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PubMed1999

Mhc class I and non-class I gene organization in the proximal H2-M region of the mouse.

A bacterial artificial chromosome (BAC) contig was constructed across the proximal part of the H2-M region from the major histocompatibility complex (Mhc) of mouse strain 129 (H2bc). The contig is composed of 28 clones that span approximately 1 megabasepair (Mb), from H2-T1 to Mog, and contains three H2-T genes and 18 H2-M genes. We report the fine mapping of the H2-M class I gene cluster, which includes the previously reported M4-M6, the M1 family, the M10 family, and four additional class I genes. All but two of the H2-M class I genes are conserved among haplotypes H2k, H2b, and H2bc, and only two genes are found in polymorphic HindIII fragments. Six evolutionarily conserved non-class I genes were mapped to a 180 kilobase interval in the distal part of the class I region in mouse, and their order Znf173-Rfb30-Tctex5-Tctex6- Tctex4-Mog was found conserved between human and mouse. In this Znf173-Mog interval, three mouse class I genes, M6, M4, and M5, which are conserved among haplotypes, occupy the same map position as the human HLA-A class I cluster, which varies among haplotypes and is diverged in sequence from the mouse genes. These results further support the view that class I gene diverge and evolve independently between species.

Animals↗

PubMed1988

The detection of conventional class I and class II I-E homologue major histocompatibility complex molecules on feline cells.

The presence on feline cells of class I and class II I-E type major histocompatibility complex (MHC) homologues was demonstrated using cross-reacting monoclonal antibodies (mAb). The feline class I antigen homologues were detected with both immunofluorescent and biochemical techniques, using the anti-human class I mAb W6/32. The class I antigens were detected on in vitro cultured feline fibroblasts and lymphoid cells, but not on fresh lymphoid cells, apparently as a result of the association of bovine beta-2 microglobulin with feline class I heavy chains which generated the determinant(s) recognized by mAb W6/32. Class II I-E-like molecules could be detected with immunofluorescent techniques using the species cross-reactive anti-mouse I-E antibody 40D only when peripheral blood mononuclear cells were activated, for example, with the mitogens staphylococcus enterotoxin A or lipopolysaccharide. The predominant expression of I-A-like molecules by resting class II-positive feline cells could explain some of the functional difference we have seen in comparison with those of most other mammalian species.

Animals↗

PubMedDate not supplied

Expression of MhcCyca class I and class II molecules in the early life history of the common carp (Cyprinus carpio L.)

In this study transcription of class I alpha chain (Cyca-UA), beta2-microglobulin (Cyca-B2m) and class II alpha (Cyca-DXA) and beta (Cyca-DAB) during the early stages of embryo development was investigated by semiquantitative PCR. No transcripts of the genes under investigation were detected in the unfertilized egg. The expression of the genes encoding for the class II molecules revealed to be synchronized starting at day 1, unlike those for the class I molecules. Transcription of Cyca-B2m was first detected at day 7, whereas Cyca-UA was already present on day 1. This discrepancy would suggest absence of class I molecules during early development. The transcription of the Mhc genes in lymphoid organs was well established on day 21, with the exception of the spleen. In later stages of ontogeny cell surface expression of class I molecules was studied using polyclonal antibodies to Cyca-UA and Cyca-B2m in conjunction with detection of surface Ig. In week 3-10 Cyca-B2m was found on a higher percentage of cells from pronephros, spleen and thymus compared to Cyca-UA, suggesting the use of an alternative class I alpha chain. In the thymus, unlike the other organs, this difference remained present in the adult stage. The most likely candidates are alpha chains encoded by non-classical class I genes.

Animals↗

PubMed1999

Effect of isolation techniques, in vitro culture and IFNgamma treatment on the constitutive expression of MHC Class I and Class II molecules on goat neutrophils.

Previous studies on the ability of human neutrophils to synthesize cytokines and express MHC Class I and inducible Class II molecules have suggested a possible role of these cells as accessory or antigen presenting cells (APC). There is no information available to date concerning this aspect in ruminants. Therefore, as the first step of these investigations, we have studied the cell surface expression of MHC molecules on goat neutrophils. We show that goat neutrophils can be distinguished from eosinophils with monoclonal antibody (MoAb) ILA-24 which recognizes cattle monocytes and neutrophils. Goat neutrophils constitutively express MHC Class II molecules. However, cell surface expression of MHC Class I and Class II molecules is dramatically reduced on neutrophils purified by density gradient centrifugation in comparison to neutrophils obtained from whole blood after lysis of erythrocytes. Also, the level of expression of MHC Class I antigens is seasonal and donor-dependent and rapidly decreases after in vitro culture despite negligible necrosis and apoptosis of neutrophils. Although treatment with IFNgamma partially prevents the loss of MHC Class I molecules on neutrophils, it fails to induce MHC Class II antigens. Implications of these results for further studies on the potential role of neutrophils as APC are discussed.

Animals↗

PubMed2000

Nitric oxide inhibits INFgamma-induced increases in CIITA mRNA abundance and activation of CIITA dependent genes--class II MHC, Ii and H-2M. Class II TransActivator.

BACKGROUND: Nitric oxide (NO) has been recently implicated as a powerful inhibitor of immune responses during allograft rejection, and some autoimmune and infectious diseases. We previously showed that one potential regulatory effect of NO is inhibition of IFNgamma-stimulated expression of Class II MHC on macrophages. Activation of this gene is mediated by the "Class II TransActivator" (CIITA). We now ask whether NO inhibits CIITA and thus the family of genes regulated by CIITA--Class II MHC, Ii, and H-2M. The latter two genes participate in antigen processing and formation of the cell-surface peptide-Class II MHC complex. METHODS: Murine macrophages--both peritoneal macrophages and the RAW264.7 macrophage line--were stimulated in vitro with IFNgamma. NO production was measured by the Greiss reagent. Transcription of Class II MHC was measured by nuclear run-on assay. mRNA abundance of Class II MHC, Ii, H-2M, and CIITA was measured by Northern blotting and RT-PCR. RESULTS: NO inhibits IFNgamma-induced increases in the abundance and transcription of the Class II MHC Ab gene. The increases in mRNA abundance of CIITA, Ii, and H-2M are also inhibited. As a control, we found that NO did not inhibit LPS-induce increases in TNFalpha mRNA abundance. CONCLUSIONS: NO inhibits IFNgamma-induced increases in CIITA, and thus inhibits the CIITA-regulated genes: Class II MHC, Ii, and H-2M. Early during rejection, NO production by macrophages may result after stimulation by IFNgamma produced by CD4+ T cells, and be an effector of allograft damage. High concentrations of NO may then act as a feedback inhibitor which decreases antigen presentation by macrophages and thus decreases CD4 T cell activation.

Animals↗

PubMed1992

MHC class II interaction with CD4 mediated by a region analogous to the MHC class I binding site for CD8.

Interactions between major histocompatibility complex (MHC) molecules and the CD4 or CD8 coreceptors have a major role in intrathymic T-cell selection. On mature T cells, each of these two glycoproteins is associated with a class-specific bias in MHC molecule recognition by the T-cell receptor. CD4+ T cells respond to antigen in association with MHC class II molecules and CD8+ T cells respond to antigen in association with MHC class I molecules. Physical interaction between the CD4/MHC class II molecules and CD8/MHC class I molecules has been demonstrated by cell adhesion assay, and a binding site for CD8 on class I has been identified. Here we demonstrate that a region of the MHC class II beta-chain beta 2 domain, structurally analogous to the CD8-binding loop in the MHC class I alpha 3 domain, is critical for function with both mouse and human CD4.

Animals↗

PubMed1996

Contribution of HLA class I and class II alleles to the regulation of antibody production to hepatitis B surface antigen in humans.

The HLA multigene family consists of HLA class I (HLA-A, B and C) and class II (HLA-DR, DQ and DP) genes, and plays a central role in the regulation of immune response. To investigate how each HLA gene and each HLA allele contribute to the human immune response, we immunized 339 healthy Japanese medical students with recombinant hepatitis B surface antigen (rHBsAg) and determined the HLA types of all vaccinated subjects at the DNA level. The anti-HBs antibody titers showed a log-normal distribution, implying that the immune response to HBsAg in humans is a multifactorial and continuous trait. A stepwise multiple regression analysis demonstrated the alleles at the HLA-class I (HLA-A and B) and class II (HLA-DRB1, DQA1, DQB1, DPA1 and DPB1) loci significantly contributed to antibody production to HBsAg. The predicting equation of anti-HBs antibody levels for individuals with any HLA phenotype was proposed based on a multiple regression analysis. The multiple correlation coefficient of antibody production to HBsAg with the HLA-DRB1 locus was highest (0.34) among all of the HLA loci, whereas those with whole HLA class I or class II loci were 0.36 or 0.44 respectively. The incorporated correlation coefficient of the presence of all HLA gene families with antibody production became 0.50, suggesting that HLA class I and class II loci within the HLA multigene family are dynamically involved in regulation of the immune response to HBsAg.

Alleles↗

PubMed1994

The role of host T cell subsets in bone marrow rejection directed to isolated major histocompatibility complex class I versus class II differences of bm1 and bm12 mutant mice.

An expanded pool of unrelated donors (URD) is now being utilized for clinical allogeneic bone marrow transplantation. Because URD transplants can involve a mismatch at least at one genotypic MHC locus, we developed a C57BL/6 congenic mouse model to better understand graft rejection based exclusively on MHC class I or class II disparities. T cell-depleted (TCD) BM from class II-disparate mutant bm12 mice was transplanted into irradiated C57BL/6-Ly5.2 congenic hosts. These mice express a different allelic form of the Ly5 (CD45) marker than bm12 and thus permit definitive typing of reconstituted mice by flow cytometry. Peripheral blood typing indicated that host-mediated graft rejection was restricted to class II-reactive CD4+ cells since an anti-CD4 monoclonal antibody significantly inhibited rejection by enhancing the level of mean donor cell engraftment from 13% to 53%. The administration of anti-CD8 had no inhibitory effect on the ability of the recipient to reject the donor graft. Hematologic reconstitution studies revealed that there was a direct relationship between the level of donor cell engraftment and the extent of lymphoid, myeloid, and erythroid recovery. Mice that did not engraft had sustained reductions in in hematologic recovery. In other studies, TCD BM from bm1 mice mutated only in the MHC class I region was rejected by C57BL/6-Ly5.2 recipients. Anti-CD8 mAb infusion prevented the class I response resulting in an increase in the level of mean donor cell engraftment from 1% to 78%. Anti-CD4 alone had no effect. A CD4/CD8 T cell interaction could be important since the combination of anti-CD4 and anti-CD8 mAb resulted in significantly better donor engraftment than with the individual antibodies. Since the role of NK cells in these models has not been previously established and there is a reported association between NK cells and the rejection of BM cells that lack the expression of self-MHC antigens, we tested the role of NK cells. The elimination of NK cells using anti-NK mAb had no effect on graft rejection in either the bm1 or bm12 model. In addition to their value in exploring mechanisms of graft rejection, these models may prove useful for evaluating the efficacy of anti-BM rejection agents exclusively against class I- or class II-restricted disparities.

Alleles↗

PubMed1996

In vivo and in vitro evidence for iodide regulation of major histocompatibility complex class I and class II expression in Graves' disease.

Increases in thyroid cell major histocompatibility complex (MHC) class I and class II expression have been suggested to be an important factor in the development or perpetuation of Graves' disease. It is hypothesized that elevations result in abnormal presentation of thyroid antigens to immune cells, and that iodide and/or methimazole (MMI) are effective therapeutic agents because, at least in part, of their suppression of MHC expression. In this report, we show that Graves' patients pretreated with iodide only 4 days before surgery have lower levels of MHC class I and class II RNA levels in their thyroid tissue than do patients with no iodide pretreatment (P < 0.001 and 0.03, respectively). Because patients in both groups are treated with MMI and because the change is independent of the amounts of MMI used to treat patients, the class I and class II changes cannot be ascribed to MMI. The iodide action to decrease MHC class I and class II RNA levels was duplicated using cultured human thyroid cells in vitro; the iodide effect was dependent on the iodide concentration, was not duplicated by chloride, was not associated with an alteration in cAMP levels or with a change in thyrotropin receptor RNA levels, and was evident in gamma-interferon-treated cells. The data suggest, therefore, that the therapeutic action of iodide in Graves' patients is associated with decreased MHC gene expression, that this action is a direct effect of high concentrations of iodide on the thyroid cells, and that altered MHC gene expression in the target tissue may well be associated with the development or perpetuation of Graves' disease.

Adolescent↗

PubMed1997

Effect of interferon-gamma and glucose on major histocompatibility complex class I and class II expression by pancreatic beta- and non-beta-cells.

Surface major histocompatibility complex (MHC) class I and class II expression by pancreatic islet cells is considered a local initiator or regulator of immune processes that can lead to diabetes. Locally released cytokines, in particular interferon-gamma, are known to stimulate MHC antigen expression by islet cells. The present study quantifies MHC expression in cultured pancreatic beta- and non-beta-cells from both rat and human organs. Interferon-gamma increased MHC class I expression in endocrine beta- and non-beta-cells as well as in pancreatic ductal cells. The cytokine induced a 6-fold increase in the MHC class I messenger ribonucleic acid levels in pancreatic beta-cells; this effect was 2-fold amplified in the presence of elevated glucose levels (20 mmol/L instead of 6 mmol/L). No MHC class II expression was observed in endocrine beta- or non-beta-cells; human, but not rat, ductal cells exhibited MHC class II expression that increased in the presence of interferon-gamma. These data indicate that the increase in beta-cell MHC class I expression described in the pancreata of diabetic patients may result from stimulated transcription after exposure to locally released interferon-gamma and/or to a hyperglycemic state. The association of human islets with ductal cells in which MHC class II expression is stimulated by interferon-gamma makes these cells potential participants in the autoimmune process in diabetes.

Adolescent↗

PubMed1999

Nicotinamide decreases MHC class II but not MHC class I expression and increases intercellular adhesion molecule-1 structures in non-obese diabetic mouse pancreas.

Pancreases of untreated and nicotinamide (NIC)-treated pre-diabetic (10-week-old) and overtly diabetic (25-week-old) female NOD (non-obese diabetic) mice and of NON (non-obese non-diabetic) control mice were studied, with the following results. (1) Islets and ducts of overtly diabetic untreated NOD mice (25-week-old) were found to express low levels of MHC class I and II molecules, like NON controls, and high levels of adhesive molecules. (2) NIC was able to slightly affect glycaemia and insulitis, slowing down diabetes progression. Moreover it significantly decreased MHC class II expression (but not class I) in vivo by week 10, and significantly enhanced intercellular adhesion molecule-1 (ICAM-1) expression, mainly by week 25, within the pancreas, where 5-bromo-2'-deoxyuridine positive nuclei and insulin positive cells were present, demonstrating that a stimulation of endocrine cell proliferation occurs. (3) In addition, NIC partly counteracted the fall of superoxide dismutase levels, observed in untreated diabetic NOD animals. (4) In vitro studies demonstrated that NIC: (i) was able to significantly reduce nitrite accumulation and to increase NAD+NADH content significantly, and (ii) was able to increase the levels of interleukin-4, a T helper 2 lymphocyte (Th2) protective cytokine, and of interferon-alpha (IFN-alpha), which is known to be able to induce MHC class I and ICAM-1 but not MHC class II expression, as well as IFN-gamma, which is also known to be able to induce MHC class I and ICAM-1 expression. The latter, although known to be a proinflammatory Th1 cytokine, has also recently been found to exert an anti-diabetogenic role. This study therefore clearly shows that adhesive mechanisms are ongoing during the later periods of diabetes in pancreatic ducts of NOD mice, and suggests they may be involved in a persistence of the immune mechanisms of recognition, adhesion and cytolysis and/or endocrine regeneration or differentiation processes, as both NIC-increased ICAM-1 expression and 5-bromo-2'-deoxyuridine positivity imply. The effects of NIC on MHC class II (i.e. a reduction) but not class I, and, mainly, on ICAM-1 expression (i.e. an increase), together with the increase in Th2 protective cytokine levels are very interesting, and could help to explain its mechanism of action and the reasons for alternate success or failure in protecting against type 1 diabetes development.

Animals↗

PubMed1991

Liposome-encapsulated antigens engender lysosomal processing for class II MHC presentation and cytosolic processing for class I presentation.

Liposome-encapsulated protein Ag were used to dissect the roles of various subcellular compartments in Ag processing for class I and class II MHC-restricted presentation. Macrophages exhibited efficient processing of Ag encapsulated in acid-resistant dioleoylphosphatidylcholine/dioleoylphosphatidylserine liposomes, which sequester their contents from potential endosomal processing events and release them only after delivery to lysosomes. Lysosomal processing was demonstrated for all four Ag studied (OVA, murine hemoglobin, bovine ribonuclease A, and hen egg lysozyme), establishing the recycling of immunogenic peptides from lysosomes after Ag processing. These acid-resistant liposomes did not engender class I processing. Ag encapsulated within acid-sensitive dioleoylphosphatidylethanolamine/palmitoylhomocysteine liposomes were also processed via the class II pathway. Of the four Ag encapsulated in liposomes, one, OVA, was tested for ability to stimulate a class I-specific response. OVA in acid-resistant liposomes did not engender a class I-specific response. In contrast, OVA encapsulated in acid-sensitive liposomes was presented by class I molecules, albeit less efficiently than it was presented by class II molecules. We interpret this to be the result of the release of a minor portion of the encapsulated Ag into the cytosol.

Animals↗

PubMedDate not supplied

The differences in the chronology and calcification of second molars between angle Class III and Class II occlusions in Japanese children.

The purpose of this study was to examine the differences in the times of eruption and calcification of the permanent dentition between skeletal class III and class II groups. (And also to examine the relationship between the time of eruption and the type of malocclusion) Fifty-three children, ages seven to ten years, were selected. Of these, twenty-six children (twelve boys and fourteen girls) were Angle class III with minus ANB and twenty-seven children (eleven boys and sixteen girls) were Angle class II with five or more ANB. Panoramic radiographs and cephalometric radiographs were used. The panoramic radiographs showed that the calcification of the maxillary second molars in class II were earlier than in class III using Nolla's classification. There was no statistically significant difference, however, for mean values of calcification stages, using Nolla's classification, between boys and girls. The cephalometric and panoramic radiographs showed that the times of eruption and calcification were earlier in the maxillary second molars than in the mandibular second molars for class II. In contrast, the times of eruption and calcification were earlier in the mandibular second molars than in the maxillary second molars for class III. The times of eruption and calcification of the maxillary molars were significantly related to the length of the ANS-PNS. The longer the ANS-PNS, the earlier were the times of eruption and calcification. There was a significant relationship between the ANB angle and the time of eruption, as well as the ANB angle and calcification. The larger ANB had earlier calcification and chronology of maxillary second molars.

Cephalometry↗

PubMed1997

Linkage of LMP, TAP, and RING3 with Mhc class I rather than class II genes in the zebrafish.

The LMP2 and LMP7 genes code for subunits of the proteasome, a multimeric enzymatic complex that degrades proteins into peptides. The two subunits replace corresponding constitutively expressed subunits during the immune response. Some of the peptides generated by the proteasome in the cytosol are transported by the products of the TAP1 and TAP2 genes into the lumen of the endoplasmic reticulum and are loaded onto the assembling MHC class I molecules. In mammals, the LMP2, LMP7, TAP1, and TAP2 genes reside in the class II region of the Mhc, closely linked to the RING3 gene. In the present study we identified, cloned, and sequenced the LMP, TAP2, and RING3 genes of the zebrafish, Danio rerio. We identified variants of these genes and used them in a segregation analysis of haploid embryos derived from heterozygous mothers. The analysis revealed that in zebrafish, the LMP2, LMP7, TAP12, and RING3 loci are closely linked but, in contrast to mammals, the LMP/TAP/RING3 cluster resides not in the Mhc class II but in the class I region. We also confirmed that in the zebrafish, the class I and class II regions are not linked to each other. In this species, therefore, the LMP/TAP/RING3 genes are clustered with the class I genes on a chromosome that apparently does not contain any class II genes. The linkage of LMP/TAP/RING3/class I may be the original and the LMP/TAP/RING3/class II a derived arrangement of these genes.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed2000

Enhancement of MHC class I-stimulated alloresponses by TNF/TNF receptor (TNFR)1 interactions and of MHC class II-stimulated alloresponses by TNF/TNFR2 interactions.

In vivo TNF inhibition has been observed to ameliorate the disease process attributed to T cell-dependent immune responses such as those generated during graft-vs.-host disease. The present studies were designed to evaluate whether TNF/TNF receptor (TNFR)1 and TNF/TNFR2 interactions were involved in the generation of allospecific T cell responses. Splenic lymphocyte populations were obtained from TNFR1- or TNFR2-deficient B6 mice and from control B6 mice. These responder cells were cultured with irradiated MHC class II-disparate B6.C-H-2bm12 (bm12) or MHC class I-disparate B6.C-H-2bm1 (bm1) or irradiated syngeneic stimulator cells for 3 days before assay of [3H]thymidine incorporation. IL-2 levels of the mixed lymphocyte culture (MLC) supernatants were assessed by enzyme-linked immunosorbent assay. With MHC class II-disparate bm12 stimulator cells, a significant reduction in T cell proliferation was observed utilizing TNFR2-deficient CD4+ responder T cells, but not when using TNFR1 -deficient CD4+ responder T cells. A significant decrease in proliferation of TNFR1-deficient CD8+ responder cells, but not of TNFR2-deficient CD8 responder T cells was observed after stimulation with MHC class I-disparate bm1 stimulator cells. IL-2 levels were lower in MLC utilizing MHC class I stimulators and TNFR1-deficient responders or MHC class II stimulators and TNFR2-deficient responders. These results indicate that TNF/TNFR2 interactions promote MHC class II-stimulated alloresponses, while TNF/TNFR1 interactions promote MHC class I-stimulated alloresponses.

Animals↗

PubMed2003

The properties of the single chicken MHC classical class II alpha chain ( B-LA) gene indicate an ancient origin for the DR/E-like isotype of class II molecules.

In mammals, there are MHC class II molecules with distinctive sequence features, such as the classical isotypes DR, DQ and DP. These particular isotypes have not been reported in non-mammalian vertebrates. We have isolated the class II (B-L) alpha chain from outbred chickens as the basis for the cloning and sequencing of the cDNA. We found only one class II alpha chain transcript, which bears the major features of a classical class II alpha sequence, including the critical peptide-binding residues. The chicken sequence is more similar to human DR than to the DQ, DP, DO or DM isotypes, most significantly in the peptide-binding alpha(1) domain. The cDNA and genomic DNA sequences from chickens of diverse origins show few alleles, which differ in only four nucleotides and one amino acid. In contrast, significant restriction fragment length polymorphism is detected by Southern blot analysis of genomic DNA, suggesting considerable diversity around the gene. Analysis of a large back-cross family indicates that the class II alpha chain locus ( B-LA) is located roughly 5.6 cM from the MHC locus, which encodes the classical class II beta chains. Thus the chicken class II alpha chain gene is like the mammalian DR and E isotypes in three properties: the presence of the critical peptide-binding residues, the low level of polymorphism and sequence diversity, and the recombinational separation from the class II beta chain genes. These results indicate that the sequence features of this lineage are both functionally important and at least 300 million years old.

Alleles↗

PubMed2005

Depressed autonomic nervous system function in African Americans and individuals of lower social class: a potential mechanism of race- and class-related disparities in health outcomes.

BACKGROUND: Both race and social class influence cardiovascular outcomes, through mechanisms not yet fully understood. Minority race and lower social class are sources of chronic stress, which can alter autonomic nervous system function. Heart rate variability (HRV), a measure of autonomic function, is also an important predictor of cardiovascular outcomes. METHODS: To determine whether minority race/ethnicity and lower social class are associated with depressed HRV, we prospectively collected data on sociodemographic, clinical, psychological, and behavioral factors by survey in 360 outpatients undergoing ambulatory electrocardiographic monitoring. Heart rate variability (24-hour) was measured by frequency domain analysis. RESULTS: In unadjusted analysis, African Americans had lower HRV than whites, and individuals of lower social class as measured by education, occupation, and income had lower HRV than those of higher class. In multivariable analysis, both race and social class were independent predictors of ultralow frequency power after controlling for clinical and psychological factors. African Americans were 3.45 (95% CI 1.74-6.98, P = .0004) times as likely as whites to have depressed HRV (ultralow frequency power, lowest tertile), and non-college graduates 2.94 (95% CI, 1.71-5.14, P = .0001) times as likely as college graduates to have depressed HRV. CONCLUSIONS: Heart rate variability is lower in African Americans and individuals of lower social class, independent of the effects of measured clinical, psychological, or behavioral factors. This suggests that the adverse effects of minority race and lower social class on cardiovascular outcomes may be mediated by dysregulation of autonomic function.

Adult↗

PubMed1999

Ligation of MHC class II molecules differentially upregulates TNF beta gene expression in B cell lines of different MHC class II haplotypes.

Although the production of selected cytokines by B cells is important for their regulation, little is known about MHC class II-induced cytokine expression in these cells. We designed the present studies to investigate MHC class II-mediated TNF-beta gene expression in 19 EBV-transformed homozygote B cell lines at similar stage of differentiation but presenting different MHC class II haplotypes. Our results demonstrate that in contrast to PMA, engagement of MHC class II with staphylococcal enterotoxin A (SEA), a natural ligand, or with anti-HLA-DR mAb L243, stimulates TNF-beta gene expression in some but not all B cell lines. The differential stimulation of TNF-beta gene expression via MHC class II was not due to the cells MHC class II expression level, nor to their capacity to bind the ligands as evidenced by SEA binding affinity studies. Together these results demonstrate that ligation of MHC class II molecules can stimulate TNF-beta gene expression in a B cell line-dependent manner. The differential cytokine gene expression might be due to an influence of MHC class II haplotype either by a linkage disequilibrium with TNF-beta gene or by a differential association with effector or cell surface molecules.

Antibodies, Monoclonal↗