摘要:

SummaryImmunological mechanisms are demonstrably of central importance in preventing the development of certain virus‐associated cancers in animals and man; however, they do not appear to fulfil this role in the majority of ‘spontaneous’ tumours. This does not, however, necessarily indicate that spontaneous tumours lack potential target antigens for immunologically mediated destruction. Work in the field of transplantation immunology has clearly shown that certain cell types fail to elicit rejection reactions despite their possession of alloantigens. Similarly, some tumour cell types are poorly immunogenic to the point that they can grow in and kill animals despite a major histocompatability barrier. These tumours are, however, susceptible to destructionin vivoin appropriately allo‐sensitized animals. Thus, some tumours may be able to grow in autologous or syngeneic hosts because of their poor immunogenicity, despite the fact that they express potential (tumour‐associated) rejection antigens. It may be possible to manipulate this situation for therapeutic purposes.

ISSN:0004-945X    

DOI:10.1038/icb.1987.31

出版商:Nature Publishing Group    

年代:1987

数据来源: WILEY

ISSN:0004-945X    

DOI:10.1038/icb.1987.32

出版商:Nature Publishing Group    

年代:1987

数据来源: WILEY

ISSN:0004-945X    

DOI:10.1038/icb.1987.33

出版商:Nature Publishing Group    

年代:1987

数据来源: WILEY

摘要:

SummaryExpression of the hapten fucosyl‐N‐acetyllactosamine was correlated with ultrastructural development in human granulocyie precursors using the monoclonal antibody FMC 10 with immunogold techniques. The antigen was detectable from the myeloblast/early neutrophilic promyelocyte stage onwards and was associated with striking development of the rough endoplasmic reticular system. In addition, low levels of labelling were seen on monocytes, eosinophils and some basophil precursors. Contraction and alignment of the cisternae of the rough endoplasmic reticulum during the promyelocyte stage of neutrophilic differentiation gave the appearance of a plasma cell. However, on closer examination it was apparent that true plasma cells did not react with this antibody.

ISSN:0004-945X    

DOI:10.1038/icb.1987.34

出版商:Nature Publishing Group    

年代:1987

数据来源: WILEY

摘要:

SummaryTo investigate the mode of entry and action of the alkylating agent chlorambucil (CBL), conjugated to monoclonal antibodies (MoAbs), CBL was coupled with three different MoAbs — to the transferrin receptor, to L3T4 and to Ly‐2 molecules — and the activity of these conjugates was compared with free CBL. It was clear that CBL and CBL‐MoAb conjugates enter cells and are transported differently within the cell prior to their cytotoxic action. Evidence favouring a separate entry point of CBL and CBL‐MoAb conjugates is the differential effect of temperature and metabolic inhibitors (2‐deoxyglucose and sodium azide) on the processing of both moieties. In addition, the likely sites of cleavage of CBL‐MoAb complexes, the lysosomes, were effected by NH4Cl and chloroquine, which inhibited the activity of CBL‐MoAb but not free CBL. Thus, it is likely that CBL‐MoAb conjugates enter via the antibody binding sites and the CBL is internalised and transported as a passenger.

ISSN:0004-945X    

DOI:10.1038/icb.1987.35

出版商:Nature Publishing Group    

年代:1987

数据来源: WILEY

摘要:

SummaryThe B16 melanoma of C57BL/6 mice immunizes very poorly, even against its own major histocompatibility complex (MHC) antigens. B16 cells expressed both H‐2K and H‐2D antigensin vitroas judged by binding of monoclonal antibodies to these antigens in indirect immunofluorescence staining. Thein vivoMHC antigen expression of B16 was examined and compared with that of a second C57BL/6 tumour, the Lewis lung carcinoma (3LL). whose defective immunogenicity has been attributed to a selective deficiency‐ in H‐2K antigen expression. We found that125I‐labeiled cells of both tumours expressed sufficient allo‐antigenin vivoto be lysed in BALB/c mice which had been pre‐immunized with C57BL/6 lymphoid cells.125I‐B16 cells were also lysed in MHC‐recombinant mice which had been immunized against either H‐2Kbor H‐2Db, indicating that B16 cells express both of these MHC antigensin vivo. This contrasted with our findings with125I‐3LL cells which were destroyed in mice immunized against H‐2Dbbut not in those immunized against H‐2Kb. Thus, B16 illustrates a different deficiency in tumour cell immunogenicity which appears not to be attributable to an absence of either of the class 1 MHC antigens.

ISSN:0004-945X    

DOI:10.1038/icb.1987.36

出版商:Nature Publishing Group    

年代:1987

数据来源: WILEY

摘要:

SummaryA mathematical model is presented which may be applied to describe and analyse data from microscopic phagocytosis assays. The method has been used to investigate the phagocytosis of opsonized yeast by peripheral blood neutrophils treated with purified recombinant human granulocyte‐macrophage colony‐stimulating factor (rH GM‐CSF)in vitro. Under limiting conditions of serum opsonization, rH GM‐CSF decreased the proportion of non‐phagocytic cells and increased the mean number of ingested yeast per cell. Stimulation of phagocytosis was dose‐dependent and occurred with concentrations of rH GM‐CSF in the range 10–320 units/ml. The effect was dependent on a heat‐labile component in serum and was not attributable to endotoxin contamination of the preparation.

ISSN:0004-945X    

DOI:10.1038/icb.1987.37

出版商:Nature Publishing Group    

年代:1987

数据来源: WILEY

摘要:

SummarySince Langerhans cells (LC) are normally the only cells within the epidermis to express the class II major histocompatibility complex (MHC) transplantation antigens, depletion of LC could be expected to prolong skin allograft survival by reducing the antigenic disparity between host and recipient. To assess this hypothesis, donor C57BL mouse shaved dorsal trunk or tail skin was exposed to high (200 mJ/cm2) or low (40 mJ/cm2) doses of short wavelength ultraviolet light (UVB) before grafting on to the thorax of BALB/c mouse recipients of the same sex. These strains have different major and minor transplantation antigens. The effects of UVB treatments on LC were determined by electronmicroscopy. Skin grafted 1–14 days following a single high dose of UVB irradiation was ultrastructurally depleted of LC and survived significantly longer than unirradiated skin before being rejected. After a 21‐day interval between exposure and grafting when LC were again present in the epidermis there was no significant difference between treated and control graft survival. Exposure to low dose UVB irradiation only significantly increased graft survival for skin transplanted 1–3 days after irradiation; skin grafted 4 days following irradiation survived for a similar period to unirradiated control skin grafts. Electronmicroscopy showed that the low UVB dose did not deplete LC from the epidermis. We conclude that after low dose UVB treatment the class II MHC antigens on the LC plasma membrane were lost temporarily, thus prolonging graft survival, but when the plasma membrane antigens were re‐expressed graft survival returned to normal. In contrast, high‐dose UVB irradiation prolonged graft survival by depleting LC from the epidermis, with graft survival only returning to control values as LC repopulated the epidermis.

ISSN:0004-945X    

DOI:10.1038/icb.1987.38

出版商:Nature Publishing Group    

年代:1987

数据来源: WILEY

摘要:

SummaryWe have previously identified the major antigen of elastin‐associated microfibrils as a 31kD glycoprotein which we named microfibril‐associated glycoprotein or MAGP. Affinity‐purified antibodies to MAGP were shown to localise specifically to elastin‐associated microfibrils in sections of bovine foetal nuchat ligament (20). In the present paper we compare the localisation of anti‐MAGP antibodies and anti‐tropoelaslin antibodies in a range of bovine elastic and non‐elastic tissues. The results show that anti‐MAGP antibodies invariably localised to immuno‐reactive elastic fibres, wherever they occurred. Extensive additional localisation was observed in a number of tissues. This extra distribution of anti‐MAGP antibodies was found to correspond to those structures exhibiting the oxytalan histochemical staining reaction in tissues such as skin, periodontal ligament and ocular zorule. Since these oxytalan fibres have been shown to consist of 12 nm microfibrils which are morphologically similar to those of elastic fibres (and unpublished data from this laboratory confirm this conclusion), the results suggest that MAGP is a component of 12 nm microfibrils in both elastic and non‐elastic tissues. Anti‐tropoelastin antibodies did not localise to these oxytalan fibres, suggesting that tropoetastin is not a component of 12 nm microfibrils. MAGP was also detected in extracellular matrix regions of tissues such as skeletal muscle. Achilles tendon and spleen, suggesting that 12 nm microfibrils, containing one or more macromolecular constituents in common, make up an important structural system within the extracellular matrix in a wide range of elastic and non‐elastic tissues.

ISSN:0004-945X    

DOI:10.1038/icb.1987.39

出版商:Nature Publishing Group    

年代:1987

数据来源: WILEY

摘要:

SummarySerum rat mucosal mast cell protease II (RMCPII) was measured in protein‐deficient rats to assess mucosal mast cell (MMC) activation during primary infection with the nematode,Nippostrongylus brasiliensis, and during systemic anaphylaxis produced byNippostrongylusantigen in immune animals. In the first study, serum RMCPII increased 4‐fold by day 15 after infection. By day 20, serum RMCPII continued to rise in protein‐deficient animals, but decreased in nutritionally normal animals. This was associated with impaired worm rejection in protein‐deficient rats. During systemic anaphylaxis, serum RMCPII was elevated in three groups of protein‐deficient rats on 6%, 8% and 10% low protein diets and in nutritionally normal rats. All protein‐deficient rats exhibited 3 to 7‐fold less mucosal permeability of the small intestine to Evan's blue dye injected intravenously compared to nutritionally normal animals following anaphylactic stimulation. These results demonstrated that MMC are activated during infection in protein deficiency, and suggest that reduced MMC function does not explain delay in worm expulsion. Impaired mucosal anaphylaxis in protein deficiency could not be attributed to a failure of MMC response.

ISSN:0004-945X    

DOI:10.1038/icb.1987.40

出版商:Nature Publishing Group    

年代:1987

数据来源: WILEY