Beta-2 microglobulin is synthesized in all nucleated cells and forms the light chain subunit of the major histocompatibility complex class I antigen. Despite its potential role as a convenient and non-invasive prognostic indicator in malignant lymphomas, the influence of serum beta2 microglobulin is currently underestimated, and therapeutic decision making is rarely affected by this marker. Recent studies that included relatively large numbers of patients with specific histologic subtypes showed that serum beta2 microglobulin is a potent prognostic marker in malignant lymphomas. In follicular lymphoma, this effort led to the incorporation of serum beta2 microglobulin as an indicator in a new prognostic model. In this review, we summarize the current evidence supporting the role of serum beta2 microglobulin as a prognostic factor in patients with malignant lymphoma and discuss perspectives for future investigations.
Decision Making ; Humans ; Lymphoma* ; Lymphoma, Follicular ; Major Histocompatibility Complex

Recently developed computational methods allow the imputation of human leukocyte antigen (HLA) genes using intergenic single nucleotide polymorphism markers. To improve the imputation accuracy in HLA imputation, it is essential to increase the sample size and the diversity of alleles in the reference panel. Our software, MergeReference, helps achieve this goal by providing a streamlined pipeline for combining multiple reference panels into one.
Alleles ; HLA Antigens ; Humans ; Leukocytes ; Major Histocompatibility Complex ; Polymorphism, Single Nucleotide ; Sample Size

BACKGROUND: The major histocompatibility complex class I, G (human leukocyte antigen-G [HLA-G]) gene plays a vital role in the suppression of immune responses. Recently, a number of studies have reported an association between HLA-G and diseases (pregnancy complications, organ transplantation, and tumors). Some of the studies have revealed that the 14-bp insertion/deletion polymorphism might be associated with various diseases. The aim of the present study was to explore a possible influence of the 14-bp insertion/deletion polymorphism on osteosarcoma. METHODS: Genomic DNA was extracted from 75 formalin-fixed, paraffin-embedded tumor tissues derived from patients with conventional osteosarcoma (OSA) and 183 peripheral blood samples of healthy controls. Fifty-eight cases were South Korean patients with OSA and 17 cases were Argentine patients with OSA. The HLA-G 14-bp insertion/deletion polymorphism at exon 8 of the HLA-G locus was analyzed by polymerase chain reaction. RESULTS: There was a significantly different distribution profile for the 14-bp genotypes between the Korean OSA and Korean control groups. Specifically, there were more heterozygote 210 bp/224 bp genotypes in the Korean OSA group when compared to the Korean control group (62.1% vs 40.4%, p=0.002). CONCLUSIONS: The results suggest that HLA-G heterozygote patients may be more susceptible to OSA in the Korean population.
DNA ; Exons ; Genotype ; Heterozygote ; HLA-G Antigens ; Humans ; Leukocytes ; Major Histocompatibility Complex ; Organ Transplantation ; Osteosarcoma ; Transplants

In the present study, we investigated if priming of autoreactive CD8+ T cells would be inhibited by competitive peptides for major histocompatibility complex (MHC) class I binding. We used a mouse model of vitiligo which is induced by immunization of Kb-binding tyrosinase-related protein 2 (TRP2)-180 peptide. Competitive peptides for Kb binding inhibited IFN-gamma production and proliferation of TRP2-180-specific CD8+ T cells upon ex vivo peptide restimulation, while other MHC class I-binding peptides did not. In mice, the capability of inhibition was influenced by T-cell immunogenicity of the competitive peptides. The competitive peptide with a high T-cell immunogenicity efficiently inhibited priming of TRP2-180-specific CD8+ T cells in vivo, whereas the competitive peptide with a low T-cell immunogenicity did not. Taken together, the inhibition of priming of autoreactive CD8+ T cells depends on not only competition of peptides for MHC class I binding but also competitive peptide-specific CD8+ T cells, suggesting that clonal expansion of autoreactive T cells would be affected by expansion of competitive peptide-specific T cells. This result provides new insights into the development of competitive peptides-based therapy for the treatment of autoimmune diseases.
Animals ; Autoimmune Diseases ; Immunization ; Major Histocompatibility Complex ; Mice ; Peptides ; T-Lymphocytes ; Vitiligo

Through the recent study, we have come to know that the gene group, which has an important function, is closely existed in the part of 6 chromosome short arm of a human being. Gene group consists of a major histocompatibility complex which develops rejective reaction in the process of kidey tranplantation, the gene group which controls immune response and the gene group which decides serum compliment component. These are called HLA in total. Through HLA-a.B.C. typhing, we may be able to find the following: 1. It is polymorphic, the gene group of A.B.C.D. DR locus is found along with many haplo-type. 2. Antigen differs accorbing to race. Example: HLA B8=White people 0.1% Oriental people 0.001% 3. It is related to disease. 4. There are few cases in the Department of Pediatrics but the result Shows A2, A9, B5 and B40 which is very similar to that of Japanese. There has been no Korean specific antigen founb yet.
Arm ; Asian Continental Ancestry Group ; Continental Population Groups ; Humans ; Major Histocompatibility Complex ; Pediatrics

Antigen processing (TAP, HLA-DM and LMP) genes map within the major histocompatibility complex (MHC) class II region between the HLA-DQB1 and -DPB1 loci, and are involved in the processing of peptides bound to HLA class I or class II molecules. In order to determine the allele frequencies of antigen processing genes and the various linkage disequilibria existing among these genes, we have analyzed TAP1, TAP2, HLA-DMA, and HLA-DMB, LMP2, LMP7 polymorphisms in 184 unrelated healthy Koreans using the rnethod of PCR-SSCP, ARMS-PCR and PCR-RFLP. The frequencies of antigen processing genes were TAP1A (77.7%), TAP1*B (17.1%), TAP1*C (5.2%), TAP2*A (41.6%), TAP2*B (31.3%), TAP2*C (3.3%), TAP2*D (0.8%), TAP2*E (6.5%), TAP2*G (0.8%), HLA-DMA*0101 (81.5%), HLA-DMA*0102 (18.2%), HLA-DMA*0103 (0.3%), HLA-DMB*0101 (42.9%), HLA-DMB*0102 (19.0%), HLA-DMB*0103 (38.0%), LMP2*R (78.8%), LMP2*H (21.2%), LMP7*A (35.3%), LMP7*B (56.0%), LMP7*C (4.9%), and LMP7*D (3.8%). We also analysed two- locus association among each locus. Many significant positive associations were observed between these two loci, such as between HLA-DMB and TAP1, between HLA-DMA and HLA-DMB, between LMP2 and LMP7, and between TAP1 and LMP7. Conversely, any significant linkage disequilibrium was not detected between HLA-DMB and LMP2. These results could be used as control data for disease association and population genetics studies in Korean population.
Antigen Presentation* ; Gene Frequency ; Genetics, Population ; Linkage Disequilibrium ; Major Histocompatibility Complex ; Peptides

Fresh rat corneas as well as corneas preserved in several different corneal preservation media were stained with Avidin-Biotin-peroxidase Complex method in order to evaluate major histocompatibility complex (MHC) antigen expression. In fresh corneas, class I antigen was identified in corneal epithelium, stroma and endothelium. Class II antigen was identified only in stroma. In corneas preserved in the media which contained chondroitin and dextran for 7 days, class I antigen was somewhat decreased but class II antigen was increased. In corneas preserved in the medium which contained insulin or epidermal growth factor for 7 days, class II antigens seemed to be increased compaired to the fresh cornea. Expression of MHC antigens of corneas in the medium with fetal bovine serum were similar to those of fresh corneas.
Animals ; Cornea/*metabolism ; Culture Media ; Histocompatibility Antigens Class I/*biosynthesis ; Histocompatibility Antigens Class II/*biosynthesis ; Immunoenzyme Techniques ; Major Histocompatibility Complex ; Organ Preservation/methods ; Rats ; Rats, Inbred Lew

Mucosal-associated invariant T (MAIT) cells are evolutionarily conserved T cells that are restricted by the non-classical major histocompatibility complex class-1b molecule MR1. MAIT cells recognize riboflavin (vitamin B2) derivatives in a MR1-dependent manner. Following antigen recongnition, MAIT cells rapidly produce Th1/Th17 cytokines, such as interferon-gamma and interleukin-17, in an innate-like manner. MAIT cells maintain an activated phenotype throughout the course of an infection, secrete inflammatory cytokines, and have the potential to directly kill infected cells, thus, playing an important role in controlling the host response. In this review, we discuss current knowledge regarding the role of MAIT cells in infectious diseases, cancers, and autoimmune diseases.
Autoimmune Diseases ; Communicable Diseases ; Cytokines ; Immunity, Innate* ; Interferon-gamma ; Interleukin-17 ; Major Histocompatibility Complex ; Phenotype ; Riboflavin ; T-Lymphocytes*

PURPOSE: Dendritic cells are antigen presenting cells(APC) that express class II major histocompatibility complex gene products on their surface. Recently, it was proved that dendritic cells activate antitumor immunity for intracranial germ cell tumor. The aim of the present study is to investigate the age-related changes of MHC class II-immunoreactive dendritic cells in the rat brain. METHODS: Male rats(Sprague-Dawley) were sacrificed at 1 month, 12 months and 24 months after birth. Brains were removed and sliced in rat brain matrix. Brain slices were cryosectioned coronally at interaural 5.70-6.70 mm. Brain tissue sections were immunohistochemically reacted with monoclonal MHC class II antibody. RESULTS: MHC class II-immunoreactive dendritic cells were observed in choroid plexuses and white matter(corpus callosum, cerebral peduncle and external capsule). The number of MHC class II-immunoreactive dendritic cells was slightly increased with age. As age increases, shapes of MHC class II-immunoreactive dendritic cells became more complex and aggregated together. CONCLUSION: As age increases, MHC class II-immunoreactive dendritic cells in choroid plexuses and white matter of the brain became not only more complex in shape, but also increased in number to improve immunity.
Aging ; Animals ; Brain* ; Choroid Plexus ; Dendritic Cells* ; Humans ; Major Histocompatibility Complex ; Male ; Neoplasms, Germ Cell and Embryonal ; Parturition ; Rats* ; Tegmentum Mesencephali

The CD8(+)CD28(+) T cells have known to mediate major histocompatibility complex class I-restricted cytolysis and to secret an HIV-1 inhibitory factor. As HIV infection lead to dramatic changes within the cellular immune system, the cellular cytotoxicities decrease in the duration of the HIV infection. To determine the importance of the cellular cytotoxicities in long-term nonprogression, we tried to compare CD28 expression on total T, CD4(+) T, and CD8(+) T cells as one of methods for cellular cytotoxicity measurements between long-term nonprogressor and normal person or between long-term nonprogressor and rapid progressor. The median percentages and counts of CD4(+) T cells of the norrnal, the long-term nonprogressor, and the rapid progressor groups were 39.9 and 0.96 * 10(9) cells/L, 24.6 and 0.58 * 10(9) cells/L, 9.9 and 0.15 * 10 cells/L, respectively. As a result of comparison of the cells having CD28 surface molecules on CD8(+) T cells in the long-term nonprogressor and the rapid progressor group, they showed over 5 times lower than that in the normal group. Especially, the long-term nonprogressor regarded to the healthy HIV-infected patient showed much lower CD28 expression on total T, CD4(+) T, and CD8(+) T cells than those of the normal person. The proportions of CD4'CD28 T and CD3CD28 T cell subsets showed the significant difference between the LTNP and the RP group. In conclusion, although HIV-infected patients were LTNPs having the steady CD4(+) T cell counts and no clinical symptoms, we suggested that HIV led to abnormality within the lymphocyte subsets such as the altered expression of CD28 molecules on various T cell subsets and this result would cause deficiency of host immune function and failure of control of HIV replication by anergy in T cell subsets.
Cell Count ; HIV ; HIV Infections ; HIV-1 ; Humans ; Immune System ; Lymphocyte Subsets ; Major Histocompatibility Complex ; T-Lymphocyte Subsets* ; T-Lymphocytes