bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression of HLA-DR, MB, MT and SB antigens on human mononuclear cells: identification of two phenotypically distinct monocyte populations.
Authors: Nuñez G , Giles R C , Ball E J , Hurley C K , Capra J D , Stastny P 
Published: December 2022

Abstract
The expression of HLA-DR, SB, MB, and MT antigens in different populations of human mononuclear cells was investigated with the use of monoclonal antibodies that recognize distinct human Ia-like antigens. Our results indicate that in man, as previously reported in other species, two phenotypically distinct populations of monocytes or macrophages can be identified on the basis of expression of Class II MHC antigens. Virtually all circulating monocytes displayed determinants associated with HLA-DR, SB, and MT. In addition, a subpopulation of human monocytes expressed MB/DS-associated antigens, as detected with monoclonal antibodies specific for MB1, MB3, and DS-framework determinants. Most B lymphocytes expressed antigens associated with HLA-DR, and the specificities SB2, SB3, MB1, MB3, MT2, and MT3 were also present. Resting T lymphocytes were unreactive with antibodies that recognize all of the Class II MHC antigens tested. T lymphocytes activated by soluble antigen or alloantigens, and expanded in culture, expressed DR, SB, MB, and MT. The majority of the MB/DS+ cells present in the adherent population were monocytes, because they were phagocytic and had the monocyte-specific marker 63D3. The rest of the cells were not identified. They are likely to include mostly B lymphocytes. The presence of other cells, such as dendritic cells, in this subset needs to be determined.
Depressed interleukin 2 receptor expression in acquired immune deficiency and lymphadenopathy syndromes.
Authors: Prince H E , Kermani-Arab V , Fahey J L 
Published: December 2022

Abstract
Because interleukin 2 (IL 2) production and IL 2 receptor (IL 2R) expression are essential steps in T cell proliferation, we undertook to measure these parameters, as defects in one or both seemed likely to account for the reduced proliferative response to mitogen in acquired immune deficiency syndrome (AIDS) and lymphadenopathy syndrome (LAS). Reduced proliferative responses to PHA are a well established feature of AIDS with opportunistic infection (AIDS-OI), AIDS with Kaposi's sarcoma (AIDS-KS), and LAS patient groups. IL 2R expression was significantly reduced in both AIDS groups; a similar trend was observed with the LAS group. Mean levels of IL 2 in culture supernatants for the three patient groups, however, did not significantly differ from controls. IL 2R expression was significantly correlated with proliferation and the Th:Ts ratio in the AIDS-OI and LAS groups, and a good correlation between proliferation and the Th:Ts ratio was also observed. The AIDS-KS group, in contrast, showed no significant correlations between IL 2R expression, proliferation, or Th:Ts ratio. IL 2 levels did not correlate with any of these parameters in any of the patient groups. These findings indicated that poor T cell proliferative responses to mitogen (PHA) are intrinsically related to decreased IL 2R expression in AIDS-OI and LAS. In AIDS-KS, however, a statistically significant correlational relationship between these altered immune parameters is not apparent.
Characteristics of a spontaneous monoclonal thymocytotoxic antibody from New Zealand Black mice: recognition of a specific NTA determinant.
Authors: Bray K R , Gershwin M E , Chused T , Ahmed A 
Published: December 2022

Abstract
Naturally occurring thymocytotoxic autoantibodies (NTA) have been described both in humans and in mice with SLE, and have been reported to be preferentially reactive with T suppressor as compared to T helper cells. However, although NTA has been shown by some groups of investigators to induce autoantibodies in normal strains of mice, other researchers have suggested that NTA has only a minor, if any, role in murine lupus. We have been studying the characteristics of a monoclonal antibody (TC-17) derived from the fusion of 4-mo-old NZB spleen cells with P3-X63-AG8.653 plasmacytoma cells. This monoclonal IgM reagent is cytotoxic for approximately 40% of total thymocytes, 50% of cortical thymocytes, less than 1% of cortisol-resistant thymocytes, 10% of splenocytes and lymph node cells, and less than 3% of bone marrow and fetal liver cells. The thymocytotoxicity can be absorbed by thymocytes but not by brain cells. Although NZB, NZW, NFS, and BALB/c thymocytes all manifest reactivity with TC-17, there was considerable difference between strains with respect to antigen density; NZB thymocytes have the highest density. By FACS analysis, TC-17 occurs independently of Lyt-1, Lyt-2, and T helper cell-specific antigens, and is more prevalent on larger proliferating thymocytes. TC-17 augments the response to SRBC but does not influence responses to TI-1 (TNP-BA) or TI-2 (DNP-Ficoll) antigen and production of LPS-induced B cell colonies. We believe that TC-17 recognizes a new T cell antigen, probably one involved in T cell differentiation. Because this monoclonal NTA reacts with only 40% of thymocytes, and is not absorbed with brain, it would not have been detected in mouse sera by using previously published methods. NTA are a heterogeneous group of autoantibodies; some specificities such as TC-17 went unrecognized in the past, and may be important either for disease pathogenesis or for secondary immunologic abnormalities.
Cleavage of human interleukin 1: isolation of a peptide fragment from plasma of febrile humans and activated monocytes.
Authors: Dinarello C A , Clowes G H , Gordon A H , Saravis C A , Wolff S M 
Published: December 2022

Abstract
Interleukin 1 (IL 1) is a product(s) of mononuclear phagocytes, and has multiple biologic activities that mediate several host responses to infection and inflammation. Highly purified IL 1 activates lymphocytes, induces fever, increases hepatic acute phase protein synthesis, and increases muscle protein degradation. A 4.2 kd peptide has been purified from plasma of febrile humans which also induces muscle proteolysis in vitro (termed proteolysis-inducing factor, PIF). Because IL 1 purified from activated human monocytes induces muscle proteolysis in vitro, studies were performed to determine the relationship of human monocyte-derived IL 1 to plasma-derived PIF. Purified PIF was highly active in the IL 1 thymocyte assay. After gel filtration of plasma from febrile patients, fractions with PIF activity also induced thymocyte proliferation and fever in mice. Thus, it seems likely that the plasma peptide PIF has IL 1 properties and probably represents a small m.w. cleavage product of IL 1. Further studies confirmed this finding. Highly purified 15 kd IL 1, rechromatographed over different gel filtration media, consistently fragmented into a 4 kd peptide with both muscle proteolysis-inducing and lymphocyte-activating properties. The breakdown of the 15 kd IL 1 into biologically active smaller fragments increased with time, and could be accelerated by trypsinization. The monocyte-derived IL 1 fragments were partially destroyed by heat. Highly purified 125I-labeled 15 kd IL 1 also fragmented into subunits, and these radioactive subunits produced fever in mice and were active in the thymocyte assay. Fragmentation of 125I-labeled 15 kd IL 1 was reduced by agents that inhibit proteases. These results indicate that some of the biologic activities of human IL 1 are conserved in small m.w. fragments. These studies also provide evidence that IL 1 may circulate in humans as a 4.2 kd peptide, and that this cleavage product can function as an active mediator of IL 1 effects in the host.
Interleukin 2 receptors on an insulin-specific T cell line: dynamics of receptor expression.
Authors: Reske-Kunz A B , von Steldern D , Rüde E , Osawa H , Diamantstein T 
Published: December 2022

Abstract
Long-term cultured T blasts with specificity for bovine insulin (BK-BI-1.2), which cease growing in IL 2 supplemented medium and require periodic antigenic challenge to resume proliferation, were selected as a model system to analyze the regulation of the growth of activated T cells. The use of AMT-13, a monoclonal antibody (mAb) directed at the murine IL 2 receptor, in indirect binding experiments and in FACS analysis allowed us to examine the time-dependent expression of IL 2 receptors on BK-BI-1.2 blasts after antigenic stimulation. The data reveal a transitory expression of IL 2 receptors, attaining maximal levels on day 2 after antigenic induction and having declined to low levels by day 6. mAb 10-2.16, reactive with I-Ak, did not inhibit T cell-proliferative capacity when the cells were subcultured in IL 2. This result suggests that, once induced to maximal levels by antigen, the transitory expression of IL 2 receptors on the descendent cells is not dependent on the continual presence of antigen-presenting cells. Thus, the progressive loss of IL 2 receptors apparently is not due to a mechanism operating by clearance of receptors from the cell surface on completion of each cell cycle, leading to dependency of the descendent cells on repeated contact with antigen for renewed receptor expression. The disappearance of IL 2 receptors from the surface of antigen-stimulated T cells might provide a basis for the control of immunologic specificity in vivo.
A novel antigenic cell surface protein associated with T200 is involved in the post-activation stage of human NK cell-mediated lysis.
Authors: Burns G F , Werkmeister J A , Triglia T 
Published: December 2022

Abstract
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.
Changes in the Ir gene controlled response phenotypes in mice of the Ap and Ak family of alleles expressing naturally occurring variant molecules.
Authors: Shaut D M , Wakeland E K , Maurer P H , Peck A B 
Published: December 2022

Abstract
Several wild-derived H-2 haplotype mice were recently shown by serology and tryptic peptide fingerprinting to express I-region A molecules closely related to the Ap and Ak molecules of the laboratory strains. To determine if such naturally occurring minor structural variations in the A molecule alter Ir gene-controlled responsiveness, we examined the immune responses of these strains after primary immunizations to three synthetic polypeptide antigens: G60Phe40, GLPhe9, and GAT10. Inbred strains carrying the Ap (or Aq) allele are known to be high responders to G60Phe40 and GLPhe9 but low responders to GAT10. Strains expressing the Ak allele are classified as low responders to G60Phe40 and GLPhe9, but high responders to GAT10. Of seven strains examined belonging to the Ap family, one (B10.CAS2) failed to respond to either G60Phe40 or GLPhe9 as measured by antibody production and T cell proliferation. In addition, two strains (B10.STC90 and W12A) of the Ak family were found to be of responder phenotype to GLPhe9. Both GLPhe9 responses resulted from the introduction of new E beta genes into the I region through naturally occurring intergenic recombination between A beta A alpha and E beta. All strains of mice in the Ak family proved to be of the high responder phenotype in their responses toward GAT10. These results contrast strongly with known patterns of alloreactivity against the variant Ap and Ak molecules.
On the cause and nature of C9-related heterogeneity of terminal complement complexes generated on target erythrocytes through the action of whole serum.
Authors: Bhakdi S , Tranum-Jensen J 
Published: December 2022

Abstract
The binding of C8 and C9 from human serum to target erythrocytes was quantified, and the molecular stoichiometries of C9:C8 within terminal C5b-9(m) complexes were determined. Low doses of serum generated terminal complexes with mean C9:C8 ratios of 2 to 3:1, whereas complexes generated by highest serum doses harbored an average of six to eight C9/C8 molecules. From the collective biochemical and ultrastructural data, we concluded that heterogeneous populations of terminal complexes regularly form on target membranes; those containing high numbers of C9 molecules (greater than or equal to six to eight) exhibit the structure of the classical "lesion", whereas those containing low numbers of C9 do not exhibit this typical structure, although they probably still function as small pores. A major cause for this heterogeneity of the lesions derives from shortage of C9, which is naturally present in a 2 to 1 molar ratio relative to C8 in serum. Generation of terminal complexes harboring high numbers of C9 on erythrocyte membranes is possible in spite of this natural shortage because SC5b-9 does not form in the fluid phase to compete for C9 binding. If interrupted, the process of C9-C9 oligomerization cannot be recontinued, and "incomplete" C5b-9 complexes are unable to bind additional C9 upon reincubation with this component. The demonstrated heterogeneity of terminal complexes with respect to their C9 content may explain the functional heterogeneity of complement lesions observed previously by other investigators.
Functional characteristics of histamine receptor-bearing mononuclear cells. II. Identification and characterization of two histamine-induced human lymphokines that inhibit lymphocyte migration.
Authors: Berman J S , McFadden R G , Cruikshank W W , Center D M , Beer D J 
Published: December 2022

Abstract
Although functional histamine receptors have generally been restricted to those human T lymphocytes expressing suppressor cell functions, more recent evidence suggests that histamine receptor-bearing human T lymphocytes are functionally heterogeneous and capable of other immunomodulatory activities. Lymphocyte chemoattractant factor (LCF) is a cationic sialoprotein with an apparent m.w. of 56,000, whose production is limited to histamine-type 2 receptor-bearing human T cells. LCF is selectively chemokinetic for T lymphocytes, and presumably contributes to the recruitment of unsensitized effector lymphocytes at inflammatory sites. In addition to LCF, Sephadex G-100 gel filtration of histamine-induced lymphocyte supernatants revealed two regions of migration inhibitory activity for human blood T and rat splenic lymphocytes. These regions corresponded to m.w. of 70,000 to 80,000 (LyMIF75K) and 30,000 to 40,000 (LyMIF35K). LyMIF75K had a single pI of 7.5 to 8.0, and its biologic activity was sensitive to trypsin but not to neuraminidase or heat (56 degrees C). LyMIF35K had a single pI of 8.5 to 8.8, and its biologic activity was sensitive to neuraminidase and heat but not to trypsin. These LyMIFs therefore appeared to be distinct from one another and physicochemically different from other migration inhibitory lymphokines. All three lymphokine activities appeared within 4 hr of incubation. The minimum concentration of histamine required to stimulate production of the LyMIF was 10(-6) M. Lymphocytes that did not adhere to a histamine affinity matrix were unable to produce either LyMIF upon subsequent stimulation with histamine or concanavalin A (Con A). Lymphocytes incubated with histamine and diphenhydramine produced LCF but neither LyMIF, whereas cells incubated with histamine in the presence of cimetidine produced both LyMIF but not LCF. These data suggest that a subset of lymphocytes defined by the presence of histamine-type 1 receptors are capable of producing two distinct species of lymphocyte migration inhibitory activity. These cells may contribute to the immobilization of effector T lymphocytes chemokinetically attracted to certain inflammatory sites.
The mechanism of basophil histamine release induced by pepstatin A.
Authors: Marone G , Columbo M , Soppelsa L , Condorelli M 
Published: December 2022

Abstract
Pepstatin A, a natural pentapeptide isolated from cultures of actinomycetes, induced histamine secretion from human basophils in the concentration range of 3 X 10(-7) to 10(-4) M. The characteristics of this reaction were similar to those of f-met-peptide-induced histamine release: pepstatin A-induced release required Ca2+, and the release reaction was complete within 2 min at 22 or 37 degrees C but did not occur at 4 degrees C. There was excellent correlation (r = 0.93; p less than 0.001) between the maximal histamine release induced by pepstatin A and f-met-peptide, but there was no relationship to the capacity of basophils to release with anti-IgE (r = -0.03) or the Ca2+ ionophore A23187 (r = -0.22). Release by pepstatin A was reversibly inhibited by two nonreleasing analogs of f-met-peptide, CBZ-Phe-Met and BOC-Met-Leu-Phe. BOC-Met-Leu-Phe competitively inhibited the effect of both f-met-peptide and pepstatin A on histamine release from basophils. The dissociation constant (Kd) for the BOC-Met-Leu-Phe-receptor complex in both conditions was approximately 10(-6) M. Furthermore, there was complete cross-desensitization between pepstatin A and f-met-peptide, whereas cells desensitized to pepstatin A released normally with anti-IgE and vice versa. A variety of pharmacologic agents had similar effects on both pepstatin A- and f-met-peptide-induced release (e.g., slight inhibition with cyclic AMP-active agents, no enhancement with D2O, and marked enhancement with cytochalasin B). We suggest that the natural pentapeptide pepstatin A induces histamine release from human basophils by activating a cell surface receptor(s) also activated by the synthetic tripeptide f-met-peptide.
Genetics of resistance to the African trypanosomes. III. Variant-specific antibody responses of H-2-compatible resistant and susceptible mice.
Authors: Levine R F , Mansfield J M 
Published: December 2022

Abstract
Genetically based differences in variant-specific immunity to the African trypanosomes were examined. H-2-compatible inbred mouse strains that differed in relative resistance were infected with Trypanosoma rhodesiense clone LouTat 1. Antibody responses to exposed epitopes of the LouTat 1 variant-specific surface glycoprotein (VSG) were measured. Relatively resistant B10.BR mice (H-2k) made predictable IgM antibody responses to the VSG of LouTat 1 which were associated with clearance of the LouTat 1 variant antigenic type from blood; IgG responses to LouTat 1 surface antigen appeared after clearance occurred, and were lower than peak titers of IgM. Intermediately susceptible CBA mice (H-2k) also made predictable IgM and IgG responses which followed the same pattern as the more resistant strain. Peak titers were lower for both Ig classes, however, and a delayed appearance of antibody was correlated with delayed clearance of LouTat 1. In contrast to B10.BR and CBA mice, the susceptible C3H mice (H-2k) failed to make detectable antibodies to LouTat 1 surface antigen and also failed to control the first peak of parasitemia. The absence of immunity in infected C3H mice was selective for antibody to exposed epitopes of LouTat 1 VSG because antibody was detectable to invariant VSG or internal trypanosome antigens. Also, the C3H strain was shown not to be a genetic nonresponder to LouTat 1 surface antigen because VSG-specific antibodies appeared within 1 wk after trypanocidal chemotherapy. Finally, we demonstrated that the susceptibility of C3H mice was not associated with an inability of the mononuclear phagocyte system to clear the parasites because drug cure, passive transfer of immune serum, or sensitization of trypanosomes with antibody all led to trypanosome clearance from blood by the liver. In summary, we show for the first time that major differences in variant-specific immunity occur in MHC-compatible animals after infection with the African trypanosomes.
Immune responses and immunoregulation in relation to human schistosomiasis in Egypt. II. Cimetidine reversal of histamine-mediated suppression of antigen-induced blastogenesis.
Authors: Barsoum I S , Dahawi H S , Gamil F M , Habib M , El Alamy M A , Colley D G 
Published: December 2022

Abstract
The effect of histamine on cell-mediated immune responses of chronic schistosomiasis patients was tested by peripheral blood mononuclear cell (PBMN) reactions to phytohemagglutinin-P (PHA) and soluble schistosomal antigenic preparations derived from eggs (SEA) or adult worms (SWAP). PBMN responses to PHA were suppressed by exogenous histamine (10(-5)M), and the addition of cimetidine (CIM) (10(-4)M), an H2-receptor antagonist, reversed this suppressive effect. Histamine primarily suppressed PBMN responses to suboptimal and optimal PHA concentrations. Exogenous histamine (10(-5)M) also suppressed PBMN responses of 27 schistosomiasis patients to SEA and SWAP, respectively. The addition of CIM (10(-4)M) to suppressed cultures reversed the effect of exogenous histamine. Most importantly, the addition of CIM to schistosomal antigen-induced cultures, without exogenous histamine, significantly increased patients' PBMN responses to SEA and SWAP. The mean optimal increase in SEA responses of 19 patients was 390%. With SWAP-induced responses of 21 patients this increase was 165%. The use of 10(-4)M diphenhydramine (DPH), an H1-receptor antagonist, resulted in general suppression of both PHA-induced and schistosomal antigen-induced PBMN responses. Lower concentrations of DPH lead to variable responses but did not result in consistent abrogation of the histamine-induced suppression. These data imply that an histamine-induced, H2-receptor-mediated suppressor circuit often helps modulate antigen-specific responsiveness of PBMN from patients with chronic schistosomiasis.