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   <subfield code="a">Antibody Response to Sheep Red Blood Cells in a Major Histocompatibility (B) Complex Aneuploid Line of Chickens</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[K. T. LEPAGE, S. E. BLOOM, R. L. TAYLOR]</subfield>
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   <subfield code="a">An integral part of the immune response is the production of antibodies specific for different antigenic challenges. Genes of the MHC encode products that regulate immunity. This study utilized the FCT-15 line of chickens, which is aneuploid for the chromosome containing the ribosomal RNA genes (rDNA) and the MHC or B complex to determine whether an antibody response to SRBC would vary as a function of B complex gene dose. Mating of trisomic parents (B 15 B 15 B 15) animals produced progeny having either a disomic (B 15 B 15), trisomic (B 15 B 15 B 15), or tetrasomic (B 15 B 15 B 15 B 15) B complex dosage. The number of B/rDNA chromosomes, and thus the B complex dosage, was determined by feather pulp nucleolar typing of chicks at hatch. A 5% SRBC antigenic challenge, which induces a T cell-dependent antibody response, was injected at 6 wk of age. Samples taken prior to SRBC injection as well as 5, 8, and 12 d postinjection were assayed for total and mercaptoethanol-resistant antibody. Peak antibody titers (log2), day of peak titer and rate of titer decline were calculated using a quadratic equation for each bird. Differences among the three B complex dosages were evaluated by analysis of variance. Antibody titers rose from 5 to 8 d postinjection and declined thereafter without significant differences among the three B complex doses. Calculations from the quadratic equations showed that B complex dose affected neither peak antibody titer nor day of peak titer. However, trisomic and tetrasomic animals had significantly more rapid rates of decline from the maximum titer. In aneuploid chickens, changes in antigen processing, antigen presentation, or persistence of processed antigen may maintain levels of antibody production found in disomic chickens and explain the more rapid decline of titer.</subfield>
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   <subfield code="a">© 1996 Poultry Science Association, Inc.</subfield>
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   <subfield code="a">Immunology</subfield>
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   <subfield code="a">LEPAGE</subfield>
   <subfield code="D">K. T.</subfield>
   <subfield code="u">Department of Animal and Nutritional Sciences, University of New Hampshire, Durham, New Hampshire 03824 and</subfield>
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   <subfield code="a">BLOOM</subfield>
   <subfield code="D">S. E.</subfield>
   <subfield code="u">Department of Avian and Aquatic Animal Medicine, Cornell University, Ithaca, New York 14853</subfield>
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