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At least 19 recordsLinked to original sources
PubMed1990

Induction of linked suppression in addition to the donor H-2 class I-specific unresponsiveness in recipient T cells by transfusing class I plus class II-disparate, but not class I alone-disparate, bone marrow cells.

This study was undertaken to determine whether bone marrow (BM) cells contain a cell population with the capacity to induce an unresponsiveness of T cells specific to the BM self-H-2 class I antigens in vivo, i.e., veto cell population. Recombinant or congenic mice were infused intravenously with H-2-incompatible BM cells. One to several weeks later, donor H-2-and irrelevant H-2-specific responses in mixed lymphocyte reaction cultures of recipient T cells were assessed. Transfusion of H-2-incompatible BM of C57BL/10 (B10) recombinant strains caused a long-lasting cytotoxic T lymphocyte (CTL) unresponsiveness to the donor class I antigens in recipient lymph node cells. When class I plus class II-disparate BM cells were transfused, an anti-donor class I CTL response and a response against a third-party class I antigen, which was presented on the stimulator cells coexpressing the donor class I and class II, were significantly suppressed. This linked suppression lasted for less than 2 weeks after transfusion. Transfusion of class I-alone-disparate BM induced the donor class I-specific CTL unresponsiveness, but not the linked suppression. The induction of linked suppression was prevented considerably by transfusing nylon wool-nonadherent BM or by treating recipients with cyclophosphamide 2 days before transfusion. An anti-third-party class I CTL response, stimulated in vitro with fully allogeneic spleen cells, was not hampered by the BM transfusion. Coculturing the lymph node (LN) cells obtained from the class I plus class II-disparate BM recipient with normal LN cells interfered with the generation of both anti-donor class I and anti-linked third-party class I CTL, whereas, coculturing LN cells from the class I alone-disparate BM recipient inhibited neither specificity of CTL generation. Transfusion of class I plus class II-disparate BM resulted in a significant suppression of the donor class II-specific proliferative response. In contrast, transfusion of class I alone-disparate BM did not suppress any proliferative responses, including even a "linked" third-party class II-specific response. Transfusion of bm 1, (B6 X bm 1)F1, or (bm 1 X bm 12)F1 BM to B6 did not induce unresponsiveness in bm 1-specific CTL responses. However, the transfusion resulted in a significant suppression of bm 1-reactive proliferative response of recipient LN cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

GVHR elicited by products of class I or class II loci of the MHC: analysis of the response of mouse T lymphocytes to products of class I and class II loci of the MHC in correlation with GVHR-induced mortality, medullary aplasia, and enteropathy.

A lethal graft-vs-host reaction (GVHR) was elicited by the injection into irradiated (700 rad) mice, reconstituted with T-depleted bone marrow cells (BM), of T lymphocytes incompatible for different loci of the major histocompatibility complex (MHC). The number of T cells needed to kill more than 50% of the recipients by day 40 was about 10(6) for GVHR elicited across the product of the K, D, or E locus, but about 10(5)--10--fold less-when the A locus was involved. The mortality was associated with a medullary aplasia in all strain combinations, but enteropathy was observed only in GVHR elicited by the products of class II, and not class I, loci. Mortality and medullary aplasia were diminished or absent in recipients reconstituted with BM cells from T cell donors instead of cells of the host genotype, which suggests a direct (cytolytic) T-hematopoietic cell interaction. Lymphoproliferation was evident within the host spleen and lymph node 5 days after injection of T lymphocytes incompatible for class II but not class I loci. Spleens from mice suffering from a lethal GVHR were examined by culture in limiting dilution to evaluate the frequency of anti-host T cells and to derive anti-host T cell clones and lines, whose properties were explored. In the GVHR elicited across the A or E region of the MHC, examined between days 7 and 19, a high frequency (10(-2] of anti-host cells was observed. The polyclonal cell lines isolated (16) all displayed MLR responsiveness, antigen-driven IL 2 production, and cytolysis for LPS blasts of the host genotype. However, among 13 clones isolated, two categories were observed: Lyt-2-, which were MLR responders and IL 2 producers (four of 13), and Lyt-2+, which were cytolytic but neither MLR responders nor IL 2 producers (nine of 13). In the GVHR elicited by the K or D region, examined between days 7 and 90, the frequency of anti-host cells was low (10(3) to 10(4], with a tendency to decrease during the progression of the disease. The lines (11) or clones (26) isolated from different mice were all Lyt-2+ and strongly cytolytic but proliferated poorly and produced no IL 2 in MLR. These findings suggest that the Lyt-2+ lymphocytes, recognizing the products of the class I loci, function in vivo without proliferation and without requiring helper T cells. Cell lines specific for class I or class II loci of the MHC produced interferon and colony-stimulating factors.

Animals↗
PubMed1991

Some cloned murine CD4+ T cells recognize H-2Ld class I MHC determinants directly. Other cloned CD4+ T cells recognize H-2Ld class I MHC determinants in the context of class II MHC molecules.

Murine T lymphocytes recognize nominal Ag presented by class I or class II MHC molecules. Most CD8+ T cells recognize Ag presented in the context of class I molecules, whereas most CD4+ cells recognize Ag associated with class II molecules. However, it has been shown that a proportion of T cells recognizing class I alloantigens express CD4 surface molecules. Furthermore, CD4+ T cells are sufficient for the rejection of H-2Kbm10 and H-2Kbm11 class I disparate skin grafts. It has been suggested that the CD4 component of an anti-class I response can be ascribed to T cells recognizing class I determinants in the context of class II MHC products. To examine the specificity and effector functions of class I-specific HTL, CD4+ T cells were stimulated with APC that differed from them at a class I locus. Specifically, a MLC was prepared involving an allogeneic difference only at the Ld region. CD4+ clones were derived by limiting dilution of bulk MLC cells. Two clones have been studied in detail. The CD4+ clone 46.2 produced IL-2, IL-3, and IFN-gamma when stimulated with anti-CD3 mAb, whereas the CD4+ clone 93.1 secreted IL-4 in addition to IL-2, IL-3, and IFN-gamma. Cloned 46.2 cells recognized H-2Ld directly, whereas recognition of Ld by 93.1 apparently was restricted by class II MHC molecules. Furthermore, cytolysis by both clones 46.2 and 93.1 was inhibited by the anti-CD4 mAb GK1.5. These results demonstrate that CD4+ T cells can respond to a class I difference and that a proportion of CD4+ T cells can recognize class I MHC determinants directly as well as in the context of class II MHC molecules.

Animals↗
PubMed1991

DNA binding of regulatory factors interacting with MHC-class-I gene enhancer correlates with MHC-class-I transcriptional level in class-I-defective cell lines.

Tumor cells frequently show a lack of surface class-I major histocompatibility complex (MHC) antigen expression. These molecules are key recognition structures for immune rejection of tumor cells and their absence at the surface of tumor cells could favor the progression of tumors. We have analyzed the transcriptional mechanisms that could lead to suppression of MHC-class-I expression in human tumor cell K562. The expression of MHC-class-I genes is highly controlled by regulatory factors interacting with an enhancer sequence upstream of MHC-class-I genes. In this report we show that DNA binding activity of 2 regulatory factors, KBFI and NF-kappa B, known to be essential for constitutive expression of MHC-class-I genes, is deficient in nuclear extracts from K562 cells. Induction of class-I gene expression at the surface of tumor cells by interferon-gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) shows that TNF-alpha can act in synergy with IFN-gamma to induce DNA binding of both factors NF-kappa B and KBFI to the class-I gene enhancer and that this induction of transcriptional factors is correlated with enhancement of MHC-class-I mRNA transcription and cell-surface antigen expression.

Antibodies, Monoclonal↗
PubMed1992

Class IV alcohol dehydrogenase (the gastric enzyme). Structural analysis of human sigma sigma-ADH reveals class IV to be variable and confirms the presence of a fifth mammalian alcohol dehydrogenase class.

Human gastric alcohol dehydrogenase (sigma sigma-ADH) was submitted to peptide analysis at picomole scale. A total of 72 positions were determined in the protein chain, providing information on three aspects of alcohol dehydrogenase structures in general. First, the data establish the presence of a unique class of the enzyme, now confirmed as class IV, expressed in gastric tissue and separate from another novel class, now termed class V. Second, the class IV gastric enzyme has active site relationships compatible with an ethanol-active, zinc-containing alcohol dehydrogenase. Third, this enzyme class is of the variable type, like that for the 'variable', classical liver alcohol dehydrogenase of class I, and in contrast to that for the 'constant' class III enzyme. Known human alcohol dehydrogenase structures now prove the presence of at least seven human genes for the enzyme and nine for the whole protein family.

Alcohol Dehydrogenase↗
PubMed1990

Baboon alcohol dehydrogenase isozymes: purification and properties of liver class I ADH. Moderate alcohol consumption reduces liver class I and class II ADH activities.

The major baboon liver isozyme of alcohol dehydrogenase (ADH-2) has been purified to homogeneity by affinity chromatography, and characterized as a "typical" Class I mammalian ADH isozyme. In contrast to human liver, which possesses three genetic isozymes (alpha 2, beta 2, and gamma 2) and three hybrid isozymes (alpha beta, alpha gamma, and beta gamma) of Class I ADH, baboon liver exhibits activity of a single major Class I isozyme (beta 2). Kinetic analyses, using alcohol substrates of differing chain lengths, and inhibition with pyrazole, support this classification. Agarose-IEF analyses, substrate specificity studies and immunochemical titrations of the major kidney ADH (ADH-1) also support the occurrence of a second Class I isozyme. The baboon was used as a model to study alcohol-induced changes in liver ADH phenotype following moderate and moderately high alcohol consumption. Four male and four female prepubertal baboons were fed nutritionally adequate liquid diets over a 40-week period, including control diets (weeks 1-8, 17-24, 32-40), moderate (12.5 percent of calories) alcohol diet (weeks 9-16), and a moderately high (25 percent of calories) alcohol diet (weeks 25-32). Liver ADH isozyme patterns and Class I ADH activities from biopsy samples, taken every 4 weeks, were monitored during the feeding study. Decreases in both Class I and Class II ADH activities were indicated in most animals, which may reflect adaptive mechanisms in the liver to continuing alcohol metabolism. Moreover, reversible changes were observed, with trends toward a recovery of ADH isozyme activities following return to the control liquid diets. These studies also have particular significance for human biomedical research work on alcohol, since most of the "drinking" population in typical drinking communities are moderate consumers of alcohol. This work, using the baboon as an animal model, has clearly indicated that alcohol consumption at such moderate levels, brings with it adaptations in the level of ADH isozymes in liver, which may play a protective role.

Alcohol Dehydrogenase↗
PubMed1990

Induction of transplantation tolerance by intravenous injection of allogeneic lymphocytes across an H-2 class II mismatch. Different mechanisms operate in tolerization across an H-2 class I vs. H-2 class II disparity.

Previously, we have shown that the intravenous (i.v.) injection of allogeneic lymphocytes across an H-2 class I-mutant disparity leads to specific skin allograft tolerance caused by irradiation-sensitive donor T cells, which function as veto cells. In the present study, we show that the i.v. injection of H-2 class II-incompatible spleen cells also results in specific skin allograft tolerance. However, tolerance induction depends on the presence of irradiation-resistant non-T cells in the donor cell inoculum. Thus, different mechanisms operate in tolerance induction across an H-2 class I vs. H-2 class II mismatch. I.v. injection of allogeneic spleen cells across an H-2 class I plus class II disparity does not result in skin allograft tolerance. Finally, our data show that transfusion-induced suppression of the delayed-type hypersensitivity response against alloantigens does not correlate with skin allograft tolerance induced by i.v. injected allogeneic lymphocytes. In conclusion, the type of H-2 mismatch between transfusion donor and recipient not only determines the occurrence of allograft tolerance but also the mechanism leading to tolerization.

Animals↗
PubMed1992

Comparison of tolerance inducibility to class I or class II antigens between cyclophosphamide (CP)-induced tolerance and transfusion with donor cells: general effectiveness of CP-induced tolerance and difference of skin graft prolongation in each class I antigen-disparate combination.

Transfusion with allogeneic cells alone was reported to prolong skin allograft survival in the MHC class I antigen alone-disparate combination of B6.C-H-2bm1 (bm1; Kbm1, IAb, IE-, Db)-->C57BL/6 CrSlc (B6; H-2b). Using 6 class I antigen-disparate and 2 class II antigen-disparate combinations, we compared the effectiveness for skin graft prolongation between transfusion with donor cells (TDC) and our system of CP-induced tolerance, which comprises intravenous (i.v.) injection of allogeneic cells followed by cyclophosphamide (CP), i.e., TDC followed by CP. TDC was effective only in the combination of bm1-->B6, but not at all in the other combinations. On the other hand, CP-induced tolerance was effective in the 5 class I antigen-disparate and 2 class II antigen-disparate combinations except for bm1-->B6 combination. These results suggest that CP-induced tolerance may be more general for the induction of unresponsiveness than TDC.

Animals↗
PubMed1985

Inhibition of anti-class I cytotoxicity by anti-class II monoclonal antibodies (MoAb). II. Blocking of anti-class I CTL clones by anti-DR MoAb.

Monoclonal antibodies directed at monomorphic determinants on A,B,C (w6/32) or DR (L243, S4/24, S8/8) HLA antigens were used to inhibit the cytotoxic activity of class I- or class II-reactive CTL clones. Anti-class I (HLA-Bw62) cytotoxic T lymphocyte CTL clones were inhibited by w6/32, but not by L243, when tested on PHA blasts and LCL as targets. Interestingly, S4/24 and S8/8 demonstrated a differential blocking ability of class I reactive clones; these two monoclonal antibodies could not block Bw62-directed CTL clones when using PHA blasts as targets but strongly inhibited the cytotoxic activity of the same clones on LCLs as targets.

Antibodies, Monoclonal↗
PubMed1992

Cell subsets responding to purified hepatocytes and evidence of indirect recognition of hepatocyte major histocompatibility complex class I antigen. II. In vitro-generated "memory" cells to class I+ class II- hepatocytes.

Purified hepatocytes stimulate the development of L3T4-, Ly2+ allospecific cytolytic T cells from naive splenocytes after 5 days in primary mixed lymphocyte-hepatocyte culture (MLHC). Previous studies indicate that the immunogenicity of purified hepatocytes relates to the expression of MHC class I antigen. The purpose of the following experiments was to identify the cell subsets that specifically recognize hepatocyte MHC class I antigen. We employed primed lymphocyte testing (PLT) in order to test for a "second set" response. Cells from primary MLHC reverted to a functionally quiescent state when they were grown in culture for an additional 7-9 days. The cells were then tested for cytotoxicity or rechallenged with allogeneic, syngeneic, or "third party" hepatocytes and tested for proliferation. Allocytotoxicity was low on day 12 in MLHC, but the sensitized cell population demonstrated peak proliferation in response to allogeneic hepatocytes 48 hr after restimulation. When bulk PLT cells were immunodepleted, both L3T4+, Ly2- and L3T4-, Ly2+ T cell subsets demonstrated a "second set" response to allogeneic hepatocytes consistent with specific recognition of and retention of "memory" for hepatocyte MHC class I alloantigen.

Animals↗
PubMed1975

Nose morphology in individuals with Angle Class I, Class II or Class III occlusions.

The intention of this work was to describe the nose morphology in individuals with different craniofacial patterns which dentally were characterized by Angle Class I, Class II div. 1, and Class III occlusions. The material comprised male adults (age 20--30 years), and the results are based on measurements on tracings of lateral cephalograms. Generally, the inclination of the nose in relation to the nasion-sella-line was similar in all groups, and so was the nose length as well. The depth of the nose, when related to the hard and soft tissue facial planes was, however, significantly different, apparently due to the different sagittal position of the chin.

Adolescent↗
PubMed1990

Role of T cell subsets in lethal graft-versus-host disease (GVHD) directed to class I versus class II H-2 differences. II. Protective effects of L3T4+ cells in anti-class II GVHD.

Detailed information was sought on the capacity of purified B6 L3T4+ cells to elicit lethal graft-versus-host disease (GVHD) in irradiated class II-different class I-identical (C57BL/6 (B6) x bm 12)F1 hosts. When B6 L3T4+ cells were transferred in small doses (10(5) to 10(6) together with donor bone marrow (BM) cells, the recipients all developed acute lethal GVHD and most of the mice died within 2 wk, probably from gut damage; this syndrome was conspicuous only in mice treated with very heavy irradiation, i.e., 1000 rad. In marked contrast to L3T4+ cells given in small doses, transfer of large doses of B6 L3T4+ cells to heavily irradiated (B6 x bm 12)F1 hosts paradoxically resulted in only limited mortality: most of the recipients survived for greater than 6 mo and manifested little or no evidence of ill health. It is suggested that the capacity of large doses of L3T4+ cells to protect mice against lethal GVHD is a reflection of T helper function: the cellular immunity provided by the donor L3T4+ cells enables the host to repel pathogens entering through damaged mucosal surfaces, with the result that GVHD becomes sublethal. The protective function of L3T4+ cells in the B6----bm 12 combination was only seen in hosts given donor BM. With transfer of donor L3T4+ cells plus host BM, even lightly irradiated recipients died rapidly from hemopoietic failure. Because this syndrome failed to occur in mice given a mixture of donor and host BM, it would appear that L3T4+ cells destroyed host lymphohemopoietic cells by direct cytotoxicity rather than via a bystander effect.

Animals↗
PubMed1985

Effect of monoclonal antibodies (MoAb) to class I and class II HLA antigens on lectin- and MoAb OKT3-induced lymphocyte proliferation.

We have examined the effect of several monoclonal antibodies (MoAb) to monomorphic determinants of class II HLA antigens, and MoAb to monomorphic determinants of class I HLA antigens and to beta-2-microglobulin (beta 2-mu) on lectin- and MoAb OKT3-induced proliferation of human peripheral blood mononuclear cells (PBMNC) and cultured T cells (CTC). Some, but not all, anti-class II HLA MoAb inhibited the proliferative response of PBMNC to MoAb OKT3 and pokeweed mitogen (PWM). The degree of inhibitory effect varied considerably. This effect was not limited to anti-class II HLA MoAb since anti-class I HLA MoAb and anti-beta 2-mu MoAb also inhibited MoAb OKT3- or PWM-induced proliferative responses. In contrast, the response of PBMNC to phytohemagglutinin (PHA) and concanavalin A (Con A) was not blocked by any anti-class II HLA MoAb. However, some anti-class II HLA MoAb also inhibited the proliferative response of CTC plus allogeneic peripheral blood adherent accessory cells (AC) to PHA or Con A as well as to MoAb OKT3 or PWM. This may be attributable to the substantially greater class II HLA antigen expression by CTC than by fresh lymphocytes. Pretreatment of either CTC or AC with anti-class II HLA MoAb inhibited OKT3-induced proliferation. In contrast, pretreatment of CTC, but not AC, with anti-class I HLA MoAb inhibited the proliferative response of CTC to OKT3. Pretreatment of CTC with anti-class I HLA MoAb inhibited PHA-, Con A and PWM-induced proliferation, to a greater degree than the anti-class II HLA MoAb. It appears as if lymphocyte activation by different mitogens exhibits variable requirements for the presence of cells expressing major histocompatibility determinants. Binding of Ab to membrane markers may interfere with lymphocyte-AC cooperation, perhaps by inhibiting binding of mitogens to their receptors or by interfering with lymphocyte and AC function. We also have examined the role of class II HLA antigens on CTC by depleting class II HLA-positive cells. As expected, elimination of class II HLA-positive AC with anti-class II HLA MoAb plus complement caused a decrease in proliferation of CTC in response to all the mitogens tested. In contrast, elimination of class II HLA-positive CTC was shown to clearly increase proliferation of CTC, perhaps because this may deplete class II HLA-positive suppressor cells.

Antibodies, Monoclonal↗
PubMed1992

The efficiency of promoter clearance distinguishes T7 class II and class III promoters.

Promoter strength has been defined as the relative production of transcripts from a promoter. For T7 transcription it has frequently been observed that T7 class III promoters are qualitatively stronger than T7 class II promoters. In previous work it was observed that the maximum rates of initiation of three class III and three class II promoters show no class distinctions (Ikeda, R. A., Lin, A. C., and Clarke, J. (1992) J. Biol. Chem. 267, 2640-2649). This suggests that the efficiency of the conversion of the polymerase initiation complex to a stable transcription complex contributes to the overall strength of T7 promoters. The class differences in the strengths of T7 class II and class III promoters are confirmed by measuring the relative synthesis of run-off transcripts. These results show that the relative strengths of the class III promoters, phi 6.5, phi 10, and phi 13, are all comparable ranging from 0.61 for phi 6.5 to 1.00 for phi 10, while the relative strengths of the T7 class II promoters, phi 1.1B, phi 1.3, and phi 3.8, vary widely. One T7 class II promoter, phi 1.1B (relative strength = 0.34), approaches the strength of the class III promoters, while the other T7 class II promoters, phi 1.3 (relative strength = 0.045) and phi 3.8 (relative strength = 0.070) are nearly inactive. The efficiency of promoter clearance is then determined by measuring the relative production of small transcription products in comparison with the production of run-off transcripts. These measurements clearly distinguish the T7 class III promoters from the T7 class II promoters. It is found that 68-75% of all initiations at the T7 class III promoters phi 6.5, phi 10, and phi 13 produce a run-off transcript, while only 16-36% of the initiations at the T7 class II promoters phi 1.1B, phi 1.3, and phi 3.8 produce a run-off transcript. Clearly, promoter clearance contributes to the difference in promoter strengths of the T7 class II and III promoters.

Base Sequence↗
PubMed1991

Analysis of T cells and major histocompatibility complex class I and class II mRNA and protein content and distribution in antiglomerular basement membrane disease in the rabbit.

The major interacting components of the immune system, major histocompatibility complex (MHC) class I and class II proteins and T cells were analyzed in a model of anti-GBM (glomerular basement membrane) disease in the rabbit that progresses to develop cellular crescents and glomerular and interstitial fibrosis. Class I and II mRNA and protein were measured in isolated glomeruli and whole renal cortex using cDNA probes and monoclonal antibodies. The distribution of T cells and class I and II proteins was assessed by immunofluorescence. Normal glomeruli contained no T cells and were class II negative. By day 4, glomeruli contained MHC class I and II mRNA and protein and class II positive T cells. Although some animals had T cells in the periglomerular area, these cells were class II negative. By day 7 periglomerular T cells were largely class II positive (activated) and there was increased MHC class I and II mRNA and protein in whole renal cortex. Later T cells accumulated in the tubulo-interstitial compartment, which became diffusely positive for MHC classes I and II, but to a variable extent in different animals. Those with high class II mRNA expression also had detectable T cell antigen receptor mRNA by Northern analysis. The authors conclude 1) in this model there was a close association between mRNA abundance and protein expression for both MHC classes I and II in glomeruli and renal cortex as a whole; 2) in this model of glomerular injury there are three phases of activation. The first phase takes place in the glomerulus and is associated with accumulation of activated T cells and MHC class I and II protein in the glomerulus. Phase 2 is associated with the accumulation of periglomerular T cells and their becoming class II positive. There is subsequent dissemination (phase 3) of activated T cells and accumulation of class I and II mRNA and protein throughout the interstitial compartment. This spacial progression of glomerulocentric inflammation is likely associated with degree of injury and permanent loss of renal function.

Animals↗
PubMed1990

[Morphological study of open bite. Skeletal Class I and Class II open bite].

The purpose of this study was to quantify the morphological features of class I and II openbite. The subjects were 151 female patients, over 7 years old, and as a control group, 180 female cases of normal overbite. The subjects were classified into 6 subgroups by ANB angles and ages as follows: 1. Class I A group (7 y less than or equal to age les than 10 y): openbite (30 cases), control (34 cases) 2. Class I B group (10 y less than or equal to age less than 15 y): openbite (23 cases), control (31 cases) 3. Class I C group (15 y less than or equal to age): openbite (20 cases), control (23 cases) 4. Class II A group (7 y less than or equal to age less than 10 y): openbite (38 cases), control (45 cases) 5. Class II B group (10 y less than or equal to age less than 15 y): openbite (20 cases), control (26 cases) 6. Class II C group (15 y less than or equal to age): openbite (20 cases), control (21 cases) The following results were obtained: 1. The combined features of class I and II openbite groups in all the 6 groups were an especially large anterior facial height and remarkable downward of lower occl. pl. angle. Mand. pl. angle was large, and the lower part of the face was tapered. 2. The primary factors of openbite were not only over-eruption of the upper molars but also vertical excess of the mandible with a large alveolar bone. 3. The clearest differences between classes I and II openbite were the mand. pl. and lower occl. pl. angles. The class I openbite groups had a large gonial angle, depending on the subgroup. On the other hand, the class II openbite groups exhibited backward and downward shifting of the mandible depending on the subgroup. 4. In the lower age groups (7 y less than or equal to age less than 10 y) both class I and class II openbite already had denture and alveolar factors, as well as skeletal problems. In the class II openbite, especially in adult cases there were unusual morphological problems both in antero-posterior and vertical relations. 5. Contrary to most reports, the nasal floor did not show an upward cant. In the adult class II openbite even a downward cant, resulting from the backward and downward shifting of the mandible was observed.

Adolescent↗
PubMed1991

HLA-class-I and -class-II expression on renal tumor xenografts and the relation to sensitivity for alpha-IFN, gamma-IFN and TNF.

In this study we evaluated the usefulness of the histocompatibility leucocyte antigen (HLA) class-I and class-II expression on renal-cell carcinoma (RCC) xenografts as predictive markers for response to cytokine therapy. Eight different RCC xenografts growing in BALBC nu/nu mice were treated with 0.5 or 5.0 ng/g recombinant human alpha- or gamma-interferon (IFN), or 500 ng/g recombinant human tumor necrosis factor (TNF). Modulation of HLA class-I, -II expression was evaluated immunohistochemically using the monoclonal antibodies (MAbs) W6.32 and B8.11.2 and at the mRNA level using the plasmids pDP001 and DR alpha 120. HLA class-I expression in all lines was upregulated by alpha- and gamma-IFN and was highest in the high-IFN-dose-treated tumors. TNF also stimulated HLA-class-I expression and up-regulated class-I expression still further when combined with IFN. Highest up-regulation of HLA-class-I in all tumors was measured in the alpha-IFN-5.0/TNF-500-ng/g-treated mice, although this was not necessarily the treatment regimen resulting in the most pronounced effect on tumor growth. Hence, maximum upregulation of class-I antigens at a given regimen was not always indicative for the highest achievable anti-tumor effect. HLA-class-II expression which was present on only 3 of the untreated tumors was up-regulated by both alpha and gamma-IFN. TNF itself did not up-regulate class-II expression but enhanced the class-II expression on the alpha-IFN-treated tumors but not on the gamma-IFN-treated tumors. Irrespective of the basic expression level, inducibility of both HLA-class-I and -class-II antigens appear to be correlated to the direct effects on growth of renal-tumor xenografts towards alpha-IFN, gamma-IFN and TNF. Modulation of HLA antigens was studied in the nude mouse, hence T-cell-mediated effector mechanisms cannot explain the good correlation between inducibility and response. Nonetheless, our studies indicate that the extent of modulation of HLA-class-I and -II can serve as predictive marker for response to cytokine therapy, which may serve as a valuable criterion for inclusion of patients in cytokine treatment regimens.

Animals↗