Allergie und Immunologie最新文献

Studies were undertaken to evaluate the effect of hepatitis B virus (HBV) immune complexes (HBV-IC) on IL-2 dependent human lymphocyte proliferation. The following parameters were studied: 1) Effect of HBV-IC (HBsAg-IgG or HBeAg-IgG) on PHA-mediated lymphocyte proliferation; 2) Influence of HBV-IC on the ability of PHA-stimulated peripheral blood lymphocytes (PBL) for IL-2 production and IL-2 receptor expression. HBV-IC induced a dose dependent and antigenic dependent suppression of PHA stimulated lymphocytes. The suppressor effect exerted by HBsAg-IgG was irreversible. In contrast, the suppression mediated by HBeAg-IgG was reversible: lymphocytes preincubated with this preparation washed and activated with PHA responded well to mitogen. The presence of HBV-IC in the cultures of PHA-activated PBL decreased their ability to produce IL-2: HBeAg-IgG exerted a stronger suppressor effect. This effect was partially reversible: removal of HBV-IC from the culture by washing and subsequent stimulation of PBL with PHA increased the capacity of lymphocytes to produce IL-2. This was particularly evident with HBeAg-IgG. Decreased activity of IL-2 observed in the cultures, was also partially dependent on the ability of HBV-IC to bind IL-2 present in the culture medium. Experiments performed using ultracentrifugation indicated that HBV-IC, especially HBsAg-IgG, may bind to IL-2 and inactivate it. HBV-IC had also an effect on IL-2 receptor expression: 1) their presence in the cultures of PHA-stimulated PBL decreased the number of Tac positive cells; 2) the response of HTCL to exogenous IL-2 was decreased by HBV-IC present in the culture medium. This was especially observed in the case of HBsAg-IgG. We suggest that the observed inhibition of PHA-induced lymphocyte proliferation exerted by immune complexes containing HBsAg-IgG or HBeAg-IgG may be caused mainly by their influence on IL-2 dependent mechanism of lymphoproliferation.

The combination of Epstein-Barr-Virus (EBV)-permitted immortalization and somatic hybridization (fusion with a myeloma partner) may be the method of choice to produce human monoclonal antibodies. We show here that the fusion of EBV-infected human B-lymphocytes to the HAT-sensitive, ouabain-resistent heteromyeloma (human x mouse) fusion line CB-F7, resulted in stable growing hybridomas producing much more immunoglobulin than the parental lymphoblastoid lines. A more efficient clonability was shown for hybridoma cultures too. The loss of B cell markers (HLA-class II antigen, CD-22, CD-37) was detected. Limiting dilution experiments showed a better fusionability of IgM-producing EBV-transformed B cells in comparison to IgG-secreting counterparts.

Peripheral blood mononuclear cells were cultured for 72 hours in presence of phytohaemagglutinin (PHA), phytohaemagglutinin/phorbolmyristate acetate (PHA/PMA), pokeweed mitogen (PWM) and in absence of these stimulators. The IL-2 concentrations of cultural supernatants were determined by an IL-2 dependent cell line. There was no IL-2 determined in absence of any mitogenic stimulators. Induction of IL-2 by PWM does not require the presence of PMA in contrast to stimulation by PHA/PMA, where PMA was found to be necessary for stimulation of production of IL-2. PHA/PMA induced IL-2 release shows only a weak maximum at 24 hours, whereas PWM induced IL-2 release was found to have a clear maximum at 48 hours. Stimulation by PWM enables comparative examination of DNA synthesis (lymphocyte transformation test) and IL-2 production in the same cell system using only one mitogen.

Immune thrombocytopenia remains a diagnosis per exclusionem. There are no specific clinical symptoms or laboratory parameters to ensure diagnosis. In otherwise caused thrombocytopenias many authors found increased platelet-associated immunoglobin (PaIg) and platelet-binding serum immunoglobulin (PbSIg). Methods to determine PaIg and PbSIg are described and their clinical relevance is discussed. Determinations of PaIg and PbSIg with Ig-L-chain-specific ELISA are recommended. They improve diagnostic possibilities to distinguish ITP from nonimmune thrombocytopenias.

The hyposensitization in IgE-mediated insect venom reactions is presently the sole causal method of treatment. In more than 90% it is possible to prevent life-threatening anaphylactic reactions after insect stings. Essential, hitherto unresolved or only partly resolved questions include, for instance, objective parameters of success and, in this connection, the necessary duration of therapy. The determination and assessment of the course of specific IgE- and IgG-antibodies with the venom skin titration yield, for the single case, no absolutely safe information regarding the therapeutic effect. An alternative is the provocative sting under clinical conditions, the limitation chiefly results from personal and temporal restrictions.

10 patients have been treated by subcutaneous injections of placebo three times weekly for 4 weeks within a phase-I trial of BCH-069. Immunological, hematological and biochemical parameters were observed at different times: preseasonal, seasonal and postseasonal. --Some new observations are reported, which are induced by the seasonal inflammation. For example there was a strong increase of C-reactive protein and also an increase in the triglyceride level. --The parameters could be useful for trials of new antiallergic drugs in hay fever in the future.

A monoclonal antibody with a high affinity for digoxin (KA = 5.5 x 10(10) M-1) and digitoxin KA = 5.0 x 10(10) M-1) was produced by somatic cell fusion. This antibody, designated 2A3, displayed little cross reactivity with other glucosides and no cross reactivity with endogenous steroids. It was shown that 2A3 is a suitable tool in an enzyme immunoassay for digoxin and digitoxin.

In the sera of 58 bronchial cancer patients with different TNM progression stage the relative 125I-C1q binding activities (BA) were determined before, after an induction of polychemotherapy and after a simultaneous polychemo- plus X-rays therapy. Only a statistically non-significant decrease of the 125I-C1q-BA was measured in the sera of patient groups with a stronger metastatic spread in the regional lymph nodes or distant metastasis. The tumor therapy cycles changed the serum 125I-C1q-BA differently and non significantly. The determination of serum 125I-C1q-BA of bronchial cancer patients is not relevant clinically.

Interleukins are well defined biologically active factors serving the intercellular communication. Here is given a review on the interleukins 1-8.

An enzyme-linked immunosorbent assay (ELISA) has been developed to detect antibodies against surface components of rat islet and spleen lymphocytes. Live islet tumor RIN5 AH cells expressing characteristic ganglioside target antigens or rat spleen cells were immobilized onto wells of microtiter polystyrene plates precoated with poly-l-lysine and then incubated with test or normal rat sera. Cell surface-bound antibodies were quantitated after reaction with horseradish peroxidase-conjugated rabbit anti-rat Ig. With this assay, 46% (6/13) of sera from diabetes-prone BB rats and 100% (8/8) of sera from rats treated with complete Freund's adjuvant/streptozotocin (CFA/STZ) prior to immunization with RIN cells had islet cell surface antibodies: 54% (7/13) and 75% (6/8), respectively, were positive for lymphocyte antibodies (defined as the HRP anti-rat Ig binding exceeding the mean + 2SD of control group values). SDS polyacrylamide gel electrophoresis followed by immunoblotting analysis suggested that the islet cell antibodies in sera from the BB and CFA/STZ rats recognized RIN-cell components that were different in their molecular weights. These antigens were not detectable on spleen cells indicating that the ELISA described can be used to quantitate levels of islet cell specific antibodies which possibly reflect beta cell damage with progression to islet degeneration in the rat.