MHC Genes, Immune Response, and Vaccines

Author(s):  
R. E. Bontrop
Keyword(s):  
2003 ◽  
Vol 77 (2) ◽  
pp. 99-109 ◽  
Author(s):  
J.M. Behnke ◽  
F. Iraqi ◽  
D. Menge ◽  
R.L. Baker ◽  
J. Gibson ◽  
...  

AbstractThe host-protective immune response to infection with gastrointestinal (GI) nematodes involves a range of interacting processes that begin with recognition of the parasite's antigens and culminate in an inflammatory reaction in the intestinal mucosa. Precisely which immune effectors are responsible for the loss of specific worms is still not known although many candidate effectors have been proposed. However, it is now clear that many different genes regulate the response and that differences between hosts (fast or strong versus slow or weak responses) can be explained by allelic variation in crucial genes associated with the gene cascade that accompanies the immune response and/or genes encoding constitutively expressed receptor/signalling molecules. Major histocompatibility complex (MHC) genes have been recognized for some time as decisive in controlling immunity, and evidence that non-MHC genes are equally, if not more important in this respect has also been available for two decades. Nevertheless, whilst the former have been mapped in mice, only two candidate loci have been proposed for non-MHC genes and relatively little is known about their roles. Now, with the availability of microsatellite markers, it is possible to exploit linkage mapping techniques to identify quantitative trait loci (QTL) responsible for resistance to GI nematodes. Four QTL for resistance to Heligmosomoides polygyrus, and additional QTL affecting faecal egg production by the worms and the accompanying immune responses, have been identified. Fine mapping and eventually the identification of the genes (and their alleles) underlying QTL for resistance/susceptibility will permit informed searches for homologues in domestic animals, and human beings, through comparative genomic maps. This information in turn will facilitate targeted breeding to improve resistance in domestic animals and, in human beings, focused application of treatment and control strategies for GI nematodes.


2018 ◽  
Vol 9 (3) ◽  
pp. 363-368 ◽  
Author(s):  
T. M. Suprovych ◽  
M. P. Suprovych ◽  
T. V. Koval ◽  
T. M. Karchevska ◽  
V. A. Chepurna ◽  
...  

The major histocompatibility complex (MHC) determines the immune response, and the MHC genes are promising candidate genes for identifying associations with diseases. The decisive role in the resistance of cattle to diseases belongs to the major histocompatibility complex of (BoLA). The BoLA system consists of several jointly operating genes that provide antigen presentation by MHC system molecules followed by an immune response to pathogenic microorganisms. The most functional is the BoLA-DRB3 gene. Its exon 2 is highly polymorphic and encodes the peptide antigen-binding cleft. Alleles, for which a close connection with disease susceptibility or disease resistance has been detected, are considered as DNA markers. These play a decisive role in the breeding of cattle to create herds resistant to diseases, including mastitis. This paper presents the results of a study of BoLA-DRB3 gene polymorphism in two commercial cattle breeds: the Ukrainian black-pied dairy (UBPD) and the Ukrainian red-pied dairy (URPD) and its association with mastitis. The UBPD and the URPD cows were genotyped at the bovine lymphocyte antigen DRB3.2 locus by a genotyping system that used polymerase chain reaction and restriction fragment length polymorphisms (PCR-RLFP). In 276 UBPD cows, 32 BoLA-DRB alleles have been found. Six alleles (*03, *08, *10, *22, *24 and *28) were identified with a frequency of more than 5% (total amount of 50.4%). The allele BoLA-DRB3.2*24 was the most frequent (19.2%). In the UBPD population (n = 162), four BoLA-DRB3.2 alleles are truly associated with mastitis: *24 and *26 with susceptibility and *13 and *22 with resistance. In 117 URPD cows, 22 alleles were identified, of which the most frequent were *07, *22, *11, *24, *01, *03 and *16 (total frequency 64.5%). Allele BoLA-DRB3.2*07 (present in 25.6% of cows) was the most commonly found. In the URPD population studied, four alleles truly associated with mastitis were identified. Animals susceptible to the disease had alleles *07 and *08, and resistant animals had alleles *22 and *24. Breeding activities for the creation of cattle resistant to mastitis using alleles of the BoLA-DRB3 gene are much more effective than treatment and special care for animals. Similar research should be carried out for other Ukrainian breeds in relation to various diseases (leukemia, necrobacteriosis, etc.).


1999 ◽  
Vol 37 (2) ◽  
pp. 123-129 ◽  
Author(s):  
B. R. Mignon ◽  
T. Leclipteux ◽  
CH. Focant ◽  
A. J. Nikkels ◽  
G. E. PIErard ◽  
...  

2015 ◽  
Vol 21 ◽  
pp. 93
Author(s):  
Merrell Magelli ◽  
Ronald Swerdloff ◽  
John Amory ◽  
Gregory Flippo ◽  
Wael Salameh ◽  
...  

Author(s):  
Barbara Kronsteiner ◽  
Panjaporn Chaichana ◽  
Manutsanun Sumonwiriya ◽  
Kemajitra Jenjaroen ◽  
Fazle Rabbi Chowdhury ◽  
...  

2004 ◽  
Vol 146 (4) ◽  
pp. 159-172 ◽  
Author(s):  
D. Müller-Doblies ◽  
S. Baumann ◽  
P. Grob ◽  
A. Hülsmeier ◽  
U. Müller-Doblies ◽  
...  

2015 ◽  
Vol 29 (3) ◽  
pp. 119-129 ◽  
Author(s):  
Richard J. Stevenson ◽  
Deborah Hodgson ◽  
Megan J. Oaten ◽  
Luba Sominsky ◽  
Mehmet Mahmut ◽  
...  

Abstract. Both disgust and disease-related images appear able to induce an innate immune response but it is unclear whether these effects are independent or rely upon a common shared factor (e.g., disgust or disease-related cognitions). In this study we directly compared these two inductions using specifically generated sets of images. One set was disease-related but evoked little disgust, while the other set was disgust evoking but with less disease-relatedness. These two image sets were then compared to a third set, a negative control condition. Using a wholly within-subject design, participants viewed one image set per week, and provided saliva samples, before and after each viewing occasion, which were later analyzed for innate immune markers. We found that both the disease related and disgust images, relative to the negative control images, were not able to generate an innate immune response. However, secondary analyses revealed innate immune responses in participants with greater propensity to feel disgust following exposure to disease-related and disgusting images. These findings suggest that disgust images relatively free of disease-related themes, and disease-related images relatively free of disgust may be suboptimal cues for generating an innate immune response. Not only may this explain why disgust propensity mediates these effects, it may also imply a common pathway.


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