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Journal articles on the topic 'Histocompatibilty complex'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Qin, J., C. Mamotte, N. E. Cockett, J. D. Wetherall, and D. M. Groth. "A map of the class III region of the sheep major histocompatibilty complex." BMC Genomics 9, no. 1 (2008): 409. http://dx.doi.org/10.1186/1471-2164-9-409.

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2

Olufowobi, Olanrewaju Teslim, Babatunde Moses Ilori, Olajide Olowofeso, Olajide Mark Sogunle, and Adewunmi Omolade Omotoso. "Genetic variation of the major histocompatibilty complex-B haplotypes in Nigerian local chicken populations." Agricultura Tropica et Subtropica 53, no. 4 (December 1, 2020): 175–81. http://dx.doi.org/10.2478/ats-2020-0017.

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AbstractTo understand the genetic basis and mechanism underlying the differences in the level of immunity among and within chicken populations in Nigeria, it is important to start from the Major Histocompability Complex (MHC) region particularly as it serves as a reservoir for genes of the immune system. The B-complex of chicken major histocompatibility complex, located on microchromosome 16, consists of gene classes responsible for immunity through antigen presentation to T cells. A highly polymorphic tandem repeat marker (LEI0258) located within the B-complex has been a marker of choice for genotyping to identify major histocompatibility complex-B haplotypes and to study the genetic diversity of chicken populations. This study was carried out to determine the genetic variations, at the LEI0258 locus, in three Nigerian local chicken populations; Normal feather, Frizzle feather and Naked neck. The allelic and genotypic profiles of each representative from each population were determined through polymerase chain reaction amplification of the repeat region. The genetic diversity parameters, analysis of molecular variance and evolutionary relationship were determined using GenAlex, FSTAT, Arlequin and POPTREEW, respectively. 76 % of the entire population was heterozygous at the LEI0258 locus. Analysis of molecular variance revealed that large proportion of the total variations across populations was due to variation between individuals (79 %), whereas variations among the populations and among individuals within populations only accounted for less than 1 % and 21 %, respectively. Using Anak Titan as an exotic outgroup, the evolutionary relationship among the Nigerian local chicken populations was studied and a Nei-based dendrogram showed two major clades separating the exotic population from the Nigerian local chicken populations. The identified diversity at the locus could be exploited for usage in further breeding programmes especially for disease resistance and fitness in locally adapted chicken populations in Nigerian.

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3

Hirata, Jun, Kazuyoshi Hosomichi, Saori Sakaue, Masahiro Kanai, Hirofumi Nakaoka, Kazuyoshi Ishigaki, Ken Suzuki, et al. "Genetic and phenotypic landscape of the major histocompatibilty complex region in the Japanese population." Nature Genetics 51, no. 3 (January 28, 2019): 470–80. http://dx.doi.org/10.1038/s41588-018-0336-0.

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4

Nikbakht-sangari, M., A. K. Qayumi, P. Keown, V. Duronio, and K. Horley. "Platelet-Activating Factor Plays a Role in the Mechanism of Major Histocompatibilty Complex in T Lymphocytes." Immunological Investigations 28, no. 4 (January 1999): 223–33. http://dx.doi.org/10.3109/08820139909060857.

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5

Lee, K. W., B. Choi, Y. M. Kim, C. W. Cho, H. Park, J. I. Moon, G. S. Choi, J. B. Park, and S. J. Kim. "Major Histocompatibilty Complex–Restricted Adaptive Immune Responses to CT26 Colon Cancer Cell Line in Mixed Allogeneic Chimera." Transplantation Proceedings 49, no. 5 (June 2017): 1153–59. http://dx.doi.org/10.1016/j.transproceed.2017.03.011.

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6

Shiels, Carol, Suhail A. Islam, Radost Vatcheva, Peter Sasieni, Michael J. E. Sternberg, Paul S. Freemont, and Denise Sheer. "PML bodies associate specifically with the MHC gene cluster in interphase nuclei." Journal of Cell Science 114, no. 20 (October 15, 2001): 3705–16. http://dx.doi.org/10.1242/jcs.114.20.3705.

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Promyelocytic leukemia (PML) bodies are nuclear multi-protein domains. The observations that viruses transcribe their genomes adjacent to PML bodies and that nascent RNA accumulates at their periphery suggest that PML bodies function in transcription. We have used immuno-FISH in primary human fibroblasts to determine the 3D spatial organisation of gene-rich and gene-poor chromosomal regions relative to PML bodies. We find a highly non-random association of the gene-rich major histocompatibilty complex (MHC) on chromosome 6 with PML bodies. This association is specific for the centromeric end of the MHC and extends over a genomic region of at least 1.6 megabases. We also show that PML association is maintained when a subsection of this region is integrated into another chromosomal location. This is the first demonstration that PML bodies have specific chromosomal associations and supports a model for PML bodies as part of a functional nuclear compartment.

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7

Mahy, Nicola L., Paul E. Perry, and Wendy A. Bickmore. "Gene density and transcription influence the localization of chromatin outside of chromosome territories detectable by FISH." Journal of Cell Biology 159, no. 5 (December 9, 2002): 753–63. http://dx.doi.org/10.1083/jcb.200207115.

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Genes can be transcribed from within chromosome territories; however, the major histocompatibilty complex locus has been reported extending away from chromosome territories, and the incidence of this correlates with transcription from the region. A similar result has been seen for the epidermal differentiation complex region of chromosome 1. These data suggested that chromatin decondensation away from the surface of chromosome territories may result from, and/or may facilitate, transcription of densely packed genes subject to coordinate regulation. To investigate whether localization outside of the visible confines of chromosome territories can also occur for regions that are not coordinately regulated, we have examined the spatial organization of human 11p15.5 and the syntenic region on mouse chromosome 7. This region is gene rich but its genes are not coordinately expressed, rather overall high levels of transcription occur in several cell types. We found that chromatin from 11p15.5 frequently extends away from the chromosome 11 territory. Localization outside of territories was also detected for other regions of high gene density and high levels of transcription. This is shown to be partly dependent on ongoing transcription. We suggest that local gene density and transcription, rather than the activity of individual genes, influences the organization of chromosomes in the nucleus.

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8

Porto, Graça, Eugénia Cruz, Maria José Teles, and Maria de Sousa. "HFE Related Hemochromatosis: Uncovering the Inextricable Link between Iron Homeostasis and the Immunological System." Pharmaceuticals 12, no. 3 (August 22, 2019): 122. http://dx.doi.org/10.3390/ph12030122.

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The HFE gene (OMIM 235200), most commonly associated with the genetic iron overload disorder Hemochromatosis, was identified by Feder et al. in 1996, as a major histocompatibilty complex (MHC) class I like gene, first designated human leukocyte antigen-H (HLA-H). This discovery was thus accomplished 20 years after the realization of the first link between the then “idiopathic” hemochromatosis and the human leukocyte antigens (HLA). The availability of a good genetic marker in subjects homozygous for the C282Y variant in HFE (hereditary Fe), the reliability in serum markers such as transferrin saturation and serum ferritin, plus the establishment of noninvasive methods for the estimation of hepatic iron overload, all transformed hemochromatosis into a unique age related disease where prevention became the major goal. We were challenged by the finding of iron overload in a 9-year-old boy homozygous for the C282Y HFE variant, with two brothers aged 11 and 5 also homozygous for the mutation. We report a 20 year follow-up during which the three boys were seen yearly with serial determinations of iron parameters and lymphocyte counts. This paper is divided in three sections: Learning, applying, and questioning. The result is the illustration of hemochromatosis as an age related disease in the transition from childhood to adult life and the confirmation of the inextricable link between iron overload and the cells of the immune system.

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9

MAROSI, BÉLA, KAREN M. KIEMNEC-TYBURCZY, IOAN V. GHIRA, TIBOR SOS TIBOR SOS, and OCTAVIAN POPESCU. "Identification and characterization of major histocompatibility complex class IIB alleles in three species of European ranid frogs." Indian Journal of Applied Research 3, no. 9 (October 1, 2011): 4–6. http://dx.doi.org/10.15373/2249555x/sept2013/2.

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10

Zorc, Minja, Jernej Ogorevc, and Peter Dovc. "The new bovine reference genome assembly provides new insight into genomic organization of the bovine major histocompatibility complex." Journal of Central European Agriculture 20, no. 4 (2019): 1111–15. http://dx.doi.org/10.5513/jcea01/20.4.2679.

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11

Kharmayani, Made Ryan, Haris Lutfi, and Danu Soesilowati. "Pengaruh Simvastatin Terhadap Kadar Proliferasi Limfosit Mencit Balb/C yang Diinduce Sepsis dengan LPS." JAI (Jurnal Anestesiologi Indonesia) 5, no. 3 (November 1, 2013): 193. http://dx.doi.org/10.14710/jai.v5i3.6309.

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Latar Belakang : Statin, inhibitor 3-hidroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase merupakan agen yang paling efektif dalam menurunkan lipid dan mempunyai efek pleiotrofik yaitu anti inflamatori dan immunomodulatori. Statin juga memodifikasi interaksi interseluler dan kemotaksis seluler pada sistem imun serta berpotensi mempengaruhi limfosit T dengan cara menghambat iinteraksi antara adhesi molekul seluler leukocyte function-associated antigen-1 (LFA-1) dan intercellular adhesion molecule-1 (ICAM-1), juga menurunkan interferon gamma (IFN -ɣ) yang berperan dalam ekspresi class II major histocompatibilty complex (MHC II) pada antigen precenting cells (APC) dan merupakan proses penting dalam aktivasi sel T. Penurunan ekspresi MHC II berakibat pada inhibisi aktivasi CD 4 limfosit, sehingga mengakibatkan penurunan diferensiasi T helper-1 (Th1) dan pelepasan sitokin proinflamasi juga menurun.Tujuan : Membuktikan efek simvastatin dosis bertingkat peroral pada mencit yang diberi LPS intraperitoneal terhadap penurunan kadar proliferasi limfosit.Metode : Penelitian eksperimental laboratorik dengan desain randomized post test only controlled group pada 20 ekor mencit Balb/c yang disuntik lipopolisakarida 10 mg/KgBB intraperitoneal dan simvastatin dosis 0,03 mg, 0,06 mg dan 0,12 mg peroral. Mencit dibagi menjadi 4 kelompok secara random, yaitu K1 sebagai control, K2 yang mendapat simvastatin 0,03 mg, K3 yang mendapat simvastatin 0,06 mg dan K4 yang mendapat simvastatin 0,12 mg. Pemeriksaan limfosit diambil dari kultur limpa setelah 72 jam pemberian simvastatin. Uji statistik yang digunakan adalah parametrik ANOVA dan dilanjutkan PosterioriHasil : Kadar rerata limfosit kelompok K1 (1,546 ± 0,106), K2 (0,541 ± 0,046), K3 (0,471 ± 0,013) dan K4 (0,553 ± 0,02). Terdapat penurunan kadar limfosit secara signifikan pada kelompok K2, K3 dan K4 dibanding K1 dengan p <0,05. Tidak terdapat perbedaan bermakna antara kadar limfosit kelompok K2 dengan kelompok K3 dan K4 ( p>0,05) tetapi didapatkan perbedaan bermakna antara kelompok K3 dibandingkan kelompok K4 ( p<0,05).Simpulan : Simvastatin secara signifikan menurunkan kadar proliferasi limfosit pada mencit yang diberi LPS intraperitoneal. Dosis 0,06 mg memiliki efek menekan kadar proliferasi limfosit paling besar.

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12

Cadavid, Luis F., Anahid E. Powell, Matthew L. Nicotra, Maria Moreno, and Leo W. Buss. "An Invertebrate Histocompatibility Complex." Genetics 167, no. 1 (May 2004): 357–65. http://dx.doi.org/10.1534/genetics.167.1.357.

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13

VAIMAN, M., P. CHARDON, and M. F. TOTHSCHILD. "Porcine major histocompatibility complex." Revue Scientifique et Technique de l'OIE 17, no. 1 (April 1, 1998): 95–107. http://dx.doi.org/10.20506/rst.17.1.1093.

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14

Nepom, Gerald T. "The Major Histocompatibility Complex." Clinical Immunotherapeutics 2, no. 2 (August 1994): 79–83. http://dx.doi.org/10.1007/bf03259257.

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15

Steinmetz, Michael. "The major histocompatibility complex:." Clinical Immunology Newsletter 7, no. 9 (September 1986): 134–37. http://dx.doi.org/10.1016/0197-1859(86)90009-9.

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16

Spieker-Polet, H., N. Sittisombut, P. C. Yam, and K. L. Knight. "RABBIT MAJOR HISTOCOMPATIBILITY COMPLEX IV. EXPRESSION OF MAJOR HISTOCOMPATIBILITY COMPLEX CLASS II GENES." European Journal of Immunogenetics 17, no. 1-2 (February 1990): 123–32. http://dx.doi.org/10.1111/j.1744-313x.1990.tb00865.x.

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17

Dorak, M. Tevfik, and Alan K. Burnett. "Major histocompatibility complex, t-complex, and leukemia." Cancer Causes and Control 3, no. 3 (May 1992): 273–82. http://dx.doi.org/10.1007/bf00124261.

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18

Stosik, Michał, Beata Tokarz-Deptuła, and Wiesław Deptuła. "Major histocompatibility complex in Osteichthyes." Journal of Veterinary Research 64, no. 1 (March 24, 2020): 127–36. http://dx.doi.org/10.2478/jvetres-2020-0025.

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AbstractBased on analysis of available genome sequences, five gene lineages of MHC class I molecules (MHC I-U, -Z, -S, -L and -P) and one gene lineage of MHC class II molecules (MHC II-D) have been identified in Osteichthyes. In the latter lineage, three MHC II molecule sublineages have been identified (MHC II-A, -B and -E). As regards MHC class I molecules in Osteichthyes, it is important to take note of the fact that the lineages U and Z in MHC I genes have been identified in almost all fish species examined so far. Phylogenetic studies into MHC II molecule genes of sublineages A and B suggest that they may be descended from the genes of the sublineage named A/B that have been identified in spotted gar (Lepisosteus oculatus). The sublineage E genes of MHC II molecules, which represent the group of non-polymorphic genes with poor expression in the tissues connected with the immune system, are present in primitive fish, i.e. in paddlefish, sturgeons and spotted gar (Lepisosteus oculatus), as well as in cyprinids (Cyprinidae), Atlantic salmon (Salmo salar), and rainbow trout (Oncorhynchus mykiss). Full elucidation of the details relating to the organisation and functioning of the particular components of the major histocompatibility complex in Osteichthyes can advance the understanding of the evolution of the MHC molecule genes and the immune mechanism.

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19

Rothbard, J. B. "Major histocompatibility complex-peptide interactions." Current Opinion in Immunology 2, no. 1 (October 1989): 99–105. http://dx.doi.org/10.1016/0952-7915(89)90104-0.

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20

Bradbury, Jane. "Human major histocompatibility complex sequenced." Lancet 354, no. 9189 (October 1999): 1531. http://dx.doi.org/10.1016/s0140-6736(99)90190-3.

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21

Danchin, Etienne, Verane Vitiello, Alexandre Vienne, Olivier Richard, Philippe Gouret, Michael F. McDermott, and Pierre Pontarotti. "The major histocompatibility complex origin." Immunological Reviews 198, no. 1 (April 2004): 216–32. http://dx.doi.org/10.1111/j.0105-2896.2004.00132.x.

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22

Raff, Robert F., H. Joachim Deeg, VERNON T. Farewell, Susan DeRose, and Rainer Storb. "The canine major histocompatibility complex." Tissue Antigens 21, no. 5 (December 11, 2008): 360–73. http://dx.doi.org/10.1111/j.1399-0039.1983.tb00185.x.

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23

Loh, Jacelyn, and John Fraser. "Metal-derivatized Major Histocompatibility Complex." Journal of Experimental Medicine 197, no. 5 (March 3, 2003): 549–52. http://dx.doi.org/10.1084/jem.20022180.

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24

Ferstl, R. "Major histocompatibility complex-associated odours." Nephrology Dialysis Transplantation 13, no. 5 (May 1, 1998): 1117–19. http://dx.doi.org/10.1093/ndt/13.5.1117.

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25

Mécheri, Salah. "Major Histocompatibility Complex II Molecules." Allergy & Clinical Immunology International - Journal of the World Allergy Organization 19, no. 2 (2007): 60–64. http://dx.doi.org/10.1027/0838-1925.19.2.60.

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26

Marshall, Brendan, Chanvit Leelayuwat, Mariapia A. Degli-Esposti, Mario Pinelli, Lawrence J. Abraham, and Roger L. Dawkins. "New major histocompatibility complex genes." Human Immunology 38, no. 1 (September 1993): 24–29. http://dx.doi.org/10.1016/0198-8859(93)90516-4.

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27

Zhou, Fusheng, and Xuejun Zhang. "Major Histocompatibility Complex and Psoriasis." Journal of Investigative Dermatology Symposium Proceedings 19, no. 2 (December 2018): S79—S80. http://dx.doi.org/10.1016/j.jisp.2018.09.006.

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28

Mullen, Craig A., Yu-Chiao Hsu, Andrew Campbell, Johan Jansson, and Olena Tkachenko. "Leukemia Free Survival Is Associated with Presence of Leukemia Reactive Antibodies In Allogeneic Transplant Recipients." Blood 116, no. 21 (November 19, 2010): 2534. http://dx.doi.org/10.1182/blood.v116.21.2534.2534.

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Abstract Abstract 2534 Background: Allogeneic hematopoietic stem cell transplant is performed for high risk acute lymphoblastic leukemia (ALL). Complex allogeneic immune responses can produce graft versus host disease which is associated with antileukemia effects. The prevailing paradigm is that these antileukemia effects are mediated by allogeneic T cells. Our laboratory has been studying factors associated with long term disease free survival in murine models of allogeneic transplantation for ALL. Design/Method: We employed a well characterized murine model of MHC-matched, multiple minor histocompatibility mismatched transplantation in which C3.SW mice are donors and C57BL/6 mice are recipients. The ALL model is a recently derived C57BL/6 murine pre-B ALL driven by a bcr/abl p210 oncogene and an Ink/Arf region deletion; such lesions frequently present in human ALL. Recipients underwent myeloablation with 5-FU and total body irradiation and received hematopoietic grafts comprised of donor marrow and spleen cells. Recipients were challenged with ALL cells three weeks after transplant and followed for survival up to 3 months. Some groups of mice were treated with vaccines comprised of irradiated leukemia cells, Freund's adjuvant and GM-CSF. Serum samples were collected prior to leukemia challenge, three weeks after leukemia challenge and at the conclusion of the experiments. T cell responses were measured with ELISPOT assays specific for minor histocompatibility antigens and leukemia antigen specific responses. Antibody responses were measured by flow cytometry and ELISA. Leukemia was measured by flow cytometry. Results: Across all experiments approximately 35% of animals challenged with ALL were long term, leukemia free survivors. Interferon-gamma ELISPOT T cell responses specific for minor histocompatibilty antigens were found in none of the survivors and ELISPOT responses to leukemia antigens were seen in only 20% of long term survivors and these were very modest in magnitude. In contrast, IgM and IgG antibodies that bound leukemia cells were found in the vast majority of survivors. Antibody responses were not specific for the ALL with which the animals were challenged. Cross reactivity with other C57BL/6 ALL and AML leukemia lines were observed. In addition, lower levels of antibody cross reactivity were observed against normal C57BL/6 and C3.SW hematopoietic cells. Titers of the antibodies ranged from 1:40 to > 1:100. Antibody responses were observed in mice that had not received post-transplant vaccination. However, post-transplant vaccination significantly increased the titers of leukemia reactive antibodies. Statistical analysis was performed to determine if antibody levels at any point in the animal's course had any relationship with the risk of later death from leukemia or GVHD. Outcomes for each animal were categorized as alive, death from leukemia, death from GVHD or death of unspecified cause. Antibody levels for each animal were categorized as above or below the median for the entire experimental population. Chi square analysis demonstrated a statistically significant relationship between outcome and antibody level at the time of leukemia challenge. Few animals with high antibody levels died of leukemia (p = 0.0197). In comparison of death from leukemia with death from GVHD, higher antibody levels were associated with death from GVHD (p = 0.0099). A statistically significant difference was not observed between survivors and death from GVHD; however, the death from GVHD group was small, limiting the power of the analysis. Conclusion: Antibody responses to ALL cells were consistently observed in survivors. These studies do not prove the antibodies play a role in control of leukemia, but suggest the hypothesis that antibody responses may contribute to GVL effects. Current experiments in B cell deficient mice are underway to test the mechanistic role of antibody responses in the GVL effect. Disclosures: No relevant conflicts of interest to declare.

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29

Stet, R. J. M., and E. Egberts. "The histocompatibility system in teleostean fishes: From multiple histocompatibility loci to a major histocompatibility complex." Fish & Shellfish Immunology 1, no. 1 (January 1991): 1–16. http://dx.doi.org/10.1016/s1050-4648(06)80016-1.

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30

Abd El Halim, Zeinab, Amr Badr, Khaled Tawfik, and Ibrahim Farag. "Major Histocompatibility Complex Class II Prediction." American Journal of Bioinformatics Research 2, no. 1 (August 31, 2012): 14–20. http://dx.doi.org/10.5923/j.bioinformatics.20120201.03.

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31

Olsaker, I., and K. H. Røed. "The major histocompatibility complex of reindeer." Rangifer 10, no. 3 (September 1, 1990): 369. http://dx.doi.org/10.7557/2.10.3.881.

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The major histocompatibility complex (MHC) is a system of closely linked genes showing an extremely high degree of polymorphism. These genes are major elements in the government of specific immune reactions. Consequently they may represent a genetic marker system well suited to investigate variability in selective pressure from disease agents on different populations. On this background we have started investigation of the MHC complex in reindeer (Rangifer tarandus L). The MHC complex consist of polymorphic regions as well as regions conserved during evolution which should allow the use of cross-species reagents. We have shown that human MHC gene probes hybridize with genomic DNA from reindeer, and thus can be used as a tool in reindeer MHC research. By RFLP (restriction fragment length polymorphism) analysis using these probes we have also been able to show polymorphism in MHC related genes from reindeer.

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32

VAINIO, OLLI, PAAVO TOIVANEN, and AULI TOIVANEN. "Major Histocompatibility Complex and Cell Cooperation." Poultry Science 66, no. 5 (May 1987): 795–801. http://dx.doi.org/10.3382/ps.0660795.

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33

GRIMHOLT, U., and O. LIE. "The major histocompatibility complex in fish." Revue Scientifique et Technique de l'OIE 17, no. 1 (April 1, 1998): 121–27. http://dx.doi.org/10.20506/rst.17.1.1091.

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34

Sharma, Preeti, Pradeep Kumar, and Rachna Sharma. "THE MAJOR HISTOCOMPATIBILITY COMPLEX: A REVIEW." Asian Journal of Pharmaceutical and Clinical Research 10, no. 2 (February 1, 2017): 33. http://dx.doi.org/10.22159/ajpcr.2017.v10i2.15555.

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One of the important components of the immune system, the major histocompatibility complex (MHC) molecules allow T-lymphocytes to detect cells, such as macrophages, B-lymphocytes, and dendritic cells that ingest infectious microorganisms or the self-cells infected with microorganism. On being engulfed a microorganism, macrophage partially digests it and displays peptide fragments of the microbe on its surface, bound to MHC molecules and the T-lymphocyte recognizes the foreign fragment attached to the MHC molecule and binds to it, lead to stimulation of an immune response. The MHC molecule presents peptides from its own cell (self-peptides) in healthy self-cells to which T-cells do not normally react.Keywords: MHC, B Cells, T Cells, Antigen Processing.

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35

Altmann, D. M., and J. Trowsdale. "Major histocompatibility complex structure and function." Current Opinion in Immunology 2, no. 1 (October 1989): 93–98. http://dx.doi.org/10.1016/0952-7915(89)90103-9.

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36

Bell, J. I. "The major histocompatibility complex and disease." Current Opinion in Immunology 2, no. 1 (October 1989): 114–16. http://dx.doi.org/10.1016/0952-7915(89)90106-4.

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37

Goodsell, David S. "The Molecular Perspective: Major Histocompatibility Complex." Stem Cells 23, no. 3 (March 2005): 454–55. http://dx.doi.org/10.1634/stemcells.fcm2.

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38

Goodsell, David S. "The Molecular Perspective: Major Histocompatibility Complex." Oncologist 10, no. 1 (January 2005): 80–81. http://dx.doi.org/10.1634/theoncologist.10-1-80.

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39

Rajapakse, M., and Lin Feng. "Peptide binding to major histocompatibility complex." IEEE Engineering in Medicine and Biology Magazine 28, no. 4 (July 2009): 73–77. http://dx.doi.org/10.1109/memb.2009.932922.

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40

Trowsdale, J., and R. D. Campbell. "COMPLEXITY IN THE MAJOR HISTOCOMPATIBILITY COMPLEX." European Journal of Immunogenetics 19, no. 1-2 (February 1992): 43–55. http://dx.doi.org/10.1111/j.1744-313x.1992.tb00047.x.

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41

BLUM, ARNON, and HYLTON MILLER. "The Major Histocompatibility Complex and Inflammation." Southern Medical Journal 93, no. 2 (February 2000): 169–72. http://dx.doi.org/10.1097/00007611-200002000-00002.

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42

BLUM, ARNON, and HYLTON MILLER. "The Major Histocompatibility Complex and Inflammation." Southern Medical Journal 93, no. 2 (February 2000): 169–72. http://dx.doi.org/10.1097/00007611-200093020-00002.

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43

Afzali, Behdad, Giovanna Lombardi, and Robert I. Lechler. "Pathways of major histocompatibility complex allorecognition." Current Opinion in Organ Transplantation 13, no. 4 (August 2008): 438–44. http://dx.doi.org/10.1097/mot.0b013e328309ee31.

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44

Klein and Sato. "Birth of the Major Histocompatibility Complex." Scandinavian Journal of Immunology 47, no. 3 (March 1998): 199–209. http://dx.doi.org/10.1046/j.1365-3083.1998.00292.x.

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45

Flainik, Martin F., and Louis Du Pasquier. "The Major Histocompatibility Complex of Frogs." Immunological Reviews 113, no. 1 (February 1990): 47–63. http://dx.doi.org/10.1111/j.1600-065x.1990.tb00036.x.

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Chardon, Patrick, Christine Renard, and Marcel Vaiman. "The major histocompatibility complex in swine." Immunological Reviews 167, no. 1 (February 1999): 179–92. http://dx.doi.org/10.1111/j.1600-065x.1999.tb01391.x.

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Ayala García, Marco Antonio, Beatriz González Yebra, Andrea Liliana López Flores, and Eduardo Guaní Guerra. "The Major Histocompatibility Complex in Transplantation." Journal of Transplantation 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/842141.

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Abstract:

The transplant of organs is one of the greatest therapeutic achievements of the twentieth century. In organ transplantation, the adaptive immunity is considered the main response exerted to the transplanted tissue, since the principal target of the immune response is the MHC (major histocompatibility complex) molecules expressed on the surface of donor cells. However, we should not forget that the innate and adaptive immunities are closely interrelated and should be viewed as complementary and cooperating. When a human transplant is performed, HLA (human leukocyte antigens) molecules from a donor are recognized by the recipient's immune system triggering an alloimmune response Matching of donor and recipient for MHC antigens has been shown to have a significant positive effect on graft acceptance. This paper will present MHC, the innate and adaptive immunities, and clinical HLA testing.

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DAUSSET, JEAN. "The Major Histocompatibility Complex in Man." Scandinavian Journal of Immunology 36, no. 2 (August 1992): 146–55. http://dx.doi.org/10.1111/j.1365-3083.1992.tb03085.x.

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Lamont, S. J. "Immunogenetics and the major histocompatibility complex." Veterinary Immunology and Immunopathology 30, no. 1 (November 1991): 121–27. http://dx.doi.org/10.1016/0165-2427(91)90013-3.

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Kaufman, J. F., M. F. Flajnik, and L. Du Pasquier. "Evolution of the major histocompatibility complex." Developmental & Comparative Immunology 10, no. 1 (December 1986): 95. http://dx.doi.org/10.1016/0145-305x(86)90049-2.

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