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PubMed1979

Induction of virus specific and H-2 restricted cytotoxic T cells by UV inactivated murine cytomegalovirus.

Infection of C3H mice with live or UV-inactivated murine cytomegalovirus (MCMV) was able to generate population(s) of lymphocytes in the spleen (CTL) which could exert a lytic effect against L cells infected with MCMV but not against uninfected or those infected with HSV-1. The effector cells proved to be theta-bearing T cells and the lysis of target cells was H-2 restricted. Data presented show that early viral protein synthesis but not viral DNA synthesis was necessary for the appearance of relevant antigenic determinant(s) on target cells. The results of co-capping experiments suggest that H-2 molecules may have close association with MCMV induced product(s) as also with murine leukemia virus glycoprotein (gp70) which is carried by normal L cells. Despite this observation, anti-H-2 serum effectively blocked the cytolysis whereas anti-gp70 and anti-MCMV sera failed. Anti-MCMV serum was effective in blocking cytolysis, only if the L cells were infected for 24 hours and then used as targets. MCMV infected L cells which were coated externally with inactivated Sendai virus could be effectively recognised by MCMV as also by sendai specific CTL. That the cytotoxicity exerted on such targets was of specific nature was revealed by the results of competitive blocking experiments with unlabelled targets.

Animals↗
PubMed2003

International guidelines for the treatment of community-acquired pneumonia in adults: the role of macrolides.

The significance of community-acquired pneumonia (CAP) has led to the publication of guidelines from numerous international organisations. Because the macrolide class of antimicrobials is active against most of the key pathogens associated with CAP, agents from this class are commonly included in recommendations from these guidelines. However, there are differences among the various guidelines concerning the positioning of the macrolides for empirical therapy. An important factor concerning the use of macrolides for CAP is the emergence of resistance of Streptococcus pneumoniae over the past decade. The rate of S. pneumoniae resistance to macrolides ranges from 4 to 70% of strains in worldwide surveillance studies. The most common mechanisms of resistance include methylation of a ribosomal target encoded by the erm gene and efflux of the macrolides by a cell membrane protein transporter, encoded by the mef gene. S. pneumoniae strains with the mef gene are resistant at a lower level (with minimum inhibitory concentration [MIC] values generally 1-16 microg/ml) than erm resistant strains; and it is possible that such strains may be inhibited if sufficiently high levels of macrolide can be obtained at the infected site. Currently mef-associated resistance predominates in North America, whereas erm predominates in Europe. Until recently, reports of failure of treatment of CAP with macrolides has been rare, particularly for patients with low-risk for drug-resistant strains. However, since 2000, several patients treated with an oral macrolide who have subsequently required admission to the hospital for macrolide-resistant S. pneumoniae (MRSP) bacteraemia have been reported in the literature. Major issues, which are fundamental to the use of the macrolides as recommended in the various guidelines, include the importance of providing therapy for 'atypical' pathogens and the clinical significance of MRSP. Presently, the macrolides are more prominently recommended in the North American guidelines than in other parts of the world. The difference in the emphasis placed on the importance of the atypical pathogens as well as the expression of MRSP in North America compared with Europe partly explains this variance.

Adjuvants, Immunologic↗
PubMed1984

A novel antigenic cell surface protein associated with T200 is involved in the post-activation stage of human NK cell-mediated lysis.

A monoclonal antibody, 9.1C3, was used to investigate the mechanism of natural killer (NK) cell-mediated lysis. In addition to blocking NK cell function, the antibody blocked antibody-dependent cellular cytotoxicity against the K562 target cell at the effector cell level. The stage at which 9.1C3 antibody inhibited cytolysis was established with a Ca++ pulse technique, whereby it was shown that the antibody inhibited killing at a discrete step after the Ca++-dependent programming for lysis. The 9.1C3 antigen appeared to be associated with the T200 glycoprotein complex. Thus the 66 and 77 Kd proteins detected by 9.1C3 were also precipitated with a monoclonal antibody to T200, and in sequential immunoprecipitations, 9.1C3 antibody removed these bands from immunoprecipitates with antibody to T200. Also, in co-modulation studies, it was found that antibody to T200 co-capped the 9.1C3 antigen but that capping with 9.1C3 antibody did not induce co-modulation of the T200 antigen. Expression of the 9.1C3 and T200 antigens on different cell types, however, was not identical, and the 9.1C3 antibody did not immunoprecipitate high m.w. proteins in the region of 200 Kd. Functionally, in NK cell killing studies, the antibody to T200 used alone did not block but was synergistic with the 9.1C3 antibody. The differential effect of the enzymes pronase and trypsin on the cell surface expression of the 9.1C3 and T200 antigens reflected the ability of these enzymes to inhibit NK cell killing. These data suggest that the 9.1C3 antigen participates in a late event in the cytolytic pathway.

Antibodies, Monoclonal↗
PubMed1982

Immunohistochemical localization of concanavalin A and wheat germ lectin receptors in the normal human spermatozoa.

A semiquantitative immunohistochemical technique for the detection of N-acetyl alpha-D-neuraminic acid, N-acetyl beta-D-glucosamine and its beta-(1 leads to 4)-linked internal chains, alpha-D-glucopyranosyl and alpha-D-mannopyranosyl and its alpha-(1 leads to 2)-linked internal chains and sterically related, nonreducing, end-chain residues of oligosaccharide chains of glycoproteins or glycolipids on the surface of membranes was developed using Con A and wheat germ lectins. When this method was applied to the localization of carbohydrate receptors on the membrane of the normal human spermatozoa, it was found that the Con A and wheat germ lectin receptors were mainly located in the equatorial and post nuclear cap with few receptors located in the acrosome and neck. None of them were found in the intermediate segment plus tail. Con A receptors were alpha-D-mannopyranosyl end-chain residues and wheat germ lectin receptors were N-acetyl beta-D-glucosamine (1 leads to 4)-linked internal chains. These groups occur together in the oligomannosidic type of N-glycosidic-linked oligosaccharide chains of glycoproteins and so the use of both lectins on desialycated membranes or on those which contain nonclustered N-acetyl neuraminic acid residues may be of help to localize this type of glycoprotein oligosaccharide chains. Con A receptors were not removed after proteases digestion, suggesting the possibility that they are part of intrinsic spermatozoal antigens.

Cell Membrane↗
PubMed1976

Properties of the Fc receptor on macrophages.

Macrophages and monocytes possess a surface receptor specific for the Fc region of certain subclasses of IgG. The binding site on IgG is localized within the Cgamma3 homology regions of the heavy chains. The intrinsic affinity of the receptor for IgG ranges from 10(6) to 10(8) M-1 depending on species and subclass of IgG. The most definitive studies on mouse macrophages indicate that IgG2a rapidly associates and dissociates from the receptor. The overall reaction is exothermic; increasing temperature lowers the intrinsic affinity. The Fc receptor, in common with many other membrane components, may be capped by polyvalent ligands under permissive conditions and capping is inhibited by azide. Data on the chemistry of the receptor is both sparse and conflicting. Sensitivity of the receptor of proteolytic enzymes has been clearly demonstrated for mouse macrophages although rabbit and guinea-pig cells appeared to carry resistant receptors. IgG-binding may be inhibited if cells are treated with phospholipases and certain group-specific reagents. Evidence is reviewed indicating that the Fc receptors found on various cell types are different. The macrophage Fc receptor appears to play a role in mediating phagocytosis and in non-immune cytotoxicity. Whether the receptor serves only to concentrates sensitized target cells at the cell surface or whether occupation of the receptors results in modulation of effector cell function remains to be determined.

Amino Acid Sequence↗
PubMed1995

Determinants of cord-blood IgE concentrations in 6401 German neonates.

For screening atopy risk in 6401 (84%) of all infants born during the year 1990 in six obstetric departments of five German cities, cord-blood IgE values were determined with CAP-RAST-FEIA. After cases with elevated IgA values had been excluded, 25% of the values were above the detection limit of 0.35 kU/l, and 8.5% were above 0.9 kU/l. Boys had significantly higher values than girls (P < 0.001). The distribution of values was significantly different for different nationalities of mothers (P < 0.001). The percentage of elevated values (> 0.9 kU/l) increased significantly with the number of close family members with atopic history (P < 0.001). Regarding the atopic history of the father, siblings, and mother separately, only the mother's history had a significant association with the cord-blood IgE class (P < 0.001). The IgE values of 81 twin pairs correlated significantly with a coefficient of r = 0.4909 (P < 0.001). The smoking history of the parents during pregnancy showed an association with cord-blood IgE values (P < 0.02). No significant association could be shown between cord-blood IgE distribution and other variables, i.e., gestational age, birth size, birth modus, Apgar score, cord-blood pH value, neonatal problems, parity, age of the mother, medication during pregnancy, educational level of mother or father, time of year, or obstetric department. It is hypothesized that, in addition to some postpartum contamination or placental transfer of maternal IgE, cord-blood IgE values are also determined by the fetal immunologic reaction to intrauterine exposure to allergens and trigger factors, and by genetic influences.

Adrenal Cortex Hormones↗
PubMed1981

Influence of IgG and IgM receptor triggering on human natural killer cell cytotoxicity measured on the level of the single effector cell.

By using an agarose single cell cytotoxicity assay, in combination with rosetting with IgG- or IgM-coated ox red blood cells for detection of Fc receptors for IgG (Fc gamma R) or IgM (Fc muR), it was found that 60% of natural killer (NK) cells are Fc gamma R+ and 17% FcmuR+. This system was further used to investigate the consequence of FcmuR and FC gamma R triggering on NK killing as measured on the single effector cell level. It was found that stimulation of the Fc gamma R, but not the FCmuR, resulted in substantial NK inhibition. In order for NK cells to be inhibited by IgG-coated ox red blood cells, they must first be exposed to the IgG-containing complex prior to conjugation with the target. While exposure of the Fc gamma R to immune complexes can block up to 57% of NK activity, the particulate immune complexes do not interfere with binding of effector cells to targets. Modulation of Fc gamma R by capping at 37 degrees C does not interfere with the NK inhibition for up to 3 h, though after 20 h, when Fc gamma R+ cells are almost completely modulated, NK activity has fully returned. Although to a lesser extent, the soluble immune complex human transferrin-anti-transferrin also reduces NK cell activity when activating effector cell FC gamma R prior to target cell binding. Also, pretreatment of target cells with high concentrations of specific antibody toward membrane antigens can block NK activity while not inhibiting target cell binding as evidenced by anti-IgM IgG binding to Daudi cells. The regulatory influence of the Fc gamma R on the NK system is discussed in terms of other functions associated with this receptor and in terms of its possible biological significance.

Animals↗
PubMed1999

Progression and regression of atherosclerosis in APOE3-Leiden transgenic mice: an immunohistochemical study.

Apolipoprotein E3-Leiden (APOE3-Leiden) transgenic mice develop hyperlipidemia and are highly susceptible to diet-induced atherosclerosis. We have studied the progression and regression of atherosclerosis using immunohistochemistry. Female transgenic mice were fed a moderate fat diet to study atherosclerosis over a longer time period. Fatty streaks arose in the intima and consisted of lipid filled macrophages which differed in origin. All macrophages expressed the macrophage scavenger receptor while two thirds expressed sialoadhesin and were positive for an antibody recognizing marginal zone macrophages (MOMA-1). All macrophages were negative for the scavenger receptor MARCO and 50% were positive for CD4. Small fatty streaks contained CD-3 positive T-lymphocytes which were for more than 70% CD4-positive. ICAM-1 was positive both in atherosclerotic and control mice. In early plaques, fibrosis was observed on the luminal and medial site of the foam cells while smooth muscle cells were only observed in the fibrous cap. To study regression, we used a high fat, high cholesterol diet to rapidly induce atherosclerosis (14 weeks). The animals were then fed normal chow. Subsequently, atherosclerosis was assayed over time (4, 8, 16 weeks). Cholesterol levels dropped in 4 weeks to control levels. The animals did not show a significantly decrease in plaque size over time. but the percentage macrophages was significantly smaller in the animals after 4 weeks. In conclusion, the APOE3-Leiden mouse is a useful model to study the progression and regression of atherosclerosis.

Animals↗
PubMed1994

Purification and properties of GTP:GTP guanylyltransferase from encysted embryos of the brine shrimp Artemia.

GTP:GTP guanylyltransferase has been purified from the yolk platelets of Artemia cysts. The 480-kDa enzyme catalyzes the reversible reaction 2GTP<==>Gp4G + PPi and contains immunologically related polypeptides of 142, 88, and 45 kDa and a distinct 80-kDa component. The 88 and 45 kDa species can be covalently labeled with [alpha-32P]GTP. Even in crude extracts, the enzyme appears to be partially proteolyzed, suggesting that it is a nonfunctional residue of the pre-encystment stages of development. A native alpha 2 beta 2 structure comprising 2 mol each of the 142- and 80-kDa polypeptides is proposed. The reaction follows ping-pong kinetics with a covalent enzyme-guanylate intermediate containing a phosphoramidate linkage, probably phospholysine. The enzyme has two GTP-binding sites: a "donor" site in which the enzyme-guanylate is formed and which is highly specific for guanine nucleotides (GTP, p4G, dGTP, and GppNHp) and an "acceptor" site which additionally binds XTP, ITP, GDP, and ADP. Thus, the enzyme will form the homodinucleotides Gp4G, Gp5G, Gp3G, dGp4dG, and GppNHppG and the heterodinucleotides Gp4X, Gp4I, and Gp3A, but not Xp4X, Ip4I, or Gp4A. The Km for GTP was 6.7 mM and kcat was 1.6 s-1. XTP was a fully uncompetitive inhibitor of Gp4G synthesis while ITP was a partially uncompetitive inhibitor. In the reverse reaction, certain pyrophosphate analogs could substitute for PPi. The structure and mechanism of this enzyme suggest an evolutionary relationship to mRNA capping enzymes.

Animals↗
PubMed2002

Temperature-responsive and degradable hyaluronic acid/Pluronic composite hydrogels for controlled release of human growth hormone.

Temperature-sensitive hyaluronic acid (HA) hydrogels were synthesized by photopolymerization of vinyl group modified HA in combination with acrylate group end-capped poly(ethylene glycol)-poly(propylene glycol)-poly(ethylene glycol) tri-block copolymer (Pluronic F127). The synthesized HA/Pluronic composite hydrogels gradually collapsed with increasing temperature over the range of 5-40 degrees C, suggesting that the Pluronic component formed self-associating micelles in the hydrogel structure. Upon prolonged incubation in a buffer medium, the micelles slowly degraded due to the hydrolytic scission of the ester linkage between the Pluronic and acrylate group. The mass erosion occurred much faster at 37 degrees C than at 13 degrees C, indicating that at the higher temperature, the ester linkage between the Pluronic and acrylate group might be more exposed to an aqueous environment and thus be more readily hydrolyzed due to Pluronic micellization. Incorporation of recombinant human growth hormone in the hydrogel resulted in a sustained release profile which followed a mass erosion pattern.

Adjuvants, Immunologic↗
PubMed1979

Surface phenotyping, histology and the nature of non-Hodgkin lymphoma in 157 patients.

In a study of 157 patients with lymphoid malignancy, the phenotype of the tumour cells was correlated with the histological classification of the tumour using the Rappaport and the Kiel classifications. The markers used included E, Fc gamma, Fc micron (IgM) and C3d rosetting, estimation of SIg and CyIg, and tests for the expression of HTLA, Ia and ALL. Repeat biopsy specimens were studied in 23 of these patients. The phenotypic features of lymphoblastic malignancy indicated B-cell, T-cell and ALL-positive null-cell tumours in this group. Immunoblastic lymphomas were predominantly of non-capping B-cell type, but T-cell immunoblastic lymphoma occurred in 2 patients. Immunoblastic lymphomas of receptor-silent cells occur, and are ALL- and HTLA-negative. In the category of diffuse, poorly differentiated lymphocytic lymphomas, most cases are of centroblastic and centrocytic tumour of diffuse type, but pure centrocytic tumours and centroblastic tumours occur. The dominant phenotype in this group is of B cells expressing C3d receptors. Nodular poorly differentiated lymphocytic lymphomas (Rappaport) are classified as centroblastic and centrocytic follicular (Kiel) and most express SIg+ C3d+ phenotype. The frequency of this phenotype appeared the same in both diffuse and nodular poorly differentiated lymphocytic neoplasms. The Rappaport group of diffuse well-differentiated lymphocytic lymphoma includes 2 Kiel categories, malignant lymphoma lymphocytic, and malignant lymphoma lymphoplasmacytoid. Cells of the former tumour were considered to be immature B cells resembling those seen in CLL, and characteristically expressing SIg weakly, with a high frequency of single kappa light chain. Cells of the latter tumour are by contrast mature, and are related to the centroblastic and centrocytic follicular tumour by their histogenesis and phenotypic features. Repeat biopsy examinations indicate that T-cell predominance occurs in the prodromal phase of B-cell-predominant tumours of SIg+ C3d+ phenotype. It is concluded that non-Hodgkin lymphoma can be divided into 2 categories: (1) tumours of immature immunologically incompetent cells of lymphoblastic histology and with phenotypic features akin to T, B and Null-cell ALL, and (2) tumours of differentiated lymphocytes expressing the phenotypic features of B lymphocytes, with maturation arrested at one of several stages of an antigen-dependent immune response.

Adult↗
PubMed1999

[Peanut anaphylaxis: the problem of hidden allergens].

HISTORY: Three patients developed recurrent anaphylactic reactions after ingestion of different kinds of food (Asian food, chocolate products, bakery products). INVESTIGATIONS: In all three patients a severe peanut allergy was confirmed either by skin prick testing or serologically (specific IgE for peanut of CAP class 3,4 and 6 respectively). Peanut allergy in all patients explained the anaphylactic reactions due to ingestion of hidden peanut in the food. TREATMENT: Patients were told to avoid the allergen. Because accidental ingestion is frequent in peanut allergy, they were equipped with a document stating the severity of the allergy and emergency medication (antihistamines, oral steroids, adrenaline injector). CONCLUSIONS: Peanuts can be concealed in different kinds of food because they are cheap, rich in protein and are often used to change the viscosity of other foods. Especially the American and Asian cuisines use peanuts in a wide variety of recipes. Furthermore accidental ingestion can occur due to false or lacking declaration of peanuts in processed food. Patients with peanut allergy should be informed about these possibilities.

Adrenergic Agonists↗
PubMed1998

Evaluation of IgG RAST FEIA for the assay of venom-specific IgG antibodies during venom immunotherapy.

BACKGROUND: Successful venom immunotherapy (VIT) in Hymenoptera allergy is usually associated with a strong increase in venom-specific serum IgG antibodies (sIgG). METHODS: We evaluated a new commercial test for the assay of sIgG (Pharmacia CAP Systemtrade mark IgG RAST(R) FEIA; FEIA), in comparison with a conventional ELISA technique. Sera from 40 bee- and 40 Vespula-allergic patients were analyzed by FEIA and ELISA before and 3 months after starting VIT. RESULTS: The correlation between sIgG obtained with the two methods was significant: r = 0.862, p<0.0001 for bee venom (BV), r = 0.861, p<0.0001 for Vespula venom (VV). The geometric mean values obtained with FEIA were higher for both venoms (BV p = 0.03; VV p<0. 01). A highly significant increase (p<0.0001) was observed during VIT with both methods. This increase was concordant in 93% of VV- and 90% of BV-treated patients. Intra- and interassay relative coefficients of variation were below 10% for FEIA. CONCLUSION: IgG RAST FEIA is a reproducible and sensitive method for the assay of venom-specific sIgG.

Allergens↗
PubMed1997

Phenotypic stability of a cytotoxic T-cell line directed against an immunodominant epitope of human carcinoembryonic antigen.

CTL lines have now been generated against defined peptides of a range of human tumor-associated antigens (TAAs). One of the potential uses of these epitope-specific CTLs is in adoptive transfer immunotherapy. This is a modality, however, that will require long-term in vitro culture of CTLs. To date, little has been reported concerning the phenotypic stability of human epitope-specific CTLs as a consequence of long-term in vitro propagation via peptide stimulation. We report here the serial phenotypic characterization of a CTL line directed against an immunodominant epitope (YLSGANLNL, designated CAP-1) of human carcinoembryonic antigen (CEA). This CTL line was derived from peripheral blood mononuclear cells of a patient with metastatic carcinoma who had been treated with a recombinant CEA-vaccinia vaccine in a Phase I trial; the CTLs were analyzed through 20 in vitro cycle passages of stimulation with CAP-1 peptide and interleukin 2 in the presence of autologous antigen-presenting cells. The CTL line was shown to be phenotypically stable in terms of high levels of cytokine (IFN-gamma, tumor necrosis factor, and granulocyte-macrophage colony-stimulating factor) production, expression of homing-adhesion molecules, ability to lyse peptide-pulsed targets, and ability to lyse human carcinoma cells endogenously expressing CEA in a MHC-restricted manner. Vbeta T-cell receptor gene usage was also analyzed. These studies thus present a rationale for the use of long-term cultured epitope-specific human CTLs, directed against a human TAA for potential adoptive transfer immunotherapy protocols.

Antigens, CD↗
PubMed1987

Gelsolin is expressed in early erythroid progenitor cells and negatively regulated during erythropoiesis.

We have identified an approximately 85-kD protein in chicken erythrocytes which is immunologically, structurally, and functionally related to the gelsolin found in many muscle and nonmuscle cell types. Cell fractionation reveals a Ca2+-dependent partitioning of gelsolin into the soluble cytoplasm and the membrane-associated cytoskeleton of differentiating or mature erythrocytes. Depending on either the presence of Ca2+ during cell lysis or on the preincubation of the intact cells with the Ca2+-ionophore A23187, up to 40% of the total cellular gelsolin is found associated with the membrane skeleton. Expression of gelsolin shows a strong negative regulation during erythroid differentiation. From quantitations of its steady-state molar ratio to actin, gelsolin is abundant in early progenitor cells as revealed from avian erythroblastosis virus- and S13 virus-transformed cells which are arrested at the colony forming unit erythroid (CFU-e) stage of erythroid development. In these cells, which have a rudimentary and unstable membrane skeleton, gelsolin remains quantitatively cytoplasmic, irrespective of the Ca2+ concentration. During chicken embryo development and maturation, the expression of gelsolin decreases by a factor of approximately 10(3) in erythroid cells. This down regulation is independent from that of actin, which is considerably less, and is observed also when S13-transformed erythroid progenitor cells are induced to differentiate under conditions where the actin content of these cells does not change. In mature erythrocytes of the adult the amount of gelsolin is low, and significantly less than required for potentially capping of all membrane-associated actin filaments. We suggest that the gelsolin in erythroid cells is involved in the assembly of the actin filaments present in the membrane skeleton, and that it may provide for a mechanism, by means of its severing action on actin filaments, to extend the meshwork of the spectrin-actin-based membrane skeleton in erythroid cells during erythropoiesis.

Actins↗
PubMed1993

Different mechanisms regulate the monoclonal antibody-induced modulation of CD2, CD3, and CD5 in human lymphocytes.

The CD2, CD3, and CD5 antigens are down-modulated from the cell surface of peripheral blood mononuclear cells after a 24-hr incubation with specific monoclonal antibodies (mAb). Here we show that active (phorbol myristate acetate, phorbol dibutyrate acetate, and mezerein) but not inactive (4 beta-phorbol) tumor-promoting agents inhibit the mAb-induced modulation of CD2 and CD5, but not CD3, without concomitant changes in the surface distribution of these antigens (such as capping). This inhibitory effect is not protein synthesis dependent and is reversed by protein kinase C inhibitors (staurosporine and H-7). The use of cytoskeleton-disrupting agents shows the existence of different cytoskeletal interactions driving the mAb-induced modulation of CD2 and CD5 with respect to CD3. Treatment with cytochalasin D (an agent that inhibits microfilament polymerization) but not colchicine (an agent that inhibits microtubule polymerization) reproduced the effect of TPA on the mAb-induced modulation of CD2, CD3, and CD5. Our results indicate that the mAb-induced modulation of CD2 and CD5 is dependent on microfilament (namely actin) polymerization and PKC activation, while the modulation of CD3 is not.

Antibodies, Monoclonal↗
PubMed1983

Naturally occurring cytotoxic human antibodies recognize H-2-controlled murine lymphocyte antigens.

Human sera contain cytotoxic naturally occurring (CyNa) antibodies which discriminate between lymph node cells from mice differing only at the H-2 complex. Sera from three healthy subjects (normal human sera, NH sera) and one serum from a patient with multiple sclerosis reacted with cells expressing Db, Kd, Kk, and Kp molecules, respectively. However, the following observations suggested that the binding specificity of these CyNa antibodies is to antigens that are distinct from the classical H-2 antigens: (i) the NH sera did not contain cytotoxic anti-HLA antibodies, (ii) redistribution (capping) of H-2 antigens did not induce resistance to lysis for CyNa antibodies, and (iii) individual variation was demonstrated in the expression of the murine lymphocyte antigens detected by the human CyNa antibodies. The reason for this variation appeared to be different for individual NH serum. A maternal effect influenced the expression of the murine lymphocyte antigen detected by one NH serum (anti-H-2b). The differences detected by another NH serum (anti-H-2p) appeared to be inherited, as shown by progeny testing. We hypothesize that the human CyNa antibodies may be directed against antigens controlled or modified by murine viruses (milk borne or endogenous), whose expression is under the influence of the H-2 complex, and that their production might have been stimulated by the products of human genes homologous to murine viruses.

Aged↗
PubMed1987

Induction of H-2-specific antibodies by injections of syngeneic Sendai virus-coated cells.

The capacity of the B cell immunoglobulin receptor to recognize complexes of Sendai viral and H-2b antigens was investigated by studying the antibody response to injections of syngeneic Sendai virus-coated (SV+) spleen cells in C57BL/6 (B6) mice. Almost all mice produced alloreactive anti-H2 lymphocytotoxic antibodies. In contrast, such antibodies were found very exceptionally in mice injected with normal (SV-) cells or with Sendai virus (SV) only. The reaction pattern of the cytotoxic antibodies induced was variable and ranged from almost anti-private to widely cross-reactive serotypes. The results of reactions on H-2-congenic, -recombinant and -mutant mouse strains, and of capping and immunoprecipitation experiments showed that the cytotoxic antibodies were directed against H-2 class I molecules. The anti-H-2 antibodies exhibited enhanced binding for SV+ target cells, but absorption experiments showed that this was not the result of cross-reactions with cell surface Sendai viral determinants or with a molecular complex of H-2 plus SV. This conclusion was supported by the observation that syngeneic SV+ cells were not the predominant targets for the induced lymphocytotoxic antibodies. Our results do not support the existence of MHC-restricted antiviral antibodies, but show the induction of anti-class I H-2 alloantibodies by injections with syngeneic SV-coated cells. We present a model for regular induction of anti-H-2 antibodies without intentional alloimmunization.

Animals↗