bluuebunny/crossref_metadata_2025_split huggingface dataset:
OCCURRENCE OF 19S AND 7S ANTI-IGGS DURING HYPERIMMUNIZATION OF RABBITS WITH STREPTOCOCCI
Authors: Bokisch Viktor A. , Bernstein David , Krause Richard M. 
Published: June 2004

All 110 rabbits immunized with Group A, A-variant, and C streptococcal vaccines produced 19S anti-IgG in addition to antibodies to the streptococcal carbohydrates. 19S anti-IgG was detected by hemagglutination of rabbit red blood cells coated with rabbit anti-blood group F antibody. Antisera of 88 of these animals were also tested for 7S anti-IgG with a coprecipitation assay. This assay is based on the coprecipitation of 7S anti-IgG with complexes of streptococcal carbohydrate and anti-carbohydrate antibody. 50 of the 88 anti-Group C streptococcal antisera contained 7S anti-IgGs. In eight antisera the concentration was greater than 5 mg/ml.
The data suggest a genetic influence on the occurrence of 7S anti-IgG. The eight rabbits which produced more than 5 mg/ml of 7S anti-IgG belonged to three related families. Moreover, there were families in which almost every member produced 7S anti-IgG and other families in which only 30% of the members manufactured 7S anti-IgG.
The streptococcal vaccine was an especially efficient stimulus for the production of 19S anti-IgG, whereas the pneumococcal vaccine was much less effective in this respect. Furthermore, 7S anti-IgGs were not detected in antipneumococcal antisera, although the concentration of anti-capsular antibodies was similar to that of anti-carbohydrate antibodies in antistreptococcal antisera.
STUDIES IN PORPHYRIA
Authors: Kappas Attallah , Bradlow H. Leon , Gillette Peter N. , Gallagher T. F. 
Published: June 2004

A variety of 5ß steroid metabolites derived from hormones natural to man are potent inducers experimentally of δ-aminolevulinate synthetase, the rate-limiting enzyme in porphyrin-heme formation. This mitochondrial enzyme is found at high levels of activity in the livers of patients with the genetic disease, acute intermittent porphyria (AIP). In this study the metabolism of 14C-labeled testosterone was examined in AIP patients to determine whether there was a disproportionate conversion of the hormone to its 5ß, compared to its 5α metabolite. The results indicate that AIP subjects do generate a substantially greater than normal fraction of 5ß metabolite from this steroid; the excessive degree of ring A reduction of testosterone taking place via the 5ß pathway in the porphyric patients averages 350% greater than in the nonporphyric subjects. In one asymptomatic AIP patient the disproportionate generation of 5ß metabolite from the hormone reached a level 10 times the normal mean. Studies with a second 14C-labeled hormone, dehydroisoandrosterone, whose metabolism in man resembles that of testosterone, confirmed the derangement in reductive transformation of steroids found in the individuals carrying the genetic lesion of AIP.
These findings define a new endocrine abnormality in AIP patients and raise the possibility that endogenously derived 5ß steroids may contribute by an induction mechanism to the increased levels of hepatic δ-aminolevulinate synthetase activity found in AIP patients.
ANTIGEN-INDUCED STIMULATION OF GLUCOSAMINE INCORPORATION BY GUINEA PIG PERITONEAL MACROPHAGES IN DELAYED HYPERSENSITIVITY
Authors: Hammond M. Elizabeth , Dvorak Harold F. 
Published: June 2004

The interaction between sensitized lymphocytes and specific antigen occurring in delayed hypersensitivity causes bystander macrophages to undergo a variety of light-microscopic, ultrastructural, and biochemical changes, which are reflected in alterations in cell movement and intercellular contacts. Since such alterations involve functions of the cell periphery, we postulated that metabolic changes in this polysaccharide-rich zone would accompany the expression of delayed hypersensitivity.
We here demonstrate that the incorporation of radioactive glucosamine by peritoneal macrophages into TCA-precipitable, membrane-associated material is regularly enhanced when these are cultured in the presence of specific antigen and nonadherent cells (lymphocytes) primed for delayed hypersensitivity. Lymphocytes from unsensitized animals, or from animals immunized so as to form antibody but not delayed hypersensitivity, do not stimulate such incorporation. Antigen-induced glucosamine incorporation is maximal at 2 or 3 days of culture and is not observed earlier; it may be elicited with as little as 0.1 µg/ml PPD, and affords an exceedingly reproducible and sensitive index of delayed hypersensitivity.
Radioautographic studies indicate that nearly all plastic adherent cells (90% macrophages) incorporate glucosamine and that grains are concentrated in the regions of the perinuclear zone and cell membrane. Subcellular fractionation indicates that nearly 30% of counts and the highest specific activity are associated with the membrane-rich microsomal fraction; the microsomal distribution of counts increases in both absolute and relative terms when macrophages are cultured in the presence of specific antigen and sensitized lymphocytes.
Taken together, these data indicate that a sizable fraction of incorporated glucosamine is localized to the vicinity of the cell periphery but lack sufficient resolution to determine whether this material is associated with the cell membrane itself or with the extramembranous cell coat. This last possibility is of particular interest since we have previously shown that macrophage cell coat material is lost or altered as a consequence of an interaction between sensitized lymphocytes and specific antigen.
DISTRIBUTION OF LABELED LYMPH NODE CELLS IN MICE DURING THE LYMPHOCYTOSIS INDUCED BY BORDETELLA PERTUSSIS
Authors: Taub Robert N. , Rosett Walter , Adler Andy , Morse Stephen I. 
Published: June 2004

The mechanism by which Bordetella pertussis organisms and their products induce lymphocytosis in mice was analyzed in terms of the localization of syngeneic Cr-51-labeled lymph node cells. Labeled lymphoid cells incubated in vitro with the supernatant of B. pertussis cultures and then injected intravenously into normal recipients, or labeled cells injected into pertussis-treated recipients were unable to "home" to lymphoid organs but persisted for long periods in the blood. In animals "equipped" with a population of Cr-51-labeled lymphoid cells, administration of B. pertussis organisms or culture supernatant effected a shift of radioactivity from lymph nodes and spleen into the peripheral blood, coincident with the lymphocytosis.
In in vitro experiments it was found that the active principle could bind to both erythrocytes and lymphocytes and could spontaneously elute from these cells onto labeled lymphocytes which were then unable to home efficiently.
The data suggest that Bordetella pertussis-induced lymphocytosis involves a reversible attachment of the pertussis factor onto the surfaces of lymphocytes which prevents their recirculation to lymphoid organs. Recirculating lymphocytes are presumably affected as they emerge from lymphoid organs to enter the blood.
EVIDENCE FOR THE LINKAGE OF THE IGCH LOCUS TO A GENE CONTROLLING THE IDIOTYPIC SPECIFICITY OF ANTI-p-AZOPHENYLARSONATE ANTIBODIES IN STRAIN A MICE
Authors: Pawlak Laura L. , Mushinski Elizabeth B. , Nisonoff Alfred , Potter Michael 
Published: June 2004

Anti-p-azophenylarsonate (anti-Ar) antibodies elicited in all strain A/J mice tested share one or more idiotypic specificities. These specificities are also found in the anti-Ar antibodies of mice of the closely related strain, AL/N, but not in those of BALB/c mice.
Anti-Ar antibodies were elicited in congenic mice in which the IgCH locus of AL/N mice, which controls allotypic markers in the constant regions of heavy chains, had been introgressively backcrossed for nine generations onto a BALB/c background; the mice were then rendered homozygous for the AL/N allotypic determinant. On the average, these antibodies were quantitatively equivalent, with respect to content of the cross-reactive idiotype, to those of AL/N mice. This indicates that the gene controlling the idiotype is closely linked to the IgCH locus. Since idiotype must be a function of V region sequences, the results suggest close linkage of VH and CH genes. The cross-reactive idiotype was found in nearly all F1 mice (C57/BL x A/J or BALB/c x A/J) tested.
AN ENZYMATIC FUNCTION ASSOCIATED WITH TRANSFORMATION OF FIBROBLASTS BY ONCOGENIC VIRUSES
Authors: Unkeless J. C. , Tobia A. , Ossowski L. , Quigley J. P. , Rifkin D. B. , Reich E. 
Published: June 2004

Chick embryo fibroblast cultures develop fibrinolytic activity after transformation by Rous sarcoma virus (RSV). This fibrinolytic activity is not present in normal cultures, and it does not appear after infection with either nontransforming strains of avian leukosis viruses or cytocidal RNA and DNA viruses. In cultures infected with a temperature sensitive mutant of RSV the onset of fibrinolysis appears after exposure to permissive temperatures and precedes by a short interval the appearance of morphological evidence of transformation.
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The rate of fibrinolysis in transformed cultures depends on the nature of the serum that is present in the growth medium: some sera (e.g., monkey or chicken serum) promote high enzymatic activity, while others (calf, fetal bovine) do not. Some sera contain inhibitors of the fibrinolysin.
Based on the effect of a small number of known inhibitors, at least one step of the fibrinolytic process shows specificity resembling that of trypsin.
The sera of sarcoma-bearing chickens contain an inhibitor of the fibrinolysin, whereas normal chicken sera do not.
For general discussion, conclusions, and summary see the accompanying paper, part II, (J. Exp. Med. 137:112).
REGULATION OF AUTOSENSITIZATION
Authors: Cohen Irun R. , Wekerle Hartmut 
Published: June 2004

We studied the mechanisms underlying the natural tolerance of thymus-derived (T) lymphocytes for self-antigens. Lymphocytes from the thymus or lymph nodes of inbred rats were autosensitized in vitro against monolayers of autochthonous thymus reticulum cells or syngeneic fibroblasts. Receptors for self-antigens were detected by the specific adherence of normal lymphocytes to syngeneic cells. The achievement of active cell-mediated autosensitization was assayed by measuring the immunospecific lysis of syngeneic target cells in vitro, or graft-versus-host (GvH) reactions in vivo. The following observations were made using these systems.
(a) A fraction of normal lymphocytes was found to have specific surface receptors that are able to recognize self-antigens which seem to be accessible in vivo. These potentially self-reactive lymphocytes were activated by incubation with syngeneic or autochthonous cells in vitro. Hence, the elimination of potentially self-reactive lymphocytes cannot be the only basis for natural self-tolerance. Therefore, the maintenance of self-tolerance in vivo appears to involve suppression of the immune reactivity of such self-tolerant lymphocytes.
(b) We found that control of autosensitization depends upon the inhibition of the recognition of self-antigens. A GvH reaction in vivo could not be suppressed once recognition of self-antigens had occurred in vitro. Moreover, studies of the kinetics of antigen recognition indicated that several hours of incubation in vitro were needed for the inactivation of factors specifically inhibiting self-recognition.
(c) We found that factors which inhibit self-recognition are present in fresh autologous serum. Treatment of the lymphocytes, but not syngeneic adsorbing cells, with autologous serum prevented recognition of syngeneic antigens. Allogeneic serum did not prevent self-recognition, and autologous serum did not inhibit the recognition of foreign antigens.
These findings indicate that natural tolerance of T lymphocytes to self-antigens can be regulated by serum factors which act on the lymphocytes. The immunospecificity of the inhibitory effect suggests that these factors may be soluble self-antigens in a tolerogenic form.
CROSS-IDIOTYPIC SPECIFICITY AMONG MONOCLONAL IGM PROTEINS WITH ANTI-γ-GLOBULIN ACTIVITY
Authors: Kunkel H. G. , Agnello V. , Joslin F. G. , Winchester R. J. , Capra J. D. 
Published: June 2004

Through the use of absorbed idiotypic antisera prepared against single isolated monoclonal IgM anti-γ-globulins, partial cross-idiotypic specificity was demonstrated with other IgM anti-γ-globulins. Such antisera classified these proteins into at least three groups. The major group which included 60% of the anti-γ-globulins was particularly homogeneous. The anti-γ-globulin specific antigens were detected best in hemagglutination and hemagglutination inhibition systems. They were not found in monoclonal IgM proteins that lacked anti-γ-globulin activity although related antigens were detected at low concentrations in pooled immunoglobulin preparations as well as in heterogeneous anti-Rh antibodies.
Several lines of evidence were obtained indicating that the antibody combining site was involved in the specific determinants. Attempts were made to analyze the fine specificity of each anti-γ-globulin for the Fc fragment of different subclasses of human immunoglobulins as well as those of other species. Differences were observed but these were not readily related to the cross-specificity antigens.
The anti-γ-globulin specific antigens were very analogous to those previously described for monoclonal IgM cold agglutinins. Although each protein could be distinguished from all the others on the basis of individual idiotypic antigens, the antigens common to the specific groups of proteins with each of these activities were prominent and readily detected with multiple antisera. The results indicate basic similarities between proteins of a given activity even in unrelated individuals.
INDEPENDENCE OF H-2K AND H-2D ANTIGENIC DETERMINANTS ON THE SURFACE OF MOUSE LYMPHOCYTES
Authors: Neauport-Sautes Catherine , Lilly Frank , Silvestre Danielle , Kourilsky François M. 
Published: June 2004

At 37°C, fluorescein-conjugated anti-H-2 alloantibodies specifically induce, at the surface of living mouse lymphocytes, the redistribution of the corresponding H-2 antigens, which cluster as patches and sometimes single caps at one pole of the cell. This aggregation is inhibited at 0°C and the H-2 antigens, stained by fluorescent antibodies in the cold, appear evenly spread over the cell surface.
This phenomenon was used to define the relationships between the membrane structures bearing the antigens coded by the H-2K and the H-2D genes of the H-2 region. Monospecific anti-H-2 antibodies coupled to either tetramethyl rhodamine isothiocyanate or fluorescein isothiocyanate were used to induce the redistribution of H-2D and H-2K antigens of the H-2b and H-2k haplotype at the surface of lymph node cells from homozygous and F1 hybrid mice. It was observed that the diffuse distribution of H-2K antigens labeled at 0°C was not affected by the prior antibody-induced aggregation of H-2D antigens and vice versa. The results were the same for H-2 antigens governed by genes located either in cis or in trans position.
These data indicate that the H-2K and H-2D antigens migrate independently at the cell surface, and suggest that the gene products from the D and the K end of the H-2 region are expressed on independent molecules or structures at the cell membrane.
THE GLOMERULAR MESANGIUM
Authors: Mauer S. Michael , Sutherland David E. R. , Howard Richard J. , Fish Alfred J. , Najarian John S. , Michael Alfred F. 
Published: June 2004

A mechanism of immune glomerular injury is described based on the fixation of antibody (Ab) to an antigen (Ag) that has localized in the glomerular mesangium. Rabbits were given, intravenously (i.v.), aggregated human IgG (AHIgG) or albumin (AHSA) and 10 h later, when the Ag by immunofluorescent microscopy was present in the mesangium, a kidney was removed and transplanted into a normal rabbit. The recipient then received, i.v., rabbit anti-HIgG or anti-HSA.
Within minutes of Ab infusion, glomeruli of the donor kidney had polymorphonuclear (PMN) infiltration that over the next few hours became marked and was associated with glomerular cell swelling. At 24 h a decrease in PMN's and early mesangial proliferation was seen. By 3 days there was marked mesangial hypercellularity and increased mesangial matrix. Within minutes after Ab administration rabbit IgG, C3, and fibrin were seen in the glomerular mesangium. There was a fall in complement titer by 1 min after Ab infusion that was due to complement consumption by the donor kidney. Complement then returned to normal levels by 48 h.
Significant glomerular injury did not occur (a) in the recipient's own kidney, (b) from Ag administration and transplantation without recipient Ab administration, or (c) from transplantation and Ab administration without prior Ag administration.
These studies demonstrated that Ag localized in the glomerular mesangium can react with circulating Ab and complement resulting in severe glomerular injury.
A STUDY OF ALLOGRAFT KIDNEY REJECTION OCCURRING SIMULTANEOUSLY IN WHOLE ORGAN AND EAR CHAMBER GRAFTS IN THE RABBIT
Authors: Hobbs J. B. , Cliff W. J. 
Published: June 2004

When portions of adult renal tissue are allografted into the rabbit ear chamber, they usually survive for periods of up to several months (6). When a kidney from the same donor is grafted as a whole organ, the ear chamber grafts then reject with the whole organ in 7 days. During that time serial needle biopsies of the whole organ are compared with the in vivo appearance of the ear chamber grafts. This establishes that the changes occurring in the ear chamber grafts are monitoring the rejection process proceeding in the whole organ grafts.
Dramatic vascular changes herald the earliest stages of unmodified rejection. A highly characteristic form of individual discrete platelet adhesion to both endothelium and adherent leukocytes is observed which is associated with the release reaction. At times as many as 20 such discrete platelets are clearly visible in profile in one high-power field. This demonstrates in vivo a mechanism whereby vascular and parenchymal damage may be produced by platelet contents, without previous aggregation or thrombus formation being necessary.
INHIBITION OF THE IMMUNE RESPONSE BY 7S ANTIBODY
Authors: Abrahams S. , Phillips R. A. , Miller R. G. 
Published: June 2004

A cell culture system was used to investigate the mechanism of action of the feedback inhibition caused by specific 7S antibody. It was found that preincubation of spleen cells with specific 7S antibody led to a marked reduction in the in vitro response of the treated spleen cells to the antigen used to prepare the antibody. The inhibition was not caused by a carry-over of free antibody nor by the release of 7S antibody from the cells. Rather, the preincubation appeared to specifically inactivate one of the cells required for initiation of an in vitro response. Since the suppression could be reversed by addition of untreated cells, it was possible to characterize the properties of the reconstituting cell. This cell is identified as the nonlymphoid accessory cell (A cell) by several criteria. (a) Suppression can be demonstrated only in assay systems requiring functional A cells. (b) The most active sources for reconstitution are also good sources for A cells. (c) The sedimentation velocity of the reconstituting cell is identical with that for A cells. (d) Like A cells, the reconstituting cell is resistant to high doses of ionizing radiation. (e) The reconstituting ability is not affected by anti-θ antibody. Of the three cells required for the initiation of an immune response, A cells, bone marrow-derived cells, and thymus-derived cells, the data are only compatible with the reconstituting cell being an A cell.
Additional experiments suggest that the Fc portion of 7S antibody binds to the surface of A cells. Thus, fluorescein isothiocyanate-labeled 7S antibody binds specifically to cells with properties similar to those described above, and F(ab')2 fragments, lacking Fc portion, are unable to cause immunosuppression when they are preincubated with spleen cells. It is possible that this binding is related to the specific suppression caused by 7S antibody molecules.
THE IMMUNE RESPONSE AGAINST HAPTEN-AUTOLOGOUS PROTEIN CONJUGATES IN THE MOUSE
Authors: Rubin Bent , Wigzell Hans 
Published: June 2004

Mice immunized with hapten-autologous serum albumin conjugates (DNP-mouse serum albumin) were shown to contain immune B and T cells with specificity for the conjugate. Fractionation on antigen-coated Sepharose beads showed that B cells could be subdivided in two major groups: those reacting against the haptenic group (DNP) and those reactive against the new antigenic determinants (NADs) introduced into the protein carrier by the hapten coupling. It was shown previously that humoral antibodies formed against hapten-mouse serum albumin conjugates also were directed against these two groups of antigenic determinants and that the immune response to the NADs does not follow the genetic rules of high or low response against the hapten used. All together these findings support the distinct nature of the NADs over the haptenic groups, as recognized both at the humoral and cellular level.
Absorption of mouse cells immune to hapten-autologous serum albumin conjugates on antigen-coated Sepharose beads using a variety of incubation conditions resulted in no specific retention of T cells. Therefore we had to resort to specificity studies of T cells in relation to T cell function. Relatively pure immune T cell suspensions were obtained using fractionation on anti-immunoglobulin-coated columns. DNP-MSA-specific T cells were shown to be very specific for the DNP-MSA conjugate with only one exception: they cross-reacted with antigenic determinants on DNP-rat serum albumin. As DNP-specific help was excluded in the present transfer system (as shown by the inability of cells from DNP-skin-painted mice and DNP-heterologous protein conjugate specific T cells [anti-immunoglobulin column purified] to help a DNP-MSA response), these results demonstrate the NAD specificity of the DNP-MSA-reactive T cells. The cross-reactivity pattern of DNP-MSA-specific T cells was similar to that found for humoral anti-NAD antibodies produced against the same immunogen.
Whether B and T cells are activated by the same antigenic determinants is discussed.
FORMATION OF C3a AND C5a ANAPHYLATOXINS IN WHOLE HUMAN SERUM AFTER INHIBITION OF THE ANAPHYLATOXIN INACTIVATOR
Authors: Vallota Enrique H. , Müller-Eberhard Hans J. 
Published: June 2004

Two biologically and chemically distinct anaphylatoxins (ATs) could be generated in whole human serum after removal of the AT inactivator (AI) by immune-absorption or after inhibition of AI with 1 M epsilon-aminocaproic acid (EACA). Both human ATs could be generated by treatment of serum with antigen-antibody complexes, which activate the classical complement pathway, and with inulin or yeast, both of which trigger the alternate pathway. The ATs were isolated from serum in active form and characterized as C3a and C5a.
Although human C3a had been characterized previously, C5a had not. The molecular weight of human C5a AT was 17,500; its electrophoretic mobility at pH 8.5 was –1.7 x 10–5 cm2 V–1 s–1. The minimal effective concentration in vitro was 7.5 x 10–10 M. The minimal effective doses of human C5a in producing a wheal and erythema in the human skin was 1 x 10–15 mol. The results strongly suggest a biological function for both ATs and indicate that the expression of their activity is controlled by the AI of normal blood plasma.