bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mouse alloantibodies capable of blocking cytotoxic T cell function. III. Studies of the mechanism of blocking of CML by anti-Lyt-2 antibodies.
Authors: Shinohara N , Taniguchi M , Kojima M 
Published: December 2022

Abstract
Attempts were made to analyze the mechanism of action of anti-Lyt-2 antibody in blocking of CML in the absence of complement. Preincubation of killer cells with anti-Lyt-2 antibody followed by washing was found to abrogate the inhibitory effect of the antibody on target cell lysis, whereas an equivalent amount of the antibody present throughout the culture period caused marked inhibition. The failure of pretreatment with anti-Lyt-2 antibody to cause inhibition of CML might be due to rapid turnover of Lyt-2 molecules. Delayed addition of the anti-Lyt-2 antibody to CML cultures decreased the inhibition observed, which indicated that the antibody must be present during early stages of killing in order to exert significant inhibitory effects. The partitioning of CML according to requirements for divalent cations showed that anti-Lyt-2 antibody acts on killer cells during the Mg++-dependent stage of killing. In addition, the antibody was shown to be capable of reversing certain events occurring during this stage. These data are consistent with a role for Lyt-2 molecules during the antigen recognition stage of cell-mediated lysis. However, the exact function of the Lyt-2 molecule remains unknown.
The induction of a unique procoagulant activity in rabbit hepatic macrophages by bacterial lipopolysaccharides.
Authors: Maier R V , Ulevitch R J 
Published: December 2022

Abstract
Disseminated intravascular coagulation (DIC) is a common occurrence during clinical sepsis and can be induced in the experimental host by LPS. Fibrin deposition in the hepatic microcirculation has been observed within 30 min of i.v. injection of LPS. Because mononuclear phagocytes have been shown to produce a PCA after exposure to LPS, we have examined the ability of a homogeneous population of explanted hepatic macrophages to express PCA. Addition of as little as 10 ng/ml of LPS stimulated a 15- to 20-fold increase in PCA over control culture levels within 7 1/2 hr post-treatment. The PCA was found to be membrane-associated, with approximately 90 to 95% of the total PCA present in the cellular lysates, and more than 85% was inhibited by pretreatment of the cells with the diazonium salt of sulfanilic acid, an inhibitor of ecto-enzymes. In contrast to tissue thromboplastin produced by other M phi populations, the H-M phi PCA was found to be markedly sensitive both to heat inactivation at 56 degrees C and to inhibition by 1 mM DFP. Additionally, assays involving both a 1-stage coagulation test as well as an enzyme assay with a Factor Xa-specific substrate (using normal and deficient human plasmas) demonstrated that the H-M phi PCA appears to activate Factor X directly. Unlike tissue thromboplastin, the H-M phi PCA is non-dependent of Factor VII activation. These studies: 1) demonstrate the LPS induces a unique PCA in the H-M phi, and 2) support a role for the H-M phi in the initiation of DIC in endotoxemic shock.
Effect of Leucogenenol on recovery from immunosuppressin by anti-lymphocyte globulins.
Authors: Rice F A , Koo M J 
Published: December 2022

Abstract
Daily treatment of rats with the thymothyroid hormone leucogenenol after their immunosuppression with anti-lymphocyte globulins causes the rats to regain their immunocompetency after 7 days of treatment, in contrast to well over a month, which is required for untreated controls. Immunocompetency was mesured by the ability of the rat to respond to the injection of sheep erythrocytes with the formation of normal concentrations of antibody-forming cells in their lymphoid tissues and normal titers of hemolysins in their serum. These results indicate that leucogenenol increases the rate of development of T cells, as well as B cells, from committed precursors.
Biochemical evidence for trans complementation of structural genes in the expression of I-E antigens in F1 hybrids.
Authors: Plunkett M L , David C S , Freed J H 
Published: December 2022

Abstract
Analysis of the tryptic peptides obtained from the Ia.7-positive, "I-E" antigens produced by 4 F1 combinations derived from strain A.TFR5 has provided biochemical confirmation that I-A/I-E gene complementation can occur in the transconfiguration. The data obtained support the concept that structural genes, as opposed to regulatory genes, are the essential elements involved in this complementation and support the assignment of the I-E subregion of strain A.TFR5 as I-Ek. The data support the following assignments of the genes encoding the E beta chains: B10.A(4R) as E beta k, B10.A(5R) as E beta b, and B10.HTT as E beta s. Finally, data are presented demonstrating that the E beta chain derived from the recombinant D2.GD strain partially differs from the E beta d chain derived from a conventional H-2d haplotype strain, B10.D2.
The Qa-1 alloantigens. I. Identification and molecular weight characterization of glycoproteins controlled by the Qa-1a and Qa-1b alleles.
Authors: Cook R G , Rich R R , Flaherty L 
Published: December 2022

Abstract
Splenocytes from the Qa-Tla congenic strain pairs, A and A-Tlab or B6 and B6-Tlaa, were biosynthetically labeled with 3H-amino acids or cell surface labeled with 125I. Membrane proteins were solubilized with detergent and chromatographed on lentil lectin-Sepharose, and the resulting adherent pools were immunoprecipitated with antisera specific for determinants controlled by the Qa-1a and Qa-1b alleles, Qa-1.1 and Qa-1.2, respectively. Polyacrylamide gel electrophoresis analysis of immunoprecipitates from biosynthetically labeled preparations indicated that both the Qa-1.1 and Qa-1.2 antigens were glycoproteins with a m.w. of approximately 46,000. Qa-1.2 isolated from radioiodinated spleen cells similarly had a m.w. of 46,000. Analysis of anti-Qa-1.1 precipitates from 125I-labeled Qa-1a lysates demonstrated in addition to the 46,000 m.w. component, an electrophoretically heterogeneous protein or series of proteins in the m.w. range of 55,000 to 75,000. The specificity of these reactivities was shown by both antiserum and genetic control immunoprecipitations. These findings indicate that the Qa-1.1 and Qa-1.2 antigens are cell surface glycoproteins that are distinct from the TL antigens, and suggest a further complexity at the Qa-1--Tla locus.
Accessory cell stimulation of T cell proliferation requires active antigen processing, Ia-restricted antigen presentation, and a separate nonspecific 2nd signal.
Authors: Germain R N 
Published: December 2022

Abstract
The roles of Ia+ accessory cells in H-2-restricted stimulation of antigen-specific T cell proliferation were explored in an in vitro model. L-glutamic acid60-L-alanine30-L-tyrosine10-(GAT) primed BALB/c nylon wool-passed T cells were depleted of Ia+ antigen-presenting cells (APC) by treatment with monoclonal anti-Ia antibody plus complement. Such cells failed to respond to soluble GAT, or to soluble GAT in the presence of phorbol myristic acetate (PMA), which is known to stimulate production of, or replace, IL-1 in vitro. Addition of gamma-irradiated syngeneic spleen cells reconstituted the response to soluble GAT, but addition of ultraviolet (UV) light-irradiated spleen cells did not, even in the presence of PMA. Preincubation of cells with GAT for 24 hr, followed by washing, then gamma irradiation, generated a cell population able to stimulate GAT-primed T cells to proliferate. The same pulsed cells exposed to UV irradiation failed to stimulate T cell responses unless PMA was added to the cultures. The relevant cells in this UV-irradiated population are Ia+. It is concluded that a finite period of time for interaction of metabolically intact APC with antigen is required before creation of an appropriate (Ia + antigen) signal recognized by the T cell. In addition to such Ia-restricted antigen presentation, however, a 2nd nonspecific signal, again requiring metabolically active APC for elaboration, is necessary for detectable T cell activation. These studies thus define 3 separable activities of APC during the process of H-2 restricted T cell activation.
Immunoglobulin glycopeptides from an IgG2b-producing mouse myeloma cell line and from variant cell lines.
Authors: Weitzman S , Portmore J 
Published: December 2022

Abstract
A mouse myeloma cell line, 45.6.3, produces an IgG2b immunoglobulin (Ig) with 2 carbohydrate attachment sites on the heavy chains. One site is in the CH2 domain and the other in the VH region. The oligosaccharides at each site have different structures. The ratio of radioactive glucosamine incorporated in the VH compared with the CH2 oligosaccharide is approximately 1 to 3. In an attempt to understand this observation further, variant cell lines derived from 45.6.3 were isolated and their Ig were characterized. A ricin-resistant line, R4R1.5, has the same 2 attachment sites as the wild type, but the ratio of radioactive glucosamine in VH compared with CH2 was 1:1 and not 1:3 as in the wild type. This alteration is most probably due to cellular factors, since the Ig protein is unchanged. The M3.11 cell line produces an Ig with a polypeptide deletion involving the CH3 domain. In this Ig, a 3rd carbohydrate attachment site can be demonstrated. The percentage of radioactivity glucosamine in the CH2 domain compared with the total Ig is about 25% instead of 75% as in the wild type. These results suggest that the extent of glycosylation of different sites on Ig can be affected by both cellular factors and structural changes in the Ig protein.
Stimulation with autologous lymphoblastoid cell lines: lysis of Epstein-Barr virus-positive and -negative cell lines by two phenotypically distinguishable effector cell populations.
Authors: Zarling J M , Dierckins M S , Sevenich E A , Clouse K A 
Published: December 2022

Abstract
Human lymphocytes, stimulated in vitro for 6 days with x-irradiated or glutaraldehyde-treated autologous Epstein-Barr (EB) virus-transformed lymphoblastoid cell lines (LCL), are cytotoxic for autologous and allogeneic EB+ LCLs as well as for several EB- cell lines that are also susceptible to lysis by interferon-activated natural killer (NK) cells. To determine whether the apparent nonspecific lysis mediated by LCL-stimulated cells is due to a mixture of effector cells directed against different target cells, advantage was taken of our recent finding that monoclonal antibody OKT8 reacts with human cytotoxic T lymphocytes but not with NK cells or NK-like cells generated in mixed leukocyte cultures. The depletion of OKT8+ cells from LCL-stimulated cultures by treatment with OKT8 and complement abolished or markedly depleted cytotoxicity against all EB+ target cells tested, whereas cytotoxicity against EB-, NK-sensitive cell lines including K562, MOLT-4 and HSB-2 was not or only minimally reduced. These results indicate that stimulation with autologous LCL results in the generation of OKT8+ cytotoxic T lymphocytes that lyse EB virus-transformed LCL and OKT8- NK-like cells that lyse EB-, NK-sensitive cells.
Effect of murine tumors upon delayed hypersensitivity to dinitrochlorobenzene. III. In vivo activity of the nonspecific suppressor cell.
Authors: Jessup J M , Macek C M , Kahan B D , Pellis N R 
Published: December 2022

Abstract
Tumor-induced immunosuppression was investigated in an in vivo model of delayed hypersensitivity (DH) to the chemical sensitizer, dinitrochlorobenzene (DNCB). DH to DNCB as measured in a footpad assay was decreased in C3H/HeJ mice bearing MCA-F, a 3-methylcholanthrene-induced syngeneic fibrosarcoma. Suppressor cells from the spleens of tumor-bearing mice inhibited the induction of DH to DNCB in otherwise normal syngeneic C3H/HeJ recipients. Ten million spleen cells (SpC) harvested from mice bearing MCA-F for 10 days and adoptively transferred to tumor-free mice at the time of sensitization with DNCB suppressed the response to the sensitizer. The suppressor cells were macrophages, since they were adherent to plastic, removed by treatment with a magnet after phagocytosis of carbonyl iron, resistant to exposure to gamma radiation and to treatment with anti-Thy 1.2 serum and complement. Further, the nonspecific suppressor cells were activated by progressive tumor growth rather than by induction of tumor-specific immunity using irradiated tumor cells. Titration studies revealed that suppression of DH occurred with the transfer of as few as 10(6) SpC. Thus, nonspecific suppressor cells are effective at inhibiting in vivo DH to DNCB and suggest that nonspecific suppression in the intact host occurs through mechanisms different from those involved in suppression in vitro.
Natural killing (NK) and antibody-dependent cellular cytotoxicity (ADCC) in specific pathogen-free (SPF) miniature swine and germfree piglets. III. Two distinct effector cells for NK and ADCC.
Authors: Huh N D , Kim Y B , Amos D B 
Published: December 2022

Abstract
Effect of "anti-NK" sera on NK and ADCC activities was examined to study further the relationship between the effector cells for NK and ADCC in specific pathogen-free miniature swine. An appropriate dilution of "anti-NK" sera that had no effect on ADCC activity not only inhibited NK activity but also eliminated NK cells in the presence of C which supports the presence of NK cells distinct from K cells for ADCC.
Ia specificities on parental and hybrid cells of an I-A mutant mouse strain.
Authors: Hansen T H , Walsh W D , Ozato K , Arn J S , Sachs D H 
Published: December 2022

Abstract
Splenic B cells and B cell blasts from the I-A mutant mouse strain B6.C-H-2bm12 were tested by serology with a series of new monoclonal anti-Iab antibodies. Four out of 5 of those monoclonal antibody-defined specificities that are determined by wild-type I-Ab antigens were undetectable on B6.C-H-2bm12 cells. Specificities both present and absent on mutant cells appear to be determinants on the same wild-type molecule, as indicated by sequential precipitation experiments with soluble H-2b antigens. The lack of expression of certain Ia specificities on mutant cells was found not to be the result of disparate control by the Xid gene, which was previously shown to control the expression of Ia.W39, another specificity absent in B6.C-H-2bm12 mice. Serologic testing of Ia specificities on cells and blasts from F1-hybrid mice suggested that the Iabm12 antigens are codominantly expressed, indicating a failure to detect trans regulation or complementation of the mutant phenotype. Another monoclonal antibody-defined Ia specificity dependent on the expression of the E beta polypeptide was normally expressed in B6.C-H-2bm12 mice. These data thus suggest that the lesion of these mutant mice occurred in the A alpha and/or A beta structural gene, resulting in the loss of several Ia specificities.
Membrane expression of Fc-receptors in cultured leukemic cell lines. I. Induction of Fc-receptor in undifferentiated types of cells after passive modulation of lipid viscosity.
Authors: Kyoizumi S , Kannagi R , Masuda T 
Published: December 2022

Abstract
The role of lipid environment of plasma membrane for the expression of Fc receptor (gamma) (FcR gamma) were studied by physicochemical modification of the membranes of myeloid leukemia cell line cells, M1. Sterol binding polyene antibiotics such as amphotericine B or filipin inhibit the expression of FcR gamma during the differentiation of M1- cells by the CM obtained from the culture of mouse embryonic fibroblasts, suggesting the possible involvement of cholesterol molecules in the induction mechanism of FcR gamma. Low-temperature incubation at either 20 degrees C or 4 degrees C results in the increment of their membrane microviscosity, when tested by the fluorescence depolarization method, in company with the appearance of FcR gamma on approximately 60% of M1 cells when assayed by the EA-rosetting method. FcR gamma is also induced on approximately 40% of M1- cells by incubating cells with cholesterol-phosphatidyl-choline liposomes with the concomitant increase of their membrane microviscosity. Nevertheless, no phagocytosis of EA is observed in these cells treated with such physicochemical procedures. These findings imply that FcR gamma is embedded in the membrane of M1- cells and that physicochemical modification of the membrane lipid bilayers can induce the FcR gamma independent on their functional differentiation marked by the expression of phagocytic activity.
Inhibition of T cell-mediated functions by MVM(i), a parvovirus closely related to minute virus of mice.
Authors: Engers H D , Louis J A , Zubler R H , Hirt B 
Published: December 2022

Abstract
A purified preparation of MVM(i), a murine parvovirus closely related to minute virus of mice (MVM), was found to inhibit various functions mediated by murine T cells in vitro. Addition of MVM(i) virus to secondary allogeneic mixed leukocyte cultures resulted in the inhibition of both lymphocyte proliferation (3H-thymidine incorporation) and the generation of cytolytic T lymphocyte activity but not interferon production. MVM(i) virus also inhibited the growth and cytolytic activity of several cloned, long-term Lyt-2+ cytolytic T cell lines. Furthermore, the antigen-induced proliferative responses of parasite- (Leishmania) specific Lyt-1+ T cells in vitro was abrogated by the addition of MVM(i) virus to the culture. Finally, the suppression of an in vitro antibody response to SRBC by MVM(i) virus was the result of the inhibition of T helper cells required for the B cell response. These suppressive effects were specific for MVM(i); parallel studies in which the prototype MVM parvovirus was used showed no significant inhibition in the various systems tested.
Accessory cells in the in vitro generation of type C virus-specific T killer lymphocytes. II. Demonstration of a T helper cell in the spleen of in vivo primed mice.
Authors: Gomard E , Wybier-Franqui J , Simmler M C , McKenzie I F , Levy J P 
Published: December 2022

Abstract
The existence of a helper T cell cooperating with cytolytic T lymphocytes (CTL) in cell-mediated anti-tumor responses specific for the virus-induced FMR antigens can be demonstrated by using unprimed thymocytes as CTL precursors and in vivo primed irradiated spleen cells as helper. The helper T cells express Thy-1.2 and Lyt-1.2 antigens at their surface, but not Lyt-2.2. The helper function required the presence of macrophages to be detected, is antigen specific, and appears unusually radiosensitive compared with previously described helper T cell function.
T cell-mediated cytotoxicity induced by Listeria monocytogenes. I. Activation of Listeria antigen-responsive T cells.
Authors: Woan M C , McGregor D D 
Published: December 2022

Abstract
Soon after rats are infected with Listeria monocytogenes (LM), Listeria antigen- (LMA) responsive lymphocytes are delivered to the animal's thoracic duct. These LM-responsive lymphocytes can be restimulated in vitro by LMA to generate cells that have a potent cytolytic capability. The activation of LMA responsive lymphocytes is immunologically specific and dependent upon the activity of histocompatible accessory cells. Neither cell-free LMA nor LMA-pulsed allogeneic accessory cells can promote a significant cytotoxic response by negatively selected responder lymphocytes. LM-dependent cytolytic lymphocytes differ from natural killer (NK) cells inasmuch as their activation is not facilitated by interferon (IF). Likewise, supernatants from cultures containing specifically sensitized thymus-derived (T) lymphocytes and histocompatible LMA-pulsed accessory cells fail to augment (day 2 and day 3 supernatants actually inhibit) the activation process. The results imply that the successful activation of LM dependent cytolytic lymphocytes requires the cooperative interplay of responder T cells and specific-antigen-pulsed accessory cells.
Suppression of parasite antigen-specific lymphoid blastogenesis in African trypanosomiasis.
Authors: Charoenvit Y , Campbell G H , Tokuda S 
Published: December 2022

Abstract
Inbred C57BL/6J mice were infected with either Trypanosoma rhodesiense organisms of Walter Reed Army Trypanozoon antigenic type 3 or 5 (WRATat 3 or WRATat 5) or were immunized with soluble trypanosomal antigens. Spleen cells obtained from immunized hosts undergo blastogenesis, measured by thymidine incorporation, when exposed to trypanosomal antigens in vitro. Spleens obtained from mice infected with T. rhodesiense organisms do not respond or respond only minimally to trypanosomal antigens in vitro. Spleen cells of infected mice suppress the trypanosomal antigen-induced proliferative response of spleen cells from immunized mice in co-culture experiments. The suppressive activity was found in both the plastic adherent and plastic nonadherent spleen cell populations. The in vitro responses of normal spleen cells to LPS and Con A were also suppressed by spleen cells obtained from infected mice.
Immune responsiveness of SM/J mice: hyper NK cell activity mediated by NK 1+ Qa 5- cells.
Authors: Clark E A , Engel D , Windsor N T 
Published: December 2022

Abstract
Compared with other inbred strains, SM/J mice have both abnormally high responses to B cell mitogens and hyper NK cell and K cell activity. This hyper NK cell activity is evident even in older SM/J animals, and a high proportion of SM/J nylon-nonadherent lymphocytes that bind target cells also have lytic activity. The SM/J NK cells are NK 1+, Qa 5-, but H-2v identical B10.SM congenic mice have normal NK activity and NK 1+, Qa 5+ NK cells. Together these results suggest the elevation of NK cell activity in SM/J mice is due to chronic activation or maintenance of a Qa 5- NK cell subset. The genetic control of B cell responsiveness and NK cell activity was examined in (B6 x SM)F1 x B6 backcross progeny and (A x SM)F2 intercross mice. No correlation between NK levels and mitogen responsiveness was detected. NK levels in SM/J mice appear to be under polygenic, non-H-2 gene control.
Demonstration of a circulating suppressor factor of thymocyte proliferation during endotoxin fever in humans.
Authors: Dinarello C A , Rosenwasser L J , Wolff S M 
Published: December 2022

Abstract
Sub-pyrogenic levels of human leukocytic pyrogen (LP) have been shown to enhance phytohemagglutinin-induced murine thymocyte proliferation. It was concluded that LP is similar to lymphocyte-activating factor (LAF). Since endotoxin stimulates the production of LP and LAF, we attempted to employ in vitro thymocyte proliferation to detect circulating LP/LAF in 12 normal human subjects during experimental endotoxin fever. Sera obtained before and during fever were first mixed with an immunoadsorbent that binds human LP/LAF, and then the dissociated material was added to thymocyte cultures. Material derived from sera obtained during the maximum fever (3 to 4 hr after endotoxin) was markedly suppressive for thymocyte proliferation in vitro. The appearance of this suppressive effect correlated with the profound lymphopenia observed in the subjects. This suppressor factor(s) was nondialyzable and was destroyed at 70 degrees C, and its suppressive effects inhibited the lymphocyte-activating property of LP/LAF. In addition, the suppression of PHA responses did not appear to be modulated by prostaglandin synthesis. The results demonstrate that a factor circulates during endotoxin fever in humans that suppresses in vitro thymocyte proliferation.