune disease varies in different inbred families of chickens.

Bacon, Larry D.; Rose, Noel R.

doi:10.1073/pnas.76.3.1435

Cited by 24 publications

(6 citation statements)

References 21 publications

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“…Crosses between OS and the ancestral CS birds produced an F a generation that exhibited thyroiditis, although not as severe as in the OS . Further genetic analysis on the basis of F 2 generations revealed that the disease is influenced by genes within the MHC as well as in non-MHC-associated genes (Bacon and Rose, 1979). These genes are Thyroid pathology index (± SE) of 6-wk-old chicks from B 13 B 5 x B 13 B 5 mating.…”

Section: The Obese Strain Chickenmentioning

confidence: 98%

Avian Models of Autoimmune Disease: Lessons from the Birds

Rose

1994

Poultry Science

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Many important lessons have been learned from studies of autoimmune diseases in chicken models. It is now quite clear that both cellular and humoral immune responses are important in developing the final picture of autoimmune disease. In the case of the amelanosis of Smyth line (SL) chickens, antibody appears to play the primary role, whereas the sclerosis of University of California/Davis line-200 (UCD-200) birds is mainly mediated by T cells. Chronic thyroiditis of the OS chicken is due to both humoral and cellular effector mechanisms. The Obese strain (OS) chicken is particularly valuable for studies of genetics. Multiple genetic factors converge in producing maximal susceptibility to the development of autoimmune thyroiditis. They include MHC genes responsible for immune recognition; genes affecting thymus development, critical for regulation of the immune response; and genes that control thyroid function, influencing the vulnerability of the target organ to autoimmune attack. The importance of environmental factors, such as dietary iodine, is also strongly supported by studies in the OS chicken. Thus, the birds have provided valuable clues to our understanding of human autoimmune disorders in the past and are expected to do so in the future.

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Section: The Obese Strain Chickenmentioning

confidence: 98%

Avian Models of Autoimmune Disease: Lessons from the Birds

Rose

1994

Poultry Science

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“…The MHC has been associated with development of GBS in some studies (Gorodezky et al, 1983;Monos et al, 1997). The MHC is often associated with autoimmune diseases, and has been associated with the development of spontaneous autoimmune thyroiditis in inbred sub-lines of Obese strain chickens selected for the development of spontaneous autoimmune thyroiditis (Bacon & Rose, 1979). The agent most implicated in GBS at present is the enteric bacterium Campylobacter jejuni, which influences not only cell-mediated immunity but also incites immunoglobulin (Ig)G antibodies that can block neuromuscular transmission (Toyka, 1999).…”

Section: Discussionmentioning

confidence: 99%

Characterization and experimental reproduction of peripheral neuropathy in White Leghorn chickens

Bacon¹,

Witter²,

Silva³

2001

Avian Pathology

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A clinical neurological syndrome termed peripheral neuropathy (PN) that resembles Marek's disease (MD) occurred at low frequency in a commercial layer strain for several years. Study of chickens from six field cases showed that the PN syndrome could be distinguished pathologically from MD on the basis of several factors, including onset as early as 6 weeks, presence of B-type but not A-type lesions in peripheral nerves, and absence of visceral lymphomas. Serotype 1 MD virus could not be isolated from blood from any chicken or demonstrated in tissues by histochemistry or polymerase chain reaction assays. Moreover, the syndrome was not prevented by MD vaccination, either in the field or in laboratory trials. PN was induced in 3 to 54% of commercial line chickens inoculated at 1 or 6 days of age with whole blood or buffy coat cells from clinically affected donor chickens. Sonicated cells also induced PN, but plasma was ineffective. Chickens did not develop PN if reared in isolators without cellular transfer or when vaccinated solely against MD. However, PN was observed in 9% of 57 B*2/*19 commercial chickens reared in isolators following vaccination against MD, infectious bursal disease, Newcastle disease and infectious bronchitis, suggesting that common vaccines may predispose chickens to PN. The data confirmed a strong influence of the major histocompatibility complex (B-complex) on both naturally occurring and experimentally induced PN with the B*19 haplotype conferring susceptibility compared with other alleles. It is postulated that PN may represent an autoimmune reaction to nerve tissue that may result from response to a combination of common vaccines. These studies confirmed that PN is distinct from MD, provided criteria for its differential diagnosis, identified strategies for its control, and established a model for its experimental induction.

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“…Using our three substrains of OS chickens, for example, we found that the influence of the B haplotype was marked in one, less marked but still significant in a second and barely detectable in the third substain. These differences were attributed to the overriding action of genes outside of the MHC (13). …”

Section: Major Histocompatibility Complex In the Chickenmentioning

confidence: 99%

The genetics of autoimmune thyroiditis: The first decade

Rose

2011

Journal of Autoimmunity

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Most of our current understanding of the genetic predisposition to autoimmune disease can be traced to experiments performed in the decade from 1971 to 1981. Chella David was a key contributor to this research. Many of these early steps came from studies of experimental autoimmune thyroiditis. This model has been especially valuable because essentially the same disease can occur spontaneously in selected strains of animals or can be induced by deliberate immunization. From a genetic point of view, the disease has been investigated in three different species: mice, rats and chickens. The same antigen, thyroglobulin, initiates the disease in all three species. Among the main discoveries were the relationship of autoimmune disease to the major histocompatibility complex (MHC), the interplay of different subregions within the MHC in promoting or retarding development of disease, the differing roles of MHC class II and MHC I class genes in induction and effector phases, respectively, and the cumulative effect of non-MHC genes, each of which represents a small addition to overall susceptibility. Other experiments revealed that genetic differences in thyroglobulin allotypes influence susceptibility to thyroiditis. Thyroid glands differed in different strains in vulnerability to passive transfer of antibody. The first evidence of modulatory genes on the sex-related X chromosome emerged. All of these genetic findings were concurrently translated to the human disease, Hashimoto’s thyroiditis, where thyroglobulin is also the initiating antigen.

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Influence of major histocompatibility haplotype on autoimmune disease varies in different inbred families of chickens.

Cited by 24 publications

References 21 publications

Avian Models of Autoimmune Disease: Lessons from the Birds

Avian Models of Autoimmune Disease: Lessons from the Birds

Characterization and experimental reproduction of peripheral neuropathy in White Leghorn chickens

The genetics of autoimmune thyroiditis: The first decade

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