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Biomedical subjects

B Heyman

Publications and source records attributed to B Heyman.

At least 55 records · Page 3Linked to original sources
PubMed1992

Dental needs of the elderly in residential care in Newcastle-upon-Tyne and the role of formal carers.

Interviews were carried out on 61 formal carers from 41 residential homes and 379 elderly residents from 35 homes. Formal carers were questioned about their own dental health and arrangements made to maintain the dental health of the residents. Only 46% of carers attended a dentist regularly although the majority knew that teeth and dentures should be examined regularly. Carers arranged most of the dental treatment received by residents. The percentage of residents from each home receiving treatment ranged from 0% to 52%. Residents judged by formal carers to be capable of participation were interviewed and a 40% stratified random sub-sample was examined. 96% of residents stated that they would only attend a dentist if they were experiencing problems. However, among residents reporting problems (25% of the sample), only a third wished to see a dentist. This proportion rose to half when treatment was offered. The reported barriers to seeking dental treatment included the resident's belief that he or she was coping satisfactorily, transport difficulties and ill health. Denture and oral hygiene were poor and dentures cleaned by staff were no cleaner than those cleaned by residents. A random sample of residents judged by formal carers to be confused were also examined. The condition of their teeth and dentures was similar to that of non-confused residents.

Adult↗
PubMed1991

Inhibition of immunological memory and T-independent humoral responses by monoclonal antibodies specific for murine complement receptors.

The importance of the complement system for mounting an antibody response in vivo was investigated by down-regulating and blocking the complement receptors (CR) in mice with three different monoclonal rat antibodies (mAb): mAb 8C12 recognized the C3b-binding site of CR1, mAb 7G6 recognized another site of CR1 and the C3d-binding site of CR2 and mAb 7E9 again recognized other epitopes on CR1 and CR2. We have earlier shown that 7G6, is the only mAb that completely suppresses the primary antibody response to horse erythrocytes. This antibody was also shown to suppress induction of immunological memory and a secondary antibody response. In contrast to what seems to be the case for thymus-dependent antibody responses, all three mAb could inhibit the antibody response to a thymus-independent antigen, dextran B 1355S.

Animals↗
PubMed1990

In vivo inhibition of the antibody response by a complement receptor-specific monoclonal antibody.

BALB/c mice were injected intravenously with three different monoclonal antibodies (mAbs) specific for complement receptor 1 (CR1). Two of the mAbs crossreacted with CR2. 24 h later, the mice were immunized with horse erythrocytes or keyhole limpet hemocyanin (KLH), and the primary antibody response was measured. One of the anti-CR antibodies, 7G6, suppressed greater than 99% of the direct plaque-forming cell response against horse red blood cells (HRBC). The same antibody markedly suppressed the serum antibody responses to both HRBC and KLH. To be optimally suppressive, the mAb had to be injected before suboptimal concentrations of antigen. The other two complement receptor-specific antibodies had very moderate, if any, effects on the antibody response. 7G6 was able to downregulate CR1 and CR2 on the surface of B cells and, in addition, to inhibit rosette formation with C3d-coated sheep erythrocytes (EC3d). One of the antibodies with a weak effect downregulated only CR1. The other downregulated both CR1 and CR2, although not as efficiently as 7G6, and was unable to inhibit EC3d rosette formation. We conclude that the reason 7G6 is outstanding in its suppressive capacity is that it is the only mAb tested that functionally blocks CR2. The data suggest that CR2 is of crucial importance in the initiation of a normal antibody response to physiological concentrations of antigen.

Animals↗
PubMed1990

Inhibition of processing of asparagine-linked carbohydrate chains on IgG2a by using swainsonine has no influence upon antibody effector functions in vitro.

Removal of asparagine (Asn)-linked carbohydrate chains from IgG antibody molecules reduces their antibody effector functions such as C activation and FcR binding. We have prepared IgG2a mAb with modified structure of carbohydrate chains by treating the hybridoma cells with swainsonine, which inhibits the processing of Asn-linked carbohydrate chains at the site of action of mannosidase II. These antibodies have obtained the capacity to bind lentil lectin and have become sensitive to endoglycosidase H digestion, indicating the structural changes of oligosaccharides from complex type to hybrid type. They behaved in an identical manner to the normal IgG2a antibodies with regards to extracellular secretion, Ag-binding capacity, C-mediated hemolysis and FcR-mediated functions. Critical moieties of Asn-linked carbohydrate chains on IgG molecules to retain their antibody effector functions were discussed.

Acetylglucosaminidase↗
PubMed1990

Evidence of IgG-mediated enhancement of the antibody response in vivo without complement activation via the classical pathway.

The complement (C) dependency of IgG-mediated enhancement of the antibody response was investigated by immunizing mice with trinitrophenyl-coupled keyhole limpet hemocyanin (TNP-KLH) and either a C-activating TNP-specific monoclonal IgG2a antibody (Hy-1.2) or a mutant, non-C-activating variant of Hy-1.2 (M12). Hy-1.2 as well as M12 efficiently enhanced the anti-KLH response, although Hy-1.2 was more active. In addition, also a naturally non-C-activating TNP-specific IgG1 antibody enhanced the response to TNP-coupled bovine serum albumin. Moreover, C-activating IgG could enhance the antibody response in mice depleted of C3 by treatment with cobra venom factor. These findings suggest that the classical pathway of C activation is not required for IgG-mediated enhancement.

Animals↗
PubMed1990

The immune complex: possible ways of regulating the antibody response.

B cells express antigen, Fc and complement receptors on their surfaces and can thus bind all three components of an immune complex. In addition to the direct effects that they exert on cells, immune complexes may affect localization, presentation and digestion of antigen. In this article, Birgitta Heyman discusses recent developments in antibody-mediated regulation of the humoral immune response, with emphasis on in vivo systems where antigens are injected together with highly purified IgM or IgG antibodies in the absence of adjuvants.

Animals↗
PubMed1990

Fc-dependent IgG-mediated suppression of the antibody response: fact or artefact?

IgG antibodies have been shown to suppress the antibody response to all epitopes of their specific antigen as well as those the IgG do not bind to, so-called 'non-epitope-specific suppression'. The present study was undertaken to clarify whether there is a true IgG-mediated Fc-dependent suppression of the antibody response. This question is of fundamental importance to the understanding of the mechanism behind this phenomenon. It is demonstrated that F(ab')2 fragments of a monoclonal TNP (trinitrophenyl)-specific IgG2a antibody are unable to suppress the murine in vitro non-epitope-specific plaque-forming cell response against SRBC (sheep erythrocytes) when SRBC-TNP is used as antigen. The same monoclonal IgG antibody, when administered in intact form, is able to induce up to 98% suppression of the SRBC-specific antibody response. The lack of suppression is not due to mitogenic effects of pepsin in the F(ab')2 fractions or increased breakdown of F(ab')2 fragments, as compared with intact antibody, in the cultures. These data clearly demonstrate that there is indeed a highly efficient, Fc-dependent, non-epitope-specific suppressive mechanism mediated by IgG antibodies and support a hypothesis involving binding of the antigen-antibody complexes to Fc receptors as a step in the effector mechanism.

Animals↗
PubMed1990

Community mental health care: clients' perceptions of services and an evaluation of a voluntary agency support scheme.

A questionnaire assessment of mental health and of perceptions of formal care was conducted with a sample of clients before they received a voluntary agency mental health intervention in addition to normal community psychiatric and social services. The assessment was repeated three months later. A matched control group who received only the normal services were also assessed twice over a period of three months. Both groups improved significantly on the mental health measure over the three months and there was little difference between the treatment and control group. Clients in the voluntary agency group were less satisfied with community psychiatric services and may have chosen the voluntary agency as an alternative source of help. Women in both groups showed less improvement in measured mental health than men. Community Psychiatric Nurses (CPNs) were seen more frequently than social workers, psychologists and psychiatrists. Contacts with CPNs and social workers were rate most favourably.

Adult↗
PubMed1989

Changes in nurse education and the facilitation of nursing research: an exploratory study.

This study is concerned with exploring nurses' attitudes and knowledge of nursing research, together with their perception of research priorities. A sample was drawn from five nursing groups, these being Assistant Directors of Nursing Services (ADNS), Ward Sisters, Student Nurses undertaking a conventional educational programme, students undertaking the Diploma in Professional Studies in Nursing Course (DPSN) and student nurses undertaking an ENB pilot scheme in general nursing. Whilst the results suggest that all groups held favourable attitudes towards nursing research, significant differences emerged with respect to knowledge of such research and perception of research priorities. Of particular interest are the differences observed in comparing the nursing groups who have had experience of higher education with those who have not. The former generally had more positive attitudes, a better knowledge base and clearer priorities for nursing research. Given that many countries now provide nurse education in such centres and that nurse education in the United Kingdom is steadily moving in this direction, the results are important in suggesting some of the benefits which can accrue from collaboration between schools of nursing and centres of higher education.

Attitude of Health Personnel↗
PubMed1989

Inhibition of IgG-mediated immunosuppression by a monoclonal anti-Fc receptor antibody.

IgG-antibodies can efficiently suppress the antibody response against their specific antigen. The suppressive capacity is dependent on intact Fc regions. However, it is not clear which of the Fc-mediated effector functions are necessary for the induction of immunosuppression. The monoclonal antibody 24G2, which binds to murine Fc receptors on macrophages and B cells, was used in the present study to address the question of whether IgG-mediated suppression is in fact dependent on the binding of IgG antibodies to Fc receptors on splenocytes. In a murine in vitro immunization system, 24G2 is shown to reverse efficiently the suppression of the sheep erythrocyte-specific antibody response. The role of B cells or macrophages as effector cells is discussed.

Animals↗
PubMed1989

Dual immunoregulatory effects of monoclonal IgG-antibodies: suppression and enhancement of the antibody response.

Nine monoclonal IgG-anti-TNP antibodies were investigated for their ability to modulate anticarrier responses in mice immunized with sheep red blood cells-2,4,6-trinitrophenyl (SRBC-TNP) or keyhole limpet haemocyanin-TNP (KLH-TNP). The antibodies enhanced the anticarrier response when KLH-TNP was used as antigen but suppressed it when SRBC-TNP was used. The enhancing and suppressive effects were not exerted by entirely the same sets of antibodies. The suppression was correlated to efficient antigen binding, but not complement activation, haemagglutination, or isotype of the monoclonal antibodies. In contrast, enhancement was correlated to isotype and complement activation but not to antigen binding capacity. Both the enhancing and the suppressive effects seem to require Fc-mediated functions of the IgG molecules since they modulate the anti-carrier response although they recognize hapten determinants. Thus, one and the same monoclonal hapten-specific IgG-antibody can enhance the anti-KLH response up to 38-fold whereas it suppresses the anti-SRBC response by more that 10-fold.

Adjuvants, Immunologic↗
PubMed1988

Mutant monoclonal antibodies with select alteration in complement activation ability. Impact on immune complex functions in vivo.

Mutagenesis of mAb is a useful means for studying the biologic and pathologic functions of immune complexes. Treatment of the Hy-1.2 hybridoma-producing IgG2a-anti-TNP antibodies with ethylmethanesulfonate provided us with a mutant clone, producing antibodies with reduced capacity for C activation. The antibodies retained normal Ag-binding capacity, staphylococcal protein A reactivity, and association to FcR for IgG on murine macrophages. No significant polypeptide deletion or class-switch was observed, but a significant change in clonotype was revealed by IEF. Intravenous injection of the mutant antibodies in immune complex form induced different tissue distributions of Ag in mice; i.e., more in kidneys and less in spleen, and developed more mesangial deposits in renal glomeruli compared with those of the wild type. Moreover, the production of granulomatous lesions in vivo caused by immune complexes of TNP-Sepharose was augmented by using mutant antibodies. These lesions demonstrated an enhanced accumulation of macrophages with multinucleated giant cells. Availability of this kind of mutant mAb is thus helpful in the elucidation of the biologic functions and consequences of immune complexes.

Animals↗
PubMed1988

Complement activation is required for IgM-mediated enhancement of the antibody response.

The ability of IgM antibodies to specifically enhance the thymus-dependent humoral immune response to particulate antigens is well documented. We have used two approaches to test whether complement factors play a role in this process. First, mice were depleted of C3 by treatment with cobra venom factor (CVF) and then immunized with SRBC with or without IgM-anti-SRBC. CVF treatment severely impaired the capacity of IgM to induce an enhanced anti-SRBC response. Moreover, it was shown that IgM can potentiate the response in C5-deficient AKR mice, thus demonstrating that the complement factors acting before C5 are the crucial ones. A second test compared the enhancing properties of two monoclonal IgM-anti-TNP antibodies where, because of a point mutation in the mu chain constant region, one of the antibodies is impaired in its capacity to activate complement. We show that the mutant antibody lacks the enhancing properties of the wild-type IgM. Activation of C3 by IgM antibodies as well as localization of antigen in the spleen seem to be necessary steps in the IgM-mediated enhancement of antibody responses. Our data offer an explanation to the immunosuppression described in CVF-treated animals as well as the low humoral immune responses in certain hereditary complement deficiencies. It is suggested that IgM indeed has an important physiological function in enhancing antibody responses to foreign substances.

Animals↗
PubMed1988

Complement activation is not required for IgG-mediated suppression of the antibody response.

Feedback suppression of the antibody response by IgG is known to be dependent on intact Fc regions. However, it is not clear which of the Fc-mediated effector functions is required. In the present report we have studied whether ability or inability of the IgG antibodies to activate the complement system was of consequence for their immunosuppressive effect. First, a monoclonal IgG1-anti-2,4,6-trinitrophenyl (TNP) antibody, unable to activate complement via the classical or alternate pathway, was shown to be able to inhibit more than 90% of the in vivo sheep erythrocyte-specific antibody response in mice when TNP coupled to sheep erythrocytes was used as antigen. Second, we investigated the immunosuppressive ability of a non-complement-activating mutant IgG2a-anti-TNP monoclonal antibody. The mutant differs from the wild type by a single amino acid substitution in the CH2 domain leading to inability to fix complement factor C1q. However, the mutant has the same affinity for antigen and the same Fc receptor-binding capacity as the wild type antibody. It is demonstrated that the mutant was as efficient as the wild type antibody in inhibiting an in vitro antibody response to TNP-coupled sheep erythrocytes. These findings confirm the non-determinant specificity and Fc dependence of IgG-mediated suppression, and show that the Fc-mediated effector mechanism is independent of complement activation. The results instead suggest binding to Fc receptors as a necessary step in feedback immunosuppression and favor inactivation of B cells by cross-linking of Fc and antigen receptors on their surface rather than elimination of antigen by complement-dependent phagocytosis as the effector mechanism.

Animals↗
PubMed1988

Primary and secondary IgG are equally efficient immunosuppressors in relation to antigen binding capacity.

Secondary, hyperimmune IgG antibodies can suppress the humoral immune response against the relevant antigen. Whether IgG antibodies derived from a primary antigen response also have this capacity is not clear, although the role of primary IgG is of great interest in a physiological situation. In this study we compared the in vivo immunosuppressive potential of primary and secondary IgG anti-SRBC (sheep erythrocytes) on the primary anti-SRBC PFC response in CBA/Ca mice. Both primary and secondary IgG antibodies are potent immunosuppressors causing more than 99% specific suppression. Preparations of primary and secondary IgG antibodies which, measured by an ELISA method, were shown to bind to SRBC to the same extent, also had very similar immunosuppressive potency. This emphasizes the strong correlation between the antigen binding and the immunosuppressive capacities of IgG antibodies.

Animals↗
PubMed1988

Non-determinant specificity of feedback immunosuppression by IgG antibodies injected after the antigen.

The determinant specificity of the IgG-mediated suppression of the humoral immune response in mice was studied. One hour before or 2.5, 6, 12, or 24 h after the injection of sheep erythrocytes (SRBC) or SRBC-TNP, CBA/Ca mice received SRBC-specific monoclonal IgG antibodies. The antibodies did not cross-react with TNP or goat erythrocytes, the latter an antigen which shows 30% cross-reactivity with SRBC. Five days later the determinant-specific plaque-forming cell response against SRBC and the non-determinant-specific response against goat erythrocytes and TNP were determined. Regardless of whether the antibodies were injected before or after the antigen, they suppressed not only the response to the antigenic determinant they bound to, but also the response to other epitopes on the same antigen. This shows that Fc parts of the IgG molecules play a crucial part in suppression of the in vivo antibody response even when, as in a natural situation, the antigen is presented to the immune system before the antibody.

Animals↗