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Role of class-II major histocompatibility complex (MHC)-antigen-positive donor leukocytes in transfusion-induced alloimmunization to donor class-I MHC antigens.

It has been shown that peripheral-blood mononuclear leukocytes (MNL) are responsible for transfusion-induced alloimmunization to donor major histocompatability complex (MHC) antigens. However, it is not known which subset of MNL is responsible for this immune response. Because elimination of class-II MHC antigen-positive passenger leukocytes effectively prolongs the survival of allografts, it has been hypothesized that class-II positive MNL are responsible for immunizing transfusion recipients to donor MHC antigens. To test this hypothesis, two different approaches were used. First, we compared the alloantigenicity of BALB/c mice (H-2(d)) peripheral blood MNL before and after depletion of class-II positive cells. CBA mice (H-2(k)) were used as transfusion recipients. Antibody development to donor class-I H-2 antigens was determined by flow cytometry and enzyme-linked immunoassay. After four weekly transfusions of MNL depleted for class-II positive cells, only 25% of recipient mice developed antibodies to donor H-2(d) antigens. In contrast, all mice transfused with control MNL became immunized. Second, we studied the alloantigenicity of peripheral MNL from C57BL/6 mice (H-2(b)) with homozygous deficiency of class-II MHC molecules in H-2 disparate recipient mice. After transfusions with class-II MHC molecule-deficient MNL, 0% of BALB/c, 40% of C57BR, and 25% of CBA-recipient mice developed antibodies to donor H-2(b) antigen. All control recipient mice were immunized. The antibody activities of the controls were also higher than those in the treatment group who became immunized. Thus, our study shows that class-II MHC antigen-positive MNL play a significant role in transfusion-induced alloimmunization to donor class-I MHC antigens. The results also support the hypothesis that direct antigen presentation by donor class-II positive MNL to the immune system of transfusion recipients is critical for the initiation of humoral immune response to donor MHC antigens.

Animals↗

Contrast between class I and class II MHC-mediated differentiation of a CD4+CD8+ T cell line: implications for lineage commitment.

Experiments in transgenic mice have demonstrated that thymocyte differentiation into the mature CD4+ helper or CD8+ cytotoxic T cell lineage is ultimately dependent upon the specificity of the TCR for class II or class I MHC molecules respectively. However, the initial mechanistic events involved in this process remain unclear. To address this issue, we have expressed a TCR specific for an ovalbumin peptide and the Kb class I MHC molecule in the DPK CD4+CD8+ precursor T cell line. This cell line originally expressed a TCR specific for a pigeon cytochrome c peptide and class II MHC molecules and has been shown previously to differentiate into CD4+CD8- cells upon recognition of antigen in vitro or thymic epithelial cells in vivo. Surprisingly, we find that recognition of either class I or class II MHC by these cells initiates differentiation into the CD4+ lineage and induces down-regulation of recombination associated genes. Unlike recognition of class II MHC, however, recognition of class I MHC does not induce full maturation. These results support a model in which (i) commitment to the CD4 lineage occurs prior to positive selection and (ii) CD4 lineage commitment is associated with a requirement for activation by a class II MHC-specific TCR in order to complete differentiation.

Animals↗

Biochemical analysis of class I and class II MHC antigens in cynomolgus macaques by one-dimensional isoelectric focusing.

To obtain a better estimate of major histocompatibility complex (MHC) polymorphism in the Old World macaque, Macaca fascicularis, class I and class II MHC proteins from 42 animals were analyzed by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and one-dimensional isoelectric focusing (1D-IEF). The panel represented both related and unrelated animals with a total of at least 30 serologically distinct haplotypes. Cells were sequentially immunoprecipitated with monoclonal antibody (mAb) W6/32 for class I and with mAb L243 for class II molecules, followed by neuraminidase treatment. Both sets of immunoprecipitates yielded 5-7 major bands on IEF. All bands present in offspring were present in at least 1 parent. Siblings which were serologically identical for class I and which were non-stimulatory in mixed lymphocyte culture (MLC) yielded identical IEF patterns for both class I and class II; in other sibling pairs which were serologically identical for class I antigens (Ag), IEF produced convincing evidence that the siblings were indeed nonidentical, or helped to verify that recombination had occurred within the MHC. Specific bands were found which correlated with class I specificities A8, A24, and B25 previously defined by serology. Comparison of serological and biochemical data will broaden our understanding of the MHC in Macaca fascicularis and will increase the potential use of this species in transplantation research, as a model of disease, and for comparative studies.

Alleles↗

The susceptibility to natural killer cell-mediated lysis of HLA class I-positive melanomas reflects the expression of insufficient amounts of different HLA class I alleles.

NK cells selectively lyse tumor cells which do not express one or more MHC class I alleles. The ability to discriminate between self normal or tumor cells is due to the expression of MHC class I-specific killer inhibitory receptors (KIR). In the present study we analyzed melanoma cell lines which were highly susceptible to NK cell-mediated lysis in spite of the expression of a complete set of HLA class I alleles. Quantitative analysis of the HLA class I expression using allele-specific monoclonal antibodies (mAb) revealed a down-regulation of all HLA class I molecules. Treatment of melanoma cells with IFN-gamma resulted in up-regulation of all HLA class I alleles that was paralleled by the acquisition of resistance to lysis. That resistance to lysis reflected the up-regulation of HLA class I molecules was revealed by the finding that mAb-mediated masking of either KIR or their HLA class I ligands completely restored the melanoma cell lysis. These results were obtained by the use of selected NK cell clones derived either from allogeneic or autologous donors. In addition, similar results were obtained using in vitro expanded autologous NK cell populations. Our data indicate that NK cells can lyse not only melanoma cells which have lost the expression of one or more HLA class I alleles but also cells expressing a decreased amount of class I molecules.

Alleles↗

Failure of MHC class II expression in neonatal alveolar macrophages: potential role of class II transactivator.

Neonatal peritoneal and blood macrophages are known to be ineffective in antigen-presentation functions, and this manifests as inefficient MHC class II expression in response to IFN-gamma. The underlying mechanisms responsible for this maturational deficiency have not been elucidated. We show here that MHC class II expression in alveolar macrophages (AM) from neonates is also refractory to IFN-gamma stimulation. Furthermore, by examining the intracellular pathway leading to MHC class II expression, we demonstrate that the site of the impairment is at the level of transcription. Thus, expression of mRNA encoding the class II transactivator (CIITA), MHC class II (RT1.B) and invariant chain (Ii) was low or undetectable in neonatal AM stimulated with concentrations of IFN-gamma that induced adult AM to up-regulate MHC class II expression. The failure of AM from young animals to express MHC class II was not due simply to deficient IFN-gamma receptor function since IFN-gamma-responsive genes such as IRF-1, IRF-2 and IP-10 were up-regulated in a dose-dependent manner from animals of all ages investigated. Importantly, the responsiveness of neonatal AM to IFN-gamma, as determined by MHC class II expression, could be modulated to adult levels when pre-cultured in vitro. This suggests that microenvironmental factors operative in vivo may play a role in suppressing the expression of MHC class II in AM from young animals. We have investigated the role of type I interferons but did not find them to be responsible for the inability of AM from young animals to induce MHC class II in response to IFN-gamma.

Aging↗

Regulation of MHC class II expression in glioma cells by class II transactivator (CIITA).

We first classified 12 malignant glioma cell lines into three different groups (types 1-3) with respect to major histocompatibility complex (MHC) class II expression and analyzed each group based on the different expression status of the class II transactivator (CIITA) gene. Glioma type 1 (2 of 12) showed constitutive expression of all class II molecules that might be mediated by activation of B cell-specific CIITA promoter III. Glioma type 2 represented the major phenotype (66.7 %) of malignant glioma cell lines, and MHC class II expression was induced by interferon-gamma (IFN-gamma) in this phenotype. Analysis of glioma tissue samples revealed that CIITA promoter IV was detected in 9 of 11 patients (81.8%); however, promoter III was only in two (18.2%). Moreover, cultured glioma cells obtained from a fresh tumor sample upregulated expression of CIITA and class II molecules in the presence of IFN-gamma, strongly suggesting that glioma type 2 might be predominant in glioma tissues. Glioma type 3 (2 of 12) showed CIITA transcripts but loss of MHC class II expression even in the presence of IFN-gamma. In addition, we determined that the constitutive MHC class II expression in the glioma cell lines (type 1) was the result of transcriptional activation of the CIITA gene. This phenomenon was mediated by global histone acetylation over 6 kb upstream from the transcriptional start site of CIITA promoter III. Moreover, stable transfection of CIITA promoter IV as well as promoter III into MHC class II inducible cell lines restored the constitutive expression of all class II molecules. These studies lay the foundation to understand the molecular basis for the expression of class II molecules in gliomas.

Adult↗

A novel type of class I gene organization in vertebrates: a large family of non-MHC-linked class I genes is expressed at the RNA level in the amphibian Xenopus.

A Xenopus class I cDNA clone, isolated from a cDNA expression library using antisera, is a member of a large family of non-classical class I genes (class Ib) composed of at least nine subfamilies, all of which are expressed at the RNA level. The subfamilies are well conserved in their immunoglobulin-like alpha 3 domains, but their peptide-binding regions (PBRs) and cytoplasmic domains are very divergent. In contrast to the great allelic diversity found in the PBR of classical class I genes, the alleles of one of the Xenopus non-classical subfamilies are extremely well conserved in all regions. Several of the invariant amino acids essential for the anchoring of peptides in the classical class I groove are not conserved in some subfamilies, but the class Ib genes are nevertheless more closely related in the PBR to classical and non-classical genes linked to the MHC in mammals and birds than to any other described class I genes like CD1 and the neonatal rat intestinal Fc receptor. Comparison with the Xenopus MHC-linked class Ia protein indicate that amino acids presumed to interact with beta 2-microglobulin are identical or conservatively changed in the two major class I families. Genomic analyses of Xenopus species suggest that the classical and non-classical families diverged from a common ancestor before the emergence of the genus Xenopus over 100 million years ago; all of the non-classical genes appear to be linked on a chromosome distinct from the one harboring the MHC. We hypothesize that this class Ib gene family is under very different selection pressures from the classical MHC genes, and that each subfamily may have evolved for a particular function.

Alleles↗

No recognition of MHC class II+ cells infected with a vaccinia virus encoding influenza type A nucleoprotein by class II-restricted T cells.

MHC class II is mostly charged by antigens derived from the outside of the antigen-presenting cell (APC), while class I presents endogenous antigens transported as peptides to the endoplasmic reticulum (ER) by specific transporters. Nevertheless, many antigens, especially glycoproteins, can be presented in vitro by class II even if endogenous. In order to investigate the class-II-restricted T-cell response to endogenously synthesized influenza nucleoprotein (NP) synthesized in infected cells as a model of non-glycosylated nuclear protein, class-II-restricted cytolytic T-cell (CTL) clones were established from BALB/c (H-2d) mice immunized with either influenza A/PR/8/34 (PR8) strain or with a vaccinia virus encoding the NP protein. Two of the clones were characterized in detail and turned out to be cytolytic, I-Ad-restricted and NP peptide 218-229 specific. Even though an in vivo class-II-restricted T-cell response was elicited in BALB/c mice immunized with a vaccinia virus encoding nucleoprotein (Vacc-NP), class II+ mouse lymphoma cells were not lysed by the class-II-restricted clones in vitro when they were infected with the same virus or with a vaccinia virus encoding a truncated form of NP with no karyophilic sequence, showing that the de novo synthesized protein targeted to the nucleus or remaining in the cytoplasm cannot charge class II through the same pathway as class I in murine APC. These results extend previous observations made on transfected cells to cells that express an antigen during viral infection.

Animals↗

Too much like school: social class, age, marital status and attendance/non-attendance at antenatal classes.

OBJECTIVE: To investigate patterns of attendance and non-attendance at National Health Service antenatal classes of first-time mothers in the indigenous white population of a large northern city of the UK. DESIGN: Survey using questionnaires, and selected participants were then given an in-depth interview. SETTING: Five maternity wards in two large northern hospitals in the UK. In-depth interviews took place in the respondents' homes. PARTICIPANTS: Fifty newly delivered women were surveyed of whom 18 took part in the follow-up interviews. FINDINGS: There was a clear hierarchy in attendance and non-attendance based on social class, with middle class women being the most regular attenders, closely followed by older, married, working class women. However, overall social class differences were found to be accounted for by the overwhelming non attendance of young, unmarried, working class women. Older, married, working class women were found to have attendance patterns which were close to their middle class counterparts, and what differences there were seemed to be based on material factors. KEY CONCLUSIONS: The majority of women felt that antenatal classes were too technical and did not address emotional and psychological issues. However, young, single unmarried women perceived the classes most negatively. If midwives are to attract such young women, their fears and their need for peer support will have to be recognised.

Adult↗

Characterization of HLA DR2 and DQ8 transgenic mouse with a new engineered mouse class II deletion, which lacks all endogenous class II genes.

Human autoimmune diseases are a class of complex immune system disorders characterized by loss of tolerance to self-antigens. HLA class II molecules play a central role in the initiation, propagation and prolongation of the disease process. HLA class II transgenic mice with mouse endogenous class II gene Ab knockout were used successfully in several mouse models for human autoimmune diseases, such as IDDM, SLE and EAE in our Lab. However, these mice carry the functional mouse Eb gene from the Abeta(0/0) construct and could express Ebeta/DRalpha(Ealpha) molecules and shape the T cell repertoire in these mice. Recently, we have obtained the new MHCII(Delta/Delta) mice that are devoid of all endogenous conventional mouse MHC class II genes. When these mice are mated with our HLA class II transgenic mice, only human class II genes are expressed. The DR and DQ molecules expressed in these mice shape the T cell repertoire and regulate the immune response. Therefore, this new class of HLA transgenic mice is the first to be completely "humanized" in their MHC class II genes and will be an invaluable mouse model for human MHC class II associated autoimmune diseases.

Animals↗

Recognition of pre-processed endogenous antigen by class I but not class II MHC-restricted T cells.

Class I and class II MHC-restricted T lymphocytes recognize non-native forms of antigen. The presentation of antigen to these two classes of T lymphocytes can occur through distinct pathways. Several mechanisms, including differences in antigen processing in different intracellular compartments, have been proposed to account for these pathway differences. Here we describe a T-cell epitope located on the influenza virus haemaglutinin, which is recognized by both class I and class II MHC-restricted cytolytic T lymphocytes (CTL). When expressed de novo in target cells, from a synthetic minigene encoding only the epitope, this pre-processed antigenic site is recognized by class I but not class II MHC-restricted T lymphocytes, even though target cells treated with the exogenously introduced peptide can be recognized by both classes of T cells. Because endogenous expression of the pre-processed antigenic fragment results in differential presentation to class I and class II MHC-restricted CTL, differences between the two different pathways of presentation could lie not at the level of processing but at the level of targeting and/or interaction of processed antigen with MHC.

Amino Acid Sequence↗

Dental and alveolar arch widths in normal occlusion, class II division 1 and class II division 2.

The aim of this study was to compare the transverse dimensions of the dental arches and alveolar arches in the canine, premolar, and molar regions of Class II division 1 and Class II division 2 malocclusion groups with normal occlusion subjects. This study was performed using measurements on dental casts of 150 normal occlusion (mean age: 21.6 +/- 2.6 years), 106 Class II division 1 (mean age: 17.2 +/- 2.4 years), and 108 Class II division 2 (mean age: 18.5 +/- 2.9 years) malocclusion subjects. Independent-samples t-test was applied for comparisons of the groups. These findings indicate that the maxillary interpremolar width, maxillary canine, premolar and molar alveolar widths, and mandibular premolar and molar alveolar widths were significantly narrower in subjects with Class II division 1 malocclusion than in the normal occlusion sample. The maxillary interpremolar width, canine and premolar alveolar widths, and all mandibular alveolar widths were significantly narrower in the Class II division 2 group than in the normal occlusion sample. The mandibular intercanine and interpremolar widths were narrower and the maxillary intermolar width measurement was larger in the Class II division 2 subjects when compared with the Class II division 1 subjects. Maxillary molar teeth in subjects with Class II division 1 malocclusions tend to incline to the buccal to compensate the insufficient alveolar base. For that reason, rapid maxillary expansion rather than slow expansion may be considered before or during the treatment of Class II division 1 patients.

Adolescent↗

Direct interaction of major histocompatibility complex class II-derived peptides with class Ia phosphoinositide 3-kinase results in dose-dependent stimulatory effects.

Peptides corresponding to residues 65-79 of human lymphocyte antigen class II sequence (DQA*03011) are cell-permeable and at high concentrations block activation of protein kinase B/Akt and p70-S6 kinase in T-cells, effects attributed to inhibition of phosphoinositide (PI) 3-kinase activity. To understand the molecular basis of this, we analyzed the effect this peptide had on activity of class I PI 3-kinases. Although there was no effect on the activity of class Ib PI 3-kinase or on the protein kinase activity of class I PI 3-kinases, there was a biphasic effect on lipid kinase activity of the class Ia enzymes. There was an inhibition of activity at higher peptide concentrations because of a formation of insoluble complexes between peptide and enzyme. Conversely, at lower peptide concentrations there was a profound activation of PI 3-kinase activity of class Ia PI 3-kinases. Studies of peptide variants revealed that all active peptides conform to heptad repeat motifs characteristic of coiled-coil helices. Surface plasmon resonance studies confirmed direct sequence-specific binding of active peptide to the p85alpha adapter subunit of class Ia PI 3-kinase. Active peptides also activated protein kinase B and extracellular signal-regulated kinase (ERK) in vivo in a wortmannin-sensitive manner while reducing recoverable cellular p85 levels. These results indicate that the human lymphocyte antigen class II-derived peptides regulate PI 3-kinase by direct interaction, probably via the coiled-coil domain. These peptides define a novel mechanism of regulating PI 3-kinase and will provide a useful tool for specifically dissecting the function of class Ia PI 3-kinase in cells and for probing structure-function relationships in the class Ia PI 3-kinase heterodimers.

Amino Acid Sequence↗

Evidence for involvement of dual-function T cells in rejection of MHC class I disparate skin grafts. Assessment of MHC class I alloantigens as in vivo helper determinants.

The present study further characterizes the cellular mechanisms involved in the in vivo rejection of MHC class I-disparate skin allografts. Previously, we demonstrated that class I-specific rejection responses could result from collaborations between distinct populations of lymphokine-secreting T helper (Th) and lymphokine-responsive T effector (Teff) cells. In the present study, we have assessed the possibility that class I-specific rejection responses could also result from a second cellular mechanism involving a single population of dual-function Th/Teff cells that would not have any further requirement for cell-cell collaboration. Our experimental strategy was to determine the ability of MHC class I-allospecific T cells, in response to class I allodeterminants expressed on skin grafts, to provide help in vivo for activation of helper-dependent Teff cells. We found that class I anti-Kbm1-allospecific T cells would reject bm1 skin allografts, but would not generate help for the activation of helper-dependent effector cells that were specific for third-party skin allografts (e.g., grafts expressing Kbm6, Qa1a, or H-Y allodeterminants). This failure of anti-Kbm1 T cells to provide help in response to bm1 skin allografts was not due to an inability of lymphokine-secreting anti-Kbm1 Th cells to recognize and respond in vivo to Kbm1 allodeterminants expressed on skin, since lymphokine-secreting anti-Kbm1 Th cells were specifically primed in animals engrafted with bm1 skin allografts. Nor was any evidence found that this failure was due to active suppression of anti-Kbm1 helper activity. Rather, we found that anti-Kbm1 T cells consumed nearly all of the helper factors they secreted. Taken together, these results are most consistent with the in vivo activity of dual-function Th/Teff cells that consume the lymphokines they secrete. Thus, this study demonstrates that MHC class I-disparate skin allografts can be rejected by two mechanisms, depending on the ability of the allospecific Teff cell to secrete helper lymphokines. MHC class I-disparate grafts can be rejected by (a) class I-allospecific Teff cells that are unable to produce lymphokine but are responsive to exogenous T cell help; and (b) class I-allospecific dual-function Th/Teff cells that are able to both produce and consume soluble lymphokine.

Animals↗

Molecular characterization of major histocompatibility complex class II gene expression and demonstration of antigen-specific T cell response indicate a new phenotype in class II-deficient patients.

Major histocompatibility complex (MHC) class II deficiency is an inherited autosomal recessive combined immunodeficiency. The disease is known as bare lymphocyte syndrome (BLS). BLS is characterized by a lack of constitutive MHC class II expression on macrophages and B cells as well as a lack of induced MHC class II expression on cells other than professional antigen-presenting cells (APCs) due to the absence of mRNA and protein of the human leukocyte antigen (HLA) class II molecules, designated HLA-DR, -DQ, and -DP. The defect in gene expression is located at the transcriptional level and affects all class II genes simultaneously. Here we have analyzed transcription and protein expression of class II antigens in Epstein-Barr virus (EBV)-transformed B lymphoblastoid cell lines and mononuclear cells (MNCs) of twin brothers. Whereas flow cytometric analysis failed to detect class II antigens on the cell surface of the patients' EBV-B cells and MNCs, examination of the genes coding for HLA-DR, -DQ, -DP, and the invariant chain (Ii) by reverse transcriptase-polymerase chain reaction amplification resulted in an unusual mRNA pattern in the B cell lines of the patients (HLA-DR alpha +, -DR beta, -DQ alpha +, -DQ beta -, -DP alpha -; -DP beta +, Ii+). In accordance with these findings no HLA-DR beta-specific protein was detected by immunoblotting, whereas low levels of HLA-DR alpha and normal levels of Ii were present. In contrast to EBV-B cells, the MNCs of both patients displayed a residual HLA-DR beta, -DQ beta, and -DP alpha mRNA signal. Furthermore, HLA-DR beta-specific protein was found in addition to HLA-DR alpha by immunoblotting of cell lysates, even though it was clearly decreased as compared with controls. Our results indicate that the defect in class II antigen expression is not necessarily present to the same extent in B cells and cells of other lineages. mRNA levels of HLA-DR beta were found to be enriched in adherent cells within the MNC fraction. Further investigations indicated that the MHC class II expressed is functional in antigen presentation, as the two boys' CD4+ T cells became activated and expressed interleukin-2R after stimulation of peripheral blood mononuclear cell cultures with recall antigen (tetanus toxoid). Furthermore, T cells tested in one of the two patients responded to both MHC class I and II allostimulation, and this response was inhibited by monoclonal antibodies of the respective specificity.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

Prognostic significance of HLA class I expression in osteosarcoma defined by anti-pan HLA class I monoclonal antibody, EMR8-5.

With the goal of establishing efficacious peptide-based immunotherapy for patients with bone and soft tissue sarcomas, we previously identified the cytotoxic T lymphocyte-defined osteosarcoma antigenic gene Papillomavirus binding factor. The present study was designed to determine the status of HLA class I expression in osteosarcoma and other bone and soft tissue sarcomas. Seventy-four formalin-fixed paraffin-embedded specimens of various bone and soft tissue sarcomas, including 33 osteosarcomas, were stained with the anti-HLA class I monoclonal antibody EMR8-5, which we recently generated. The expression of HLA class I was lost or downregulated in 46 of these specimens (62%). With respect to osteosarcoma, loss or downregulation of HLA class I expression was seen in 13 (52%) of 25 primary tumors and seven (88%) of eight metastatic tumors. In six of 11 HLA class I-negative osteosarcoma specimens, the expression of beta-2 microglobulin was also lost. Subsequently the prognostic significance of HLA class I expression was analyzed in 21 patients with osteosarcoma who had completed multidrug neoadjuvant chemotherapy and undergone adequate surgery. Patients with osteosarcoma highly expressing HLA class I showed significantly better overall and event-free survival than those with HLA class I-negative osteosarcoma. In contrast, such prognostic significance of HLA class I expression was not found in 15 patients with malignant fibrous histiocytoma of soft tissue. These findings suggest that the class I-restricted cytotoxic T lymphocyte pathway plays a major role in immune surveillance of patients with osteosarcoma.

Adolescent↗

Human leukocyte antigens (HLA) class I and class II on sperm cells studied at the serological, cellular, and genomic levels.

The expression of human leukocyte antigens (HLA) on highly purified human ejaculated sperm cells was studied using the sensitive enzyme-linked immunosorbent assay (ELISA) technique and a wide panel of monoclonal antibodies to class I and class II HLA. In addition, the stimulatory capacity of these cells was tested in mixed cultures of lymphocytes and spermatozoa, and the levels of RNA homologous to the HLA class I and class II genes were determined. The results obtained using the ELISA indicate that the class I and class II HLA serologically defined antigens are weakly expressed on the cell surface of the mature spermatozoa. Highly purified sperm cells consistently stimulated heterologous lymphocytes but not when HLA-DR compatibility was observed between stimulator and responder. The proliferative response of lymphocytes induced by sperm cells was lower than the response obtained in a lymphocyte-lymphocyte combination, though the kinetics of the response were similar in both cases. In addition, it was found that spermatozoa contained RNA species homologous to HLA class II DR beta and DQ beta genes sequences but not to HLA class I sequences. The levels of these RNA species were significantly reduced after interferon stimulation. Lymphocytes that served as positive control were found to contain RNA complementary to both HLA class I and class II genes.

Antibodies, Monoclonal↗

Social class and psychiatric diagnosis: differential findings in a lower-class sample.

Social class and the American Psychiatric Association Diagnostic and Statistical Manual II Diagnosis were examined for all patients contracting the Department of Psychiatry over a year at a large county hospital. This sample was primarily lower class -50 per cent Class V and 33 per cent in Class IV. All diagnoses showed average class between IV and V. Organic brain syndrome, both psychiatric and non-psychotic, and mental retardation had lower average social class than other diagnoses. A small sample of the diagnosis behaviour disorder of childhood and adolescence was also lower than other diagnoses. Class V patients with mental malfunction may present differently than patients from other social classes. The absence of differences on neurosis and functional psychosis may have been due to the predominance of lower class patients, diagnosticians more familiar with lower class patients, or the allowable choice of diagnoses.

Adolescent↗