bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ontogeny of the MHC antigens on human trophoblast cells during the first trimester of pregnancy.
Authors: Montgomery B , Lala P K 
Published: December 2022

Abstract
The presence and the ontogeny of class I and class II major histocompatibility (MHC) antigens were investigated on human trophoblast cells in single cell suspensions of collagenase dispersed placentae during the first trimester of pregnancy by using a highly sensitive radioautographic approach. Cells were treated with monoclonal anti-HLA-A,B,C or anti-HLA-DR (or anti-human Ia) antibodies followed by 125I-labeled protein A, normal mouse serum, or medium alone used as negative controls, and monoclonal antibodies against trophoblast specific antigenic markers (anti-Trop 2, NDOG-1, and NDOG-2) used as positive controls for specificity of trophoblast labeling. Tissue controls were provided by Ficoll-paque-separated adult human peripheral blood lymphocytes (PBL), and placental lymphocytes were used as additional internal controls. Results revealed variable but specific labeling of cytotrophoblast cells for class I but not class II MHC antigens at all gestational stages during the first trimester. The incidence of HLA-A,B,C antigen-bearing cytotrophoblast cells in early gestational (5 to 8 wk) placentae was high (75 to 91%) in the minority, but was low to medium (35 to 66%) in placentae at later gestational intervals (9 to 12 wk). The initial antigen density on the labeled cytotrophoblast cells as reflected by the median silver grain counts per unit area was approximately 75% of that noted on adult PBL or placental lymphocytes at 5 to 7 wk. The density then dropped to 50% of the initial level by the eighth week of gestation with no further change up to 12 wk. Syncytiotrophoblast cells revealed no appreciable labeling for either antigen class. This could not be explained by antigen stripping due to the collagenase dispersion procedure; specific labeling was not detectable on the syncytiotrophoblast cell layer in situ in histologic sections after intact chorionic villi had been directly exposed to 125I-labeled monoclonal anti-class I antibody. These results are qualitatively similar to our findings in the mouse in revealing the presence of class I MHC antigens on a major population of trophoblast cells.
The release of platelet-activating factor from human endothelial cells in culture.
Authors: Camussi G , Aglietta M , Malavasi F , Tetta C , Piacibello W , Sanavio F , Bussolino F 
Published: December 2022

Abstract
The release of platelet-activating factor (PAF) from stimulated human endothelial cells (HEC) cultured from normal term, umbilical cord veins is described. HEC in primary cultures released PAF after challenge with A23187, rabbit anti-human factor VIII (RaHu/FVIII), angiotensin II, and vasopressin. HEC subcultures maintained the ability to release PAF in the presence of A23187 and RaHu/FVIII, whereas the release of PAF in response to angiotensin II and vasopressin was not constant and was reduced. Control cultured, smooth muscle cells derived from umbilical cord veins, previously depleted of endothelial cells, did not release PAF under the above-mentioned stimulation. Plastic-adherent or cultured monocytes released PAF with A23187, but not with RaHu/FVIII, angiotensin II, and vasopressin. The release of PAF from HEC in primary cultures required the presence of extracellular cations and the activation of membrane phospholipase A2. PAF release induced by A23187, RaHu/FVIII, angiotensin II, and vasopressin was unaffected by indomethacin, an inhibitor of cyclooxygenase, which, however, favored the release of PAF from HEC stimulated with thrombin, a stimulus that did not affect HEC in the absence of indomethacin. PGI2 inhibited PAF release from stimulated HEC. The relevance of an acetylation process in the biosynthesis of PAF and HEC was supported by the following evidence: 1) the increase in PAF yield in the presence of sodium acetate and, particularly, of acetyl-CoA; 2) the incorporation of [14C]acetate into PAF molecules; 3) the loss of radioactivity and of biologic activity after treatment with phospholipase A2. These results indicate that HEC in culture are able to release PAF and that metabolic pathways similar to those described for leukocytes are involved.
Isolation of guinea pig macrophages bearing surface C4 by fluorescence-activated cell sorting: correlation between surface C4 antigen and C4 protein secretion.
Authors: Auerbach H S , Lalande M E , Latt S , Colten H R 
Published: December 2022

Abstract
Studies of complement (C) secretion by single cells indicate that only a subset of a guinea pig macrophage population is capable of secreting the second (C2) and fourth (C4) components of C. Moreover, cell-surface bound C4 antigen is also found on a proportion of guinea pig peritoneal macrophages. The availability of methods for the isolation of macrophages bearing surface membrane C4 antigen and for the detection of the secretion of C by single cells made it possible to ascertain the relationship between these two subsets. Approximately 25% of the freshly isolated peritoneal macrophages were surface C4 antigen positive. When incubated in conditioned medium containing C4 or incubated in small volumes to increase the concentration of fluid phase C4, the proportion of macrophages bearing surface C4 increased to approximately 80%. The surface C4 antigen was adsorbed from the medium and was predominantly native C4. The proportion of peritoneal macrophages secreting functionally active C4 or C2 was approximately 45% as measured by a hemolytic plaque assay technique. The proportion of C4-secreting cells decreased to 5% after incubation in conditioned medium containing preformed C4, whereas the proportion of C2-producing macrophages was unchanged, i.e., it remained at about 45%. The removal of secreted C4 with F(ab')2 anti-C4 or effectively decreasing C4 concentration by increasing the volume of the culture medium abrogated the decrease in the proportion of C4-secreting cells. Conditioned medium derived from cells genetically deficient in C4 had no effect on the proportion of C4- or C2-producing macrophages. The macrophage population bearing surface membrane C4, isolated by fluorescence-activated cell sorting, contained more than 90% of the C4-producing cells. Cells producing C2 were distributed equally in both subpopulations. Maintenance of the surface C4-positive, C4-producing cells in culture for 12 hr resulted in a decrease in the proportion of C4-secreting cells. Conversely, isolated macrophages initially surface C4 negative and not producing C4, developed the capacity to produce C4 in culture. C4 production in the isolated surface C4-negative population was inhibited by incubation in medium containing preformed C4. These results suggest the presence of a negative feedback effect on C4 secretion that is mediated by extracellular C4.(ABSTRACT TRUNCATED AT 400 WORDS)
High degree of idiotypic cross-reactivity among murine monoclonal antibodies to thyroglobulin.
Authors: Zanetti M , De Baets M , Rogers J 
Published: December 2022

Abstract
The idiotypy of five mouse monoclonal antibodies (mAb) generated against human thyroglobulin (Tg) and reacting with Tg from various species, including murine Tg, was investigated. Rabbit antisera made specific for the idiotype (Id) of three mAb (62, 1.15, and 9.1) were used. By competitive inhibition of homologous Id-anti-Id binding, a surprisingly high degree of Id cross-reactivity was found. The Id determinants on mAb appeared located in or close to the paratope because anti-Id could inhibit their binding to Tg in each instance. Interestingly enough, no true "private" Id could be identified. Id cross-reactivity was found between mAb generated in different fusion experiments and recognizing apparently distinct epitopes on Tg. These results suggest that the immune response to phylogenetically highly conserved epitopes on antigen of internal origin, such as Tg, is idiotypically restricted.
Comparison of binding characteristics of factors B and H to C3b on normal and paroxysmal nocturnal hemoglobinuria erythrocytes.
Authors: Parker C J , Baker P J , Rosse W F 
Published: December 2022

Abstract
To determine if aberrant interactions of the endogenous control proteins with cell-bound C3b contribute to the greater fixation of C3b to paroxysmal nocturnal hemoglobinuria (PNH) erythrocytes when whole serum complement is activated, we compared the characteristics of binding of factors B and H to normal and PNH red cells bearing C3b (EC3b). Factor B binding is homogeneous, there is 1:1 stoichiometry, and the affinity constant at equilibrium for factor B binding is the same for normal and PNH EC3b. In contrast, analysis by Scatchard's method of factor H binding results in a curvilinear plot, the deviation from linearity being exaggerated for the PNH EC3b. The heterogeneity of binding of factor H appears to be a consequence of the nonrandom distribution of C3b about the alternative pathway convertase site. This nonrandom distribution does not induce negative cooperativity but rather effects a biophysical milieu which enhances factor H binding. The greater heterogeneity of binding of factor H to PNH E bearing nonrandomly distributed C3b appears to be due to the presence of a greater proportion of lower affinity binding sites on the PNH EC3b. However, it appears unlikely that this greater heterogeneity of factor H binding contributes to the enhanced fixation of C3b to PNH erythrocytes.
The inhibition of the mitogenic stimulation of B lymphocytes by a serine protease inhibitor: commitment to proliferation correlates with an enhanced expression of a cell-associated arginine-specific serine enzyme.
Authors: Ku G S , Quigley J P , Sultzer B M 
Published: December 2022

Abstract
By the use of diisopropylfluorophosphate (DFP) we have been able to show that the mitogenic stimulation of murine B lymphocytes can be maximally inhibited a few hours before commitment of the cells to DNA synthesis. This inhibition was shown to be specific for a serine enzyme(s). The results of experiments designed to determine the location of this enzyme indicated that the mitogens-linked serine enzyme is not a secreted extracellular factor but is cell-associated. Fluorographic analysis of electrophoretic gels of cell homogenates labeled with [3H]DFP revealed the presence of one major and three minor bands which were arginine-specific serine enzymes. In stimulated cells, there was a clear quantitative difference in the amount of [3H]DFP bound to the major band (approx. 23,000 m.w.) suggesting that this protein may be critical to the progression of the cells through the cell cycle into the S phase of DNA synthesis.
A mechanism for inhibition of luminol-dependent neutrophil chemiluminescence by polyanions.
Authors: Brestel E P , McClain E J 
Published: December 2022

Abstract
Heparin has been reported to have antiinflammatory properties in both experimental animal and human disease states. Previous investigators assumed that the antiinflammatory properties of heparin were related to its anticoagulant effect. In this study we confirm the ability of heparin to inhibit luminol-dependent chemiluminescence by neutrophils stimulated with serum-activated zymosan. This inhibition is due to a combination of the diminished release of myeloperoxidase and the scavenging of the luminol oxidant generated by the myeloperoxidase-H2O2-chloride system. Although the polyanions heparin and dextran sulfate were effective in inhibiting luminol-dependent myeloperoxidase-H2O2-chloride chemiluminescence, the uncharged polysaccharide dextran T500 was without effect. None of the polysaccharides inhibited oxygen consumption by stimulated neutrophils. Additionally, heparin was able to reduce the myeloperoxidase release from zymosan-stimulated neutrophils by nearly 50%. Recent studies have shown that some antiinflammatory drugs scavenge peroxidase-generated oxidants of luminol. Such a property may explain the previously observed antiinflammatory effects of heparin and other polyanions.
Antigen-specific suppressor T lymphocytes (Leu-2a+3a-) in human schistosomiasis japonica.
Authors: Ohta N , Minai M , Sasazuki T 
Published: December 2022

Abstract
Immunoregulatory mechanisms in human schistosomiasis japonica were investigated through in vitro T lymphocyte-macrophage co-culture experiments. High responder T lymphocytes responded to the schistosomal adult worm antigen in the presence of HLA-DR-compatible low responder macrophages, whereas low responder T lymphocytes failed to respond to this antigen even in the presence of HLA-DR-compatible high responder macrophages. This observation strongly suggested that T lymphocytes, but not macrophages, controlled the low responsiveness to the schistosomal adult worm antigen. When high responder lymphocytes were challenged with the schistosomal antigen in the presence of low responder T lymphocytes, low responder T lymphocytes caused an antigen-specific suppression, in a dose-dependent manner, of the responsiveness of high responder lymphocytes. The suppressor T lymphocytes were mitomycin C resistant and were positive for Leu-2a, but were negative for Leu-3a. When Leu-2a+ T lymphocytes were depleted from low responder T lymphocytes, a vigorous response by the Leu-2a-depleted T lymphocytes (Leu-2a-3a+) to the schistosomal adult worm antigen was observed. By adding back the Leu-2a+ T lymphocytes into autologous T lymphocyte subpopulations, the specific response to the adult worm antigen was completely suppressed. These findings clearly demonstrate the existence of Leu-2a+3a- suppressor T lymphocytes that can control low responsiveness to the schistosomal adult worm antigen in man.
Cell receptors for the mammalian reovirus. I. Syngeneic monoclonal anti-idiotypic antibody identifies a cell surface receptor for reovirus.
Authors: Noseworthy J H , Fields B N , Dichter M A , Sobotka C , Pizer E , Perry L L , Nepom J T , Greene M I 
Published: December 2022

Abstract
We have prepared and characterized a syngeneic monoclonal anti-idiotype directed against the idiotype (Id3) of the anti-reovirus type 3 hemagglutinin B cell hybridoma 9BG5. We have shown this monoclonal antibody to be anti-idiotypic in a series of inhibition studies with purified sigma 1 (hemagglutinin) protein and with absorption studies on the idiotypic R1.1 cell line. That the idiotype Id 3 defined by the monoclonal anti-idiotype is distinct from H-2 was demonstrated by its presence on an idiotype-expressing H-2 negative cell line (R1.E). Binding of the anti-idiotype is relatively tunicamycin resistant and pronase/trypsin sensitive, which suggests that the recognition site of the anti-idiotypic receptor is poorly glycosylated. The presence of idiotype-like receptors on reovirus type 3 susceptible neurons may have important implications for the presence of related gene families between neural and lymphoid tissue. The implications of recognition by neuronal cells of an anti-idiotypic monoclonal antibody directed against the reovirus 3 attachment receptor for the pathogenesis of viral-induced auto-immunity are discussed.
Gamma-interferon is the factor in lymphokine that activates human macrophages to inhibit intracellular Chlamydia psittaci replication.
Authors: Rothermel C D , Rubin B Y , Murray H W 
Published: December 2022

Abstract
We have demonstrated previously that mitogen-induced lymphokines activate human monocyte-derived macrophages to inhibit the intracellular replication of Chlamydia psittaci. To identify the factor(s) in crude lymphokines responsible for this antimicrobial effect, we tested human Con A-induced lymphokines for interferon activity. We also attempted to neutralize the lymphokines with a monoclonal antibody directed against human gamma-interferon and examined the ability of partially purified human gamma-interferon to induce macrophage antichlamydial activity. The lymphokine-induced antichlamydial effect was measured by the inhibition of chlamydial inclusion formation in Giemsa-stained macrophage cultures. Our lymphokines were found to be rich in gamma-interferon; treatment of cells for 48 hr before infection with lymphokines containing 300 U/ml of interferon resulted in an 89% inhibition of chlamydial growth. This lymphokine effect was completely abolished by monoclonal antibody against human gamma-interferon, but not by antisera against human alpha- or beta-interferons. In addition, partially purified human gamma-interferon alone induced macrophages to restrict chlamydial growth by 95%. We conclude that it is the gamma-interferon present in human Con A-induced lymphokines that activates monocyte-derived macrophages to inhibit chlamydial replication.
Studies on the mechanism of bacterial resistance to complement-mediated killing. VI. IgG increases the bactericidal efficiency of C5b-9 for E. coli 0111B4 by acting at a step before C5 cleavage.
Authors: Joiner K A , Goldman R C , Hammer C H , Leive L , Frank M M 
Published: December 2022

Abstract
Our previous experiments showed that immune IgG and F(ab')2, but not Fab', mediated serum killing of Escherichia coli 0111B4, strain 12015 (12015), without significantly increasing the extent of terminal complement (C) component attachment to the bacterial surface. We concluded that bactericidal antibody must change either the site or the nature of C5b-9 bacterial attachment. To pursue this possibility, conditions necessary for elution of C5b-9 from the bacterial surface were examined. Forty-two to 44% of 125I-C9 was released from the serum-resistant nonpresensitized 12015 by 1 M NaCl or 0.1% trypsin, compared with the 21 to 24% release from the serum-sensitive presensitized isolate under the same condition. When strain 12015 bearing 125I-C9 was lysed in a French pressure cell, 73.1% of 125I-C9 was released with the capsular fraction if the organisms had not been presensitized. In contrast, on presensitized 12015, 70.2% of 125I-C9 remained associated with the outer membrane after such lysis. These results suggested that C5b-9 was trapped within or underneath the capsule of 12015 in the absence of bactericidal antibody, but that addition of antibody led to C5b-9 insertion into the outer membrane with bacterial killing. The requirement of C components preceding C5 for bacterial killing was next examined. Minimal killing of presensitized 12015 occurred when a terminal C complex was formed by acid activation from purified C5, C6, C7, C8, and C9 in the absence of C3 or earlier components. In contrast, between 1.2 and 3 log killing of nonpresensitized rough Salmonella minnesota and rough E. coli was observed in the same system. Killing of 12015 was examined with bacteria incubated in C5-deficient serum (C5D), followed by washing and the addition of purified C5, C6, C7, C8, and C9 to permit C5b-9 formation. Antibody was added before or after incubation in C5D serum, or after the addition of purified C5-C9. Under conditions of equivalent C3 and C9 binding, significant killing occurred only when antibody was added before incubation in C5D serum. These results show that antibody must be present at or before the time of C5 convertase formation to mediate killing of 12015 by C5b-9. Therefore, antibody is unlikely to be functioning primarily to alter the bacterial surface to expose sites for C5b-9 insertion, nor is the effect of antibody simply to increase C3 and terminal component binding. We postulate that antibody mediates killing of 12015 by localizing C5b-9 around antibody-clustered sites of C3 and C5 convertase formation.
"Nonspecific" immunoenhancing T cells in tumor-bearing mice include anti-idiotypic subsets.
Authors: Behforouz N , Eardley D D , Cerny J 
Published: December 2022

Abstract
Splenocytes from DBA/2 mice inoculated 3 wk earlier with syngeneic P815 mastocytoma tumor cells produce increased numbers of antibody plaque-forming cells (PFC) when stimulated with either sheep red blood cells (SRBC) or phosphorylcholine (PC) on Streptococcus pneumoniae R36a in vitro. The nature of this nonspecific hyperreactivity was investigated in mixed cultures of purified splenic T and B cells. The addition of T cells from P815 tumor-bearing mice (TP815) into the cultures of normal B cells produced a significant enhancement of the PFC response to both SRBC and PC, when compared with the effect of normal T cells added to control cultures. The idiotypic profile of the enhanced anti-PC response was studied by a PFC-inhibition assay with monoclonal antibodies against two distinct idiotopic determinants (Id) of the T15 family. Normal B cells produced greater than 90% of T15 Id-positive (Id+) PFC. Addition of normal T cells diminished the proportion of T15 Id+ PFC to approximately 60%, whereas the rest of PFC were Id-. Addition of the immunoenhancing TP815 cells into the normal B cells cultures elevated the number of both T15 Id+ and Id- PFC responses, proportionally. However, when TP815 cells were first incubated on T15 protein-coated dishes and the non-adherent fraction was added to B cell cultures, the anti-PC PFC response remained enhanced but consisted of predominently T15 Id- PFC. These observations suggest that the early stage of P815 tumor growth activates various populations of specific helper/amplifier T cells including subsets with anti-idiotypic activity and that the generalized increase of antibody response to various antigens in tumor-bearing mice may be regarded as a polyclonal activation of specific T cells.
Sensitized (T6 X RFM)F1 donor B cells are engrafted and synthesize antibodies without further antigenic stimulation in RFM recipients with allogenic host-vs-graft disease.
Authors: Hard R C , Carter W H , Bick P H 
Published: December 2022

Abstract
Host-vs-graft (HVG) syndrome is the fatal disease of altered immunity that may be induced in susceptible strains of inbred mice by the perinatal inoculation of semiallogenic spleen cells. The allogenic HVG reaction causes severe depletion of both the donor F1 and host T lymphocytes, but the B cell system is hyperplastic and serum immunoglobulins (Ig) are markedly elevated. Death is caused by glomerulonephropathy and coagulopathy, both thought to be due to immune complexes. Previous work indicated that RFM host B cells are poor antibody producers, and therefore are an unlikely source of the high levels of serum Ig. The present studies were undertaken to determine if (T6 X RFM)F1 donor B cells could survive the allogenic HVG reaction and then contribute to the hyperglobulinemia. Spleen cells from (T6 X RFM)F1 donors marked with the distinctive T6 chromosome, and pre-sensitized against horseradish peroxidase (HRP) or sheep red blood cells (SRBC), were inoculated into RFM perinates. Cytogenetic studies revealed that replicating (T6 X RFM)F1 donor cells were present in low numbers in the spleens, but high numbers were found in the nodes of RFM hosts. After the transplantation of F1 cells sensitized to HRP, plasmacytoid cells with intracytoplasmic antibody to HRP were detected in the spleens and nodes of RFM recipients. Hemolytic plaque-forming cells and serum hemolysins were detected in RFM hosts that were perinatally inoculated with spleen cells from F1 donors sensitized to SRBC. The results suggested that F1 donor B cells had been engrafted, and then proliferated and matured into antibody-synthesizing cells. Their maturation was attributed to the allogeneic HVG effect, because there was no further exposure of the sensitized F1 donor B cells to antigen after transplantation, and because similar levels of mature F1 donor B cell activity were not found in T6/(T6 X RFM)F1 chimeras, which never develop HVG disease but become highly tolerant. These studies suggest a possible explanation for the seeming paradox of how hyperglobulinemia can develop in HVG mice that respond poorly to primary challenge with thymus-dependent antigen. It is proposed that primed, F1 donor B cells are stimulated into excessive production by the allogeneic reaction, whereas both donor and host B cells are poor primary responders because of the T cell deficiency induced by the same reaction.