bluuebunny/crossref_metadata_2025_split huggingface dataset:
NK and T cell subsets regulate antibody production by human in vivo antigen-induced lymphoblastoid B cells.
Authors: Brieva J A , Targan S , Stevens R H 
Published: December 2022

Abstract
This study demonstrates the existence of two different suppressive systems for the regulation of antitetanus toxoid antibody production by human lymphoblastoid (LB) B cells. These B cells appear in the circulation 5 to 7 days after in vivo immunization and spontaneously secrete antibody during a 3-day in vitro culture. One suppressive system was mediated by large granular lymphocytes that exhibited high natural killer activity. This suppressive cell subset spontaneously inhibited the antibody production by autologous LB cells, and this effect could be enhanced by the addition of interferon. This inhibition of antibody synthesis could be readily reversed by the addition of as few as 10(2) K-562 cells to the culture. Additionally, the activity of this suppressive cell population could be reduced by complement (C)-mediated lysis with Leu-7 antibody. These results strongly suggest that this autologous suppression was mediated by NK cells. The other suppressor system was contained in the fraction of high density T cells depleted of Fc receptor-bearing cells, which was low in NK activity. This subset inhibited LB function in the presence of pokeweed mitogen but not interferon, and even the addition of up to 10(6) K-562 NK target cells only minimally reversed this inhibition. These results indicate that two distinct subsets of cells share regulatory functions on the in vivo induced B lymphoblastoid cells. The observation that NK cells can inhibit these highly differentiated B cells expands our view of the spectrum of natural targets recognized by NK cells.
Anti-T cell monoclonal antibodies conjugated to ricin as potential reagents for human GVHD prophylaxis: effect on the generation of cytotoxic T cells in both peripheral blood and bone marrow.
Authors: Quinones R R , Youle R J , Kersey J H , Zanjani E D , Azemove S M , Soderling C C , Lebien T W , Beverley P C , Neville D M , Vallera D A 
Published: December 2022

Abstract
Three murine anti-human monoclonal antibodies broadly reactive with human T cells were conjugated to intact ricin toxin. The purgative effects of these immunotoxins (IT) on alloreactive T cells after in vitro pretreatment was tested in an in vitro assay measuring the generation of cytotoxic T cells (CTL). Pretreatment was performed in the presence of lactose to block the native binding of ricin, thus rendering IT antibody specific. Blocking studies with free antibody showed that selective toxicity was determined by the antibody moiety of the antibody-toxin conjugate. Our assay system permitted the measurement of significant CTL levels in the bone marrow. Thus, we were able to determine the differential selectivity of IT for T cells as compared with stem cells in the same donor preparation. Our studies show that antibody-intact ricin conjugates have great potential as T cell purgative reagents for GVHD prophylaxis in human BMT.
Dietary fish oil augments the induction of arthritis in rats immunized with type II collagen.
Authors: Prickett J D , Trentham D E , Robinson D R 
Published: December 2022

Abstract
Certain dietary-induced changes in tissue levels of polyunsaturated fatty acids are known to modify inflammatory reactions, possibly through changes in the synthesis of mediators of inflammation derived from fatty acids, including prostaglandins and leukotrienes. We have therefore examined the effects of a fish oil diet, enriched in highly unsaturated (delta-17) long chain fatty acids, on collagen arthritis. Weanling female Sprague-Dawley rats were maintained on a diet with fat provided by either fish oil (containing 14.5% 5, 8, 11, 14, 17-eicosapentaenoic acid; EPA) or, as a control, beef tallow (containing less than 0.05% EPA). They were immunized with native chick type II collagen emulsified in incomplete Freund's adjuvant 5 to 6 wk later. There was an increased incidence of arthritis in the rats receiving the fish oil compared with the group receiving the beef diet (88 vs 61%, p less than 0.001), but there was no significant difference in the severity of joint inflammation of arthritic rats in the two groups. The mean serum titer of IgG antibodies to type II collagen, measured by an enzyme-linked immunosorbent assay (ELISA), was decreased in the group receiving the fish oil (p less than 0.001), whereas the hemagglutinating antibody titer and delayed-type hypersensitivity to collagen were similar in the two groups. Primary synovial explant cultures from fish oil-treated rats produced only 21 to 24% as much PGE2 as beef tallow-treated controls, and this reduction in the experimental group was not accompanied by any detectable increase in PGE3, the E-prostaglandin derived from the arachidonic acid analogue, EPA, in fish oil. These data demonstrate that inductive mechanisms in collagen arthritis can be altered by diet-induced changes in tissue fatty acid composition without essential fatty acid deficiency. The reason(s) for this effect is unknown, but it is possible that changes in the cyclooxygenase or lipoxygenase products of polyunsaturated fatty acids are involved.
Effect of iron (III) in the presence of various ligands on the phagocytic and metabolic activity of human polymorphonuclear leukocytes.
Authors: van Asbeck B S , Marx J J , Struyvenberg A , van Kats J H , Verhoef J 
Published: December 2022

Abstract
FeCl3 or Fe(III) that attached to chelating ligands such as citrate or nitrilotriacetic acid (NTA) at a molar ratio of 1:1 had a toxic effect on PMN. Uptake of radiolabeled Staphylococcus aureus by PMN, preincubated for 2 hr at 37 degrees C in a medium containing Fe(III)-citrate or Fe(III)-NTA, was significantly lower than that of control PMN preincubated without excess iron (p less than 0.002). However, at a 1:2 molar ratio of Fe(III) to citrate or NTA, the iron was not toxic. In contrast, the iron-liganding molecules transferrin and deferoxamine protected the PMN against the noxious effect of iron at concentrations just high enough to sequester all the iron. Fe(III) increased the generation of luminol chemiluminescence by stimulated PMN, whereas the oxygen consumption of the cells was not altered in the presence of Fe(III); this suggests a catalytic effect of iron on the production by PMN of oxygen metabolites at some step beyond the formation of superoxide. No effect of iron was observed when the incubation was performed at 4 degrees C, nor when an oxygen-radical scavenger such as thiourea, mannitol, or catalase was present in the incubation medium. Also, Fe(III) had much less effect on the phagocytic function of PMN of a patient with chronic granulomatous disease. The results indicate that the Fe(III)-induced defect in the phagocytic capacity of PMN depends on the nature and the concentration of the ligand attached to the iron ion, and also suggest that the noxious effect of iron on the PMN function is a result of its ability to catalyze the generation of toxic oxygen species by these cells.
Responsiveness of autoimmune and normal mice to nucleic acid antigens.
Authors: Madaio M P , Hodder S , Schwartz R S , Stollar B D 
Published: December 2022

Abstract
To test the possibility that anti-DNA antibody formation in autoimmune disease is related to an exceptional responsiveness to nucleic acid immunogens, we examined the ability of normal and autoimmune strains of mice to produce antibodies after immunization with DNA and synthetic helical DNA analogues. Autoimmune mice (MRL/++) did not respond significantly to denatured DNA-methylated BSA in adjuvant (in comparison with adjuvant alone). They did, however, respond to helical structures that differed from B-DNA, including poly-(dG) . poly(dC), poly(dT-dG) . poly(dC-dA), and left-handed Z-DNA. Normal mice (C57BL/6) responded to denatured DNA and, after immunization with the other polymers, produced antibodies of equal or higher titer than those of MRL/++ animals. Neither strain responded to native DNA. The induced anti-nucleic acid antibodies were highly selective and reacted only with the immunogen. In contrast, both lupus autoantibodies and antisera from normal animals that received adjuvant alone cross-reacted with multiple nucleic acid antigens. This result, and the finding that MRL/++ mice were poor responders to nucleic acid immunogens, suggest that different clones and pathways are involved in nucleic acid-induced and spontaneous anti-DNA antibody formation.
Six antigenic determinants in the surface layer of the archaebacterium Methanococcus vannielii revealed by monoclonal antibodies.
Authors: Conway de Macario E , König H , Macario A J , Kandler O 
Published: December 2022

Abstract
The immunogenicity and antigenic characteristics of the unique surface layer (S layer) of Methanococcus vanielii was studied with a panel of six monoclonal antibodies. Six surface determinants were identified for the first time, each recognized by one antibody exclusively. The determinants are proteins, located in the S layer, and accessible to antibody in whole, unfixed, as well as formalinized bacteria. Hence the six antigens and antibodies reported here should be useful for rapid identification of new isolates and for taxonomy of methanogens, notably Methanococcaceae. In this connection two novel applications of the slide immunoenzymatic assay were developed for analyses of monoclonal antibodies and their complementary sites in the bacterial envelope.
Antigenic structure of hepatitis B surface antigen: identification of the "d" subtype determinant by chemical modification and use of monoclonal antibodies.
Authors: Peterson D L , Paul D A , Lam J , Tribby I I , Achord D T 
Published: December 2022

Abstract
Hepatitis B surface antigens (HBsAg) of both the adw and ayw subtypes were reductively methylated with formaldehyde in the presence of sodium cyanoborohydride. The effect on antigenicity was determined by radioimmunoassay with monoclonal antibodies specific for seven different antigenic determinants. The reaction was shown to eliminate specifically the "d" antigenic activity of HBsAg/adw and to have no effect on HBsAg/ayw. Moreover, the reaction had only a slight affect on HBsAg/adw at one of the "a" antigenic determinants. The sites of modification were determined and the extent of modification of each site was compared to the loss of "d" antigenic activity. These studies demonstrated that the loss of "d" activity was due to the modification of lysine 122 in HBsAg/adw, and that although the amino terminus and lysine residues 141 and 160 of both HBsAg/adw and HBsAg/ayw are reactive, their modification does not alter any measurable antigenic activity.
Responses against single minor histocompatibility antigens. II. Analysis of cloned helper T cells.
Authors: Roopenian D C , Orosz C G , Bach F H 
Published: December 2022

Abstract
We have utilized a clonal approach to investigate functional and immunogenetic characteristics of T cells responsive to the miHA H-1.3. Our data prove the existence of H-2 I region-restricted helper T cells that are specific for H-1.3, or for determinants encoded by closely linked loci. These conclusions are based upon the following observations: 1) the cloned Th are driven to proliferate only by H-2 I-compatible stimulator cells that bear the appropriate (H-1.3) miHA; 2) antigenic stimulation causes the cloned Th to secrete lymphokine with high levels of IL 2-like activity; and 3) they are not specifically lytic for relevant target cells. These cloned Th were isolated at a rather low frequency from an H-1.3-immune MLC population compared with the observed frequency of H-1.3-specific Tc that proliferate autonomously after antigen stimulation; i.e., HITc isolated from the same MLC. They were, however, capable of promoting the clonal expansion of an H-1.3-specific HITc, suggesting that Th can collaborate with HITc in an anti-miHA response.
Surface membrane heterogeneity among human mononuclear phagocytes.
Authors: Biondi A , Rossing T H , Bennett J , Todd R F 
Published: December 2022

Abstract
Considerable information has been accumulated about the functional and metabolic differences that exist among human mononuclear phagocytes isolated from different anatomic sites. This heterogeneity may reflect the influence of environmental factors that stimulate circulating monocytes to differentiate in a distinctive manner, or may suggest the existence of predetermined subsets of macrophage precursors. The present study was designed to evaluate macrophage diversity at the membrane level by defining the expression of antigenic determinants on the surface of these cells. The expression of two new membrane differentiation antigens, BMM1 and PAM1, and of Mo1 and Mo2 were evaluated on blood monocytes, macrophages derived from cultured monocytes, breast milk macrophages (BMM), pulmonary alveolar macrophages (PAM), and peritoneal macrophages. Anti-BMM1 is a mouse IgG2a monoclonal antibody obtained by immunization with breast milk cells that recognizes an antigen expressed only on BMM but not on blood monocytes (or any other circulating cells), PAM, and peritoneal macrophages. BMM1 expression is also seen on HL60 promyelocytes induced toward macrophage differentiation by lymphokines but not by phorbol diester. Anti-PAM1, an IgG1 monoclonal antibody raised by immunization with PAM, reacts with an antigen found only on PAM. Blood monocytes, BMM, and peritoneal macrophages all share the previously described differentiation antigens, Mo1 and Mo2 (as well as Ia), whereas these markers are not found on PAM. BMM1 is associated with a two subunit surface protein of 46 and 40 Kd, and PAM1 resides on a 200 Kd polypeptide. The appearance of new antigens during differentiation (BMM1 on milk macrophages and PAM1 on PAM) and the disappearance of antigens more common to the macrophage lineage (absence of Mo1 and Mo2 on alveolar macrophages) indicate a significant heterogeneity at the membrane level among phagocytes obtained from different anatomic sites (but arising from a common myeloid precursor). The functional relevance of these structures selectively expressed by BMM and PAM is the object of further investigation.
In vitro immune response of cells of various lymphoid tissues in (NZB X NZW)F1 mice: evidence for abnormality of the mesenteric lymph node cells.
Authors: Jung L K , Good R A , Fernandes G 
Published: December 2022

Abstract
Autoimmune-prone (NZB X NZW)F1 (B/W) mice have been shown to have a variety of immunologic perturbations. However, most studies have been performed with spleen cells. By using the Mishell-Dutton culture system, we examined the in vitro immune response of the various lymphoid tissue to determine whether an imbalance at a selective lymphoid site may exist in B/W mice. It was shown that the ability of mesenteric lymph node (MLN) cells of B/W mice to generate plaque-forming cells (PFC) in response to sheep red blood cells was consistently less than that of the spleen cells. This relationship held true in the aged mice. In contrast, the ability of the MLN cells of other strains not prone to develop autoimmunity to generate PFC was higher than that of the spleen cells. No significant difference in the mitogenic response of the lymphoid cells from various lymphoid tissue in the young B/W mice was seen, as compared with normal lymphoid cells from control mice. However, it was demonstrated that a relative decrease of B cells and immunoregulatory Lyt-123+ cells in the MLN in the B/W mice occurred early in life, and it was concluded that this abnormality may account for the low PFC response observed.
Isotypes of spontaneous and mitogen-induced autoantibodies in SLE-prone mice.
Authors: Slack J H , Hang L , Barkley J , Fulton R J , D'Hoostelaere L , Robinson A , Dixon F J 
Published: December 2022

Abstract
A common cellular abnormality of all murine strains prone to systemic lupus erythematosus (SLE) is an increased spontaneous polyclonal expansion of B cells. Our findings support the existence of this SLE-associated abnormality because the numbers of B lymphocytes secreting all the different IgG subclasses and IgM in spleens of all lupus-prone mice are elevated, compared to levels of normal splenic immunoglobulin-producing cells. We also report that 1) spontaneous polyclonal stimulation of immunoglobulin in autoimmune mice is preferential for subclass, and that the preferentially stimulated isotypes in each SLE strain consistently dominate both circulating and kidney-deposited immune complexes; 2) distinct patterns of isotype preference exist among the autoimmune strains determined by inherent B cell proliferative abnormalities or by B cell proliferation affected by thymus-derived lymphocytes; and 3) chronic administration of the TI B cell mitogen Lipid A in late-life SLE-prone mice induces an early-life glomerulonephritis with auto-antibodies of an isotype composition characteristic of those spontaneously produced by inherently abnormal B cells of early-life lupus mice.
Subpopulations of antibodies to phosphocholine in human serum.
Authors: Brown M , Schiffman G , Rittenberg M B 
Published: December 2022

Abstract
We investigated the heterogeneity of anti-phosphocholine (PC) antibodies present in human serum taken from individuals before and after immunization with a multivalent pneumococcal vaccine. The fine specificity of IgM, IgG, and IgA anti-PC antibodies was determined in an ELISA by using phosphocholine or p-nitrophenyl phosphocholine (NPPC) to inhibit binding of antibody to PC-histone. We identified two populations specific for PC that differed in their binding properties. One population is inhibited by NPPC much better than by PC and is most evident in IgG antibodies. The second population has similar avidity for PC and NPPC and is consistently associated with the IgM and IgA isotypes as well as with IgG. The IgG antibodies in both populations were predominantly of the IgG2 subclass. Both populations were found in serum samples taken before immunization with pneumococcal vaccine, suggesting that they had been stimulated through prior environmental contacts with PC-containing antigens. Previously, we found populations with similar fine specificity patterns in the murine response to PC. The two murine antibody populations have been shown to derive from different immunoglobulin variable region genes. The presence of comparable antibody populations in the human suggests the possibility that these two fine specificity families have been conserved in evolution.
Identification of distinct predominant epitopes recognized by myoglobin-specific T cells under the control of different Ir genes and characterization of representative T cell clones.
Authors: Berkower I , Matis L A , Buckenmeyer G K , Gurd F R , Longo D L , Berzofsky J A 
Published: December 2022

Abstract
We characterized the fine specificity of antigen recognition of myoglobin-immune T cells from B10.D2, B10.GD, and B10.A(5R) mice. Polyclonal H-2d T cells show a predominant response to an epitope centering on Glu 109 and His 116. These residues localize a dominant epitope to one segment of the myoglobin surface, but probably are not the only amino acid residues involved. This response pattern maps genetically to I-Ad (or Kd) based on the B10.GD recombinant strain. A different epitope specificity was detected in B10.A(5R) T cells mapping to I-E beta b E alpha k or I-Cd, but no difference was detected between strains differing at the Igh locus. Thus, epitope specificity varied with Ia haplotype but not Igh allotype. Myoglobin-specific B10.D2 T cell lines were established, and five clones specific for the Glu 109, His 116 epitope were isolated; these were all restricted to I-Ad antigen-presenting cells. These clones represent the dominant specificity in the polyclonal T cell response to myoglobin and will be useful in characterizing the structure and function of T cell receptors for antigen and Ia. The differences in number and nature of T cell epitopes compared to B cell epitopes of myoglobin are discussed.
Activation of the alternative complement pathway by Leishmania promastigotes: parasite lysis and attachment to macrophages.
Authors: Mosser D M , Edelson P J 
Published: December 2022

Abstract
When exposed to normal human or guinea pig sera, promastigotes of Leishmania enriettii and L. tropica activate the complement cascade by the alternative pathway and fix C3 on their surfaces. In high (25%) serum concentrations, the result of complement activation is parasite lysis. At lower concentrations (4%), complement fixation results in enhanced parasite binding and uptake into murine peritoneal macrophages. Parasites are lysed in normal guinea pig, C4-deficient guinea pig, normal human, and C2-deficient human sera when they are incubated at 37 degrees C for 30 min. Fetal calf and normal mouse sera are poorly lytic. Lysis requires Mg++ but not Ca++, is mediated by heat labile (56 degrees C, 30 min) component(s), and does not occur when the incubations are maintained at 4 degrees C. Guinea pig serum preadsorbed with promastigotes of L. tropica in EDTA at 4 degrees C for 30 min is fully lytic. Immunofluorescence studies with anti-C3 antibodies show that under these conditions C3 is deposited on the surface of the parasite. The serum-dependent binding of parasites to macrophages is also mediated by heat-labile, nonadsorbable factor(s) present in normal guinea pig and mouse sera, as well as C2-deficient and C4-deficient sera. The serum-dependent macrophage recognition mechanism is trypsin sensitive but relatively resistant to chymotrypsin. Parasites but not macrophages can be presensitized at room temperature with low levels (8%) of serum to enhance their binding to macrophages. Presensitization does not occur at 4 degrees C. These results show that Leishmania promastigotes of several species can fix complement by activating the alternative complement pathway. This may then result either in parasite lysis or in an accelerated uptake of the parasite into phagocytic cells. In vivo, the biologic outcome of infection may reflect a balance between extracellular lysis and enhanced uptake into phagocytic cells.