Research Note: Rous sarcoma growth differs among congenic lines containing major histocompatibility (B) complex recombinants.

New arrangements of chicken major histocompatibility complex (MHC) class I BF and class IV BG genes are created through recombination. Characterizing the immune responses of such recombinants reveals genes or gene regions that contribute to immunity. Inbred Line UCD 003 (B17B17) served as the genetic background for congenic lines, each containing a unique MHC recombinant.

Major histocompatibility complex recombinant R13 antibody response against bovine red blood cells.

Recombination within the chicken major histocompatibility complex (MHC) has enabled more precise identification of genes controlling immune responses. Chicken MHC genes include BF, MHC class I; BL, MHC class II; and BG, MHC class IV that are closely linked on chromosome 16. A new recombination occurred during the 10th backcross generation to develop congenic lines on the inbred Line UCD 003 (B17B17) background.

Immune effects of chicken non-MHC alloantigens.

Alloantigen systems are a broad group of molecules found on various cell types, including erythrocytes and lymphocytes. These alloantigens, identified via specific polyclonal or monoclonal antibodies or molecular methods, have demonstrated effects on immune responses. Erythrocyte alloantigens include the A, B, C, D, E, H, I, J, K, L, N, P, and R systems.

Dramatic differences in the response of macrophages from B2 and B19 MHC-defined haplotypes to interferon gamma and polyinosinic:polycytidylic acid stimulation.

The chicken MHC has been associated with disease resistance, though the mechanisms are not understood. The functions of macrophages, critical to both innate and acquired immunity, were compared between the more infectious bronchitis virus-resistant B2 and the more infectious bronchitis virus-susceptible B19 lines. In vivo peripheral blood concentrations of monocytes were similar in B2 or B19 homozygous haplotypes.

Genetic variation at the MHC in a population of introduced wild turkeys.

Genetic variation in the major histocompatibility complex (MHC) is known to affect disease resistance in many species. Investigations of MHC diversity in populations of wild species have focused on the antigen presenting class IIβ molecules due to the known polymorphic nature of these genes and the role these molecules play in pathogen recognition. Studies of MHC haplotype variation in the turkey ( Meleagris gallopavo ) are limited.

Association of the chicken MHC B haplotypes with resistance to avian coronavirus.

Clinical respiratory illness was compared in five homozygous chicken lines, originating from homozygous B2, B8, B12 and B19, and heterozygous B2/B12 birds after infection with either of two strains of the infectious bronchitis virus (IBV). All chickens used in these studies originated from White Leghorn and Ancona linages. IBV Gray strain infection of MHC homozygous B12 and B19 haplotype chicks resulted in severe respiratory disease compared to chicks with B2/B2 and B5/B5 haplotypes.

Non-replicating adenovirus vectors expressing avian influenza virus hemagglutinin and nucleocapsid proteins induce chicken specific effector, memory and effector memory CD8(+) T lymphocytes.

Avian influenza virus (AIV) specific CD8(+) T lymphocyte responses stimulated by intramuscular administration of an adenovirus (Ad) vector expressing either HA or NP were evaluated in chickens following ex vivo stimulation by non-professional antigen presenting cells. The CD8(+) T lymphocyte responses were AIV specific, MHC-I restricted, and cross-reacted with heterologous H7N2 AIV strain. Specific effector responses, at 10 days post-inoculation (p.

Avian influenza viral nucleocapsid and hemagglutinin proteins induce chicken CD8+ memory T lymphocytes.

The avian influenza viruses (AIVs) can be highly contagious to poultry and a zoonotic threat to humans. Since the memory CD8(+) T lymphocyte responses in chickens to AIV proteins have not been defined, these responses to H5N9 AIV hemagglutinin (HA) and nucleocapsid (NP) proteins were evaluated by ex vivo stimulation with virus infected non-professional antigen presenting cells. Secretion of IFNgamma by activated T lymphocytes was evaluated through macrophage induction of nitric oxide.

BG1 has a major role in MHC-linked resistance to malignant lymphoma in the chicken.

Pathogen selection is postulated to drive MHC allelic diversity at loci for antigen presentation. However, readily apparent MHC infectious disease associations are rare in most species. The strong link between MHC-B haplotype and the occurrence of virally induced tumors in the chicken provides a means for defining the relationship between pathogen selection and MHC polymorphism.

Rous sarcoma growth in lines congenic for major histocompatibility (B) complex recombinants.

Rous sarcoma virus (RSV)-induced tumor growth was examined in congenic lines of chickens with different major histocompatibility (B) complex recombinant haplotypes on the highly inbred line UCD 003 (B17B17) genetic background. Males bearing an individual B complex recombinant were mated to UCD 003 females followed by 10 backcross generations. Matings among heterozygotes for each recombinant produced homozygous chickens estimated to contain 99.

Extended gene map reveals tripartite motif, C-type lectin, and Ig superfamily type genes within a subregion of the chicken MHC-B affecting infectious disease.

MHC haplotypes have a remarkable influence on whether tumors form following infection of chickens with oncogenic Marek's disease herpesvirus. Although resistance to tumor formation has been mapped to a subregion of the chicken MHC-B region, the gene or genes responsible have not been identified. A full gene map of the subregion has been lacking.

2004 Nomenclature for the chicken major histocompatibility (B and Y) complex.

The first standard nomenclature for the chicken (Gallus gallus) major histocompatibility (B) complex published in 1982 describing chicken major histocompatibility complex (MHC) variability is being revised to include subsequent findings. Considerable progress has been made in identifying the genes that define this polymorphic region. Allelic sequences for MHC genes are accumulating at an increasing rate without a standard system of nomenclature in place.

Non-major histocompatibility complex alloantigen genes affecting immunity.

An alloantigen is a genetically determined cell-surface molecule detected by specific antisera. An identifying letter has been assigned to each genetic locus responsible for the 12 distinct families of alloantigens: A, B, C, D, E, H, I, J, K, L, P, and R. The genes of each system segregate independently of the other systems, except that the A and E are very closely linked (0.

Resistance, susceptibility, and immunity to cecal coccidiosis: effects of B complex and alloantigen system L.

This study examined alloantigen system L effects on resistance to initial infection and acquired immunity to Eimeria tenella infection in three B complex genotypes. Experimental progeny segregating for B and L genotypes were produced from pedigree matings of B2B5 L1L2 sires and dams. Chicks were weighed and inoculated with 30,000 E.

Memory T cells protect chicks from acute infectious bronchitis virus infection.

Infectious bronchitis has remained one of the most difficult to control diseases in poultry since it was first described in 1931. Previous studies demonstrated that primary CD8(+) T lymphocytes collected at 10 days post-infection (p.i.

Single-strand conformation polymorphism (SSCP) assays for major histocompatibility complex B genotyping in chickens.

We have developed a DNA-based method for defining MHC B system genotypes in chickens. Genotyping by this method requires neither prior determination of allele-specific differences in nucleotide sequence nor the preparation of haplotype-specific alloantisera. Allelic differences at chicken B-F (class I) and B-L (class II) loci are detected in PCR single-strand conformation polymorphism (SSCP) assays.

Alloantigen system L affects the outcome of rous sarcomas.

This study was designed to examine the alloantigen system L effects on Rous sarcomas in three B complex genotypes. The parental stock was 50% Modified Wisconsin Line 3 x White Leghorn Line NIU 4 and 50% inbred Line 6.15-5.

Allelic complementation between MHC haplotypes B(Q) and B17 increases regression of Rous sarcomas.

Major histocompatibility (B) complex haplotypes B(Q) and B17 were examined for their effect on Rous sarcoma outcome. Pedigree matings of B(Q)B17 chickens from the second backcross generation (BC2) of Line UCD 001 (B(Q)B(Q)) mated to Line UCD 003 (B17B17) produced progeny with genotypes B(Q)B(Q), B(Q)B17, and B17B17. Six-week-old chickens were injected with subgroup A Rous sarcoma virus (RSV).

Alloantigen systems L and P influence phagocytic function independent of the major histocompatability complex (B) in chickens.

Synthetic parent stocks were designed to produce progeny among which alleles were simultaneously segregating for nine alloantigen systems, including the MHC (B). Chicks from Ancona-derived B19B19 females crossed with White leghorn B19B21 males were blood typed, resulting in genotypic categories for the A-E, C, D, H, I, L, and P loci with the objective of determining which, if any, of the eight non-MHC alloantigen systems influence or interact with the B system genotypes for blood monocyte phagocytic activity. Leukocytes obtained from whole blood at 2 and 4 wk were separated on a Fico/Lite LymphoH, density gradient and were allowed to adhere to glass coverslips.

Nonmajor histocompatibility complex alloantigen effects on the fate of Rous sarcomas.

Rous sarcoma virus-induced tumor outcome is controlled by the MHC (B). Additional data, using controlled segregation in families, has indicated non-MHC effects as well, but few studies have focused on blood groups other than the B complex. Segregating combinations of genes encoding erythrocyte (Ea) alloantigen systems A, C, D, E, H, I, P, and L in B2B5 and B5B5 MHC (B) backgrounds were examined for their effects on Rous sarcomas.

Further tests for genetic linkages of three morphological traits, three blood groups, and break points of two chromosome translocations on chromosome one in the chicken.

Two matings were conducted to further test the locations of the pea comb (P*), blue egg shell color (O*), and tardy feathering (T*) loci. In each mating a different chromosome rearrangement break point (R(B)) was tested against the three loci. Independent segregation was noted between the traits and the R(B) when the R(B) was on the long arm of chromosome 1.

Adoptive transfer of infectious bronchitis virus primed alphabeta T cells bearing CD8 antigen protects chicks from acute infection.

Infectious bronchitis virus (IBV) infection and associated illness may be dramatically modified by passive transfer of immune T lymphocytes. Lymphocytes collected 10 days postinfection were transferred to naive chicks before challenge with virus. As determined by respiratory illness and viral load, transfer of syngeneic immune T lymphocytes protected chicks from challenge infection, whereas no protection was observed in the chicks receiving the MHC compatible lymphocytes from uninfected chicks.

A consensus linkage map of the chicken genome.

A consensus linkage map has been developed in the chicken that combines all of the genotyping data from the three available chicken mapping populations. Genotyping data were contributed by the laboratories that have been using the East Lansing and Compton reference populations and from the Animal Breeding and Genetics Group of the Wageningen University using the Wageningen/Euribrid population. The resulting linkage map of the chicken genome contains 1889 loci.

Developmental expression of alloantigen systems in the chicken.

The different allelic forms of nine non-Mhc alloantigen systems of the chicken were examined for developmental expression on erythrocytes isolated from embryos and young chicks. Polyclonal alloantisera raised against the different antigens were used to detect these antigens on the cell surface by hemagglutination as well as by indirect immunofluorescence. The developmental stage of initial expression on erythrocytes for each of the genetic systems investigated (i.