Genetic Associations of Body Weight and Immune Response with the Major Histocompatibility Complex in White Leghorn Chicks

Abstract

Survival, body weight, and humoral immune response to sheep red blood cells (SRBC) were measured in 256 chicks of the Iowa State University S1 Leghorn line. The chicks were produced from breeders selected for serological Ea-B blood type (B1 or B19), high or low humoral immune response to the amino acid polymer, glutamic acid-alanine-tyrosine (Ir-GAT), and response to Rous sarcoma virus-induced (RSV) tumors (progression or regression). Chicks were hatched from sublines representing all eight triple homozygous genotypes. Survival was significantly (P less than .01) associated with Ir-GAT, but not with Ea-B or RSV response. Body weight was affected by Ea-B, Ir-GAT, and the interaction between Ea-B and Ir-GAT, but not by interaction with RSV response. The SRBC antibody titer was affected by the interaction of Ea-B and Ir-GAT. The SRBC antibody titer was also lowest in the B19 low group. There were positive significant correlations (.21 to .31) between SRBC antibody titer and body weights at all ages except hatch in the Ir-GAT low group, but there were no significant correlations between SRBC antibody titer and body weights in the Ir-GAT high group. In this population of White Leghorn chicks, the heritabilities of body weight ranged from .43 to .27 for weights at 2 to 6 wk of age, and the heritability of SRBC antibody titer at 4 wk was .34 +/- .25.

Production Traits and Alloantigen Systems in Lines of Chickens Selected for High or Low Antibody Responses to Sheep Erythrocytes

“…Other researchers report no effects from the B genotype on egg production (Kim et al, 1989). Body weight at 2, 4, and 6 wk of age differed among B genotypes (Kim et al, 1987), as did egg weight (Kim et al, 1989); but BW at 8,20, and 32 wk of age did not differ (Kim et al, 1989). In evaluating the apparent discrepancies between reports concerning the effects of alloantigen systems, a critical consideration would be the relationships between particular haplotypes or alleles present in the genetic stocks under consideration.…”

Analysis of B-G and Immune Response Genes in the Iowa State University S1 Chicken Line by Hybridization of Sperm Deoxyribonucleic Acid with a Major Histocompatibility Complex Class II Probe

“…A gene exerting major control over RSV tumor regression has been mapped to the MHC class I region (Plachy and Vilhelmova, 1984), but non-MHC genetic control of RSV response has also been demonstrated (Collins and Zsigray, 1984;Gilmour et al, 1986). Because selection for RSV tumor response in the SI line was conducted within each MHC haplotype (as determined by B-G antigen and IrGAT phenotype), non-MHC genes probably determined the divergence in RSV response (Kim et al, 1987). It was not, therefore, expected that MHC-probed RFLP would be associated with RSV response in the ISU SI line of chickens.…”

“…The B-G antigens (designated as class IV), of which no mammalian homolog has been identified, are expressed on erythrocytes only (Longenecker and Mosmann, 1981). ' Associations have been demonstrated, in the Iowa State University (ISU) SI chicken line, between B blood group type and mortality and egg production (Nordskog et al, 1973(Nordskog et al, , 1977, immune response to several antigens (Pevzner et al, 1975, juvenile body weight (Kim et al, 1987), and resistance to Marek's disease (Steadham et al, 1987) and to fowl cholera (Lamont et al, 1987a). Identification of the MHC in the previous studies was done serologically with anti-B-G antisera.…”

Genetic resistance to fowl cholera is linked to the major histocompatibility complex

“…In other recent studies with the Iowa StateS 1 line, resistance to Marek's disease also was associated with the B 1 B 1 blood type (Steadham et al 1987). SRBC titer also has been associated with the B-G region of the MH C, with B 1 B 1 chicks having higher antibody responses to SRBC (Kim et al 1986). In contrast, reticuloendothelial activity level was not associated with B-G but with ability to regress RSV tumors (Lamont 1986).…”