bluuebunny/crossref_metadata_2025_split huggingface dataset:
Acute-phase reactants of mice. II. Strain dependence of serum amyloid P-component (SAP) levels and response to inflammation.
Authors: Mortensen R F , Beisel K , Zeleznik N J , Le P T 
Published: December 2022

Abstract
Serum amyloid P-component (SAP) is an acute-phase reactant of mice that occurs at baseline concentrations that vary over a 10-fold range among several common inbred mouse strains. The endogenous SAP levels of all strains increased to 180 to 230 micrograms/ml 24 h after an inflammatory stimulus of either thioglycollate (TG) or lipopolysaccharide (LPS). The C57BL/6J and C57BL/10SN strains displayed 10-fold increases in SAP concentration during acute inflammation, whereas the A/J and DBA/2J strains increased levels by only 20 to 40%. These strains were therefore designated high and low SAP responders, respectively. Testing for H-2 linkage of endogenous SAP levels by using several H-2 congenic lines derived from the C57BL/10, C3H, A, and BALB parental backgrounds indicated that the levels were only weakly influenced by the H-2 complex and were influenced much more strongly by the non-H-2 background genes. F1 hybrids (B6AF1 and B6D2F1) of high and low responder strains displayed a high SAP response similar to that of C57BL/6J mice. Because IL 1-containing macrophage supernatants and semi-purified human IL 1 were previously shown by us to induce SAP in vivo, we titrated IL 1 as LAF activity in supernatants from LPS-activated macrophages from the different mouse strains. Macrophages from the high SAP responder strains displayed significantly higher IL 1 activity than macrophages from the low SAP responder strains. LPS-unresponsive C3H/HeJ or C57BL/10Sc mice did not respond to LPS with an increase in SAP synthesis. Adoptive transfer of the SAP response to C57BL 10Sc mice by using early (90 min) acute-phase sera from the different strains indicated that higher SAP inducer activity was present in the latent phase sera from the high SAP responder strains. The identification of high and low SAP responder strains should aid in determining the biologic role of this acute-phase reactant.
Natural and antibody-dependent cell-mediated activity against Salmonella typhimurium by peripheral and intestinal lymphoid cells in mice.
Authors: Nencioni L , Villa L , Boraschi D , Berti B , Tagliabue A 
Published: December 2022

Abstract
Cell-mediated immune responses were assessed employing a 2-hr in vitro cytotoxicity assay against S. typhimurium. It was observed that lymphocytes from GALT as well as from peripheral lymphoid organs possessed natural antibacterial activity, whereas macrophages were devoid of this spontaneous activity. The distribution of this newly described natural activity was PPL greater than MnL greater than IEL = SpL = PBL greater than PoL; this did not correlate with the organ distribution of NK activity against YAC-1 tumor cells, which was PBL greater than SpL = IEL greater than MnL = PoL = PPL. Moreover, the phenotype of the splenic effector cell of the natural activity against S. typhimurium showed some differences from that of NK activity. In fact, both these cells were asialo GM1+, Fc-receptor+, nonadherent, and nonphagocytic, but the former was Thy-1.2- and the latter Thy-1.2+. The effector cell of the natural antibacterial activity in the Peyer's patches had the same phenotype as the splenic one. It was then observed that the antibacterial activity could be augmented by the addition of immune antibodies against S. typhimurium. This was particularly evident employing IEL, SpL, and PBL as effector cells, whereas PPL and MnL did not show any antibody-dependent antibacterial activity. Furthermore, these last two populations could not mediate ADCC against CRBC. Employing selective methods to deplete cell populations, we observed that, at least at the splenic level, there is also a cell that differs in its phenotypic characteristics from that mediating natural antibacterial activity but that plays a role in the antibody-dependent reactions. In conclusion, these results suggest that natural and antibody-dependent antibacterial mechanisms might be important in defense against S. typhimurium, particularly at the gastrointestinal level, where many bacterial infections first take place and begin to interact with the host immune system.
Pichinde virus-specific cell-associated suppression of primary footpad swelling in an inbred strain of Syrian hamsters.
Authors: Chan M , Clark D , Rawls W E 
Published: December 2022

Abstract
Pichinde virus causes a lethal disease after i.p. inoculation of adult MHA hamsters; other strains of Syrian hamsters are resistant to this lethal infection. During studies of cell-mediated immune responses to Pichinde virus, it was noted that MHA hamsters survived infection when the virus was given in the footpad. However, unlike the resistant LSH and LVG strains of hamsters, the MHA hamsters did not manifest a footpad swelling response. Failure of the MHA hamster to respond to a footpad inoculation of Pichinde virus was shown to be virus-specific and appeared to be mediated by a cell-associated suppressor mechanism.
Immunization with idiotypic immunoglobulin protects against development of B lymphocytic leukemia, but emerging tumor cells can evade antibody attack by modulation.
Authors: Stevenson F K , Gordon J 
Published: December 2022

Abstract
Immunization of strain 2 guinea pigs with idiotypic IgM obtained from serum of animals in the terminal phase of the L2C leukemia produced high levels of circulating anti-idiotypic antibody that was cytotoxic for the tumor cells in the presence of syngeneic C. Such animals showed good protection against injected tumor cells, but after a long delay, leukemia did develop. As tumor cells appeared in the blood, anti-idiotype was consumed, but the cells displayed little or no surface Ig and could not be killed in vitro by anti-idiotype and C. However, as serum antibody levels fell, the cells displayed increasing amounts of surface IgM lambda of the same idiotype and regained their susceptibility to the antibody and C in vitro. It appears, therefore, that the ability of tumor cells to modulate their target idiotype can present a considerable problem for antibody-mediated attack.
Regulation of the immune response to tumor antigens. IX. In vitro Lyt-1+2- cell proliferative responses to cellbound or subcellular tumor antigen.
Authors: Carter R H , Drebin J A , Schatten S , Perry L L , Greene M I 
Published: December 2022

Abstract
We investigated the cellular basis of immune reactivity to the S1509a fibrosarcoma in tumor-immune A/J mice. In a Winn assay, immune Lyt-1+2- T cells are capable of retarding S1509a tumor growth in naive A/J mice. In vitro proliferation to S1509a is also mediated by tumor-immune Lyt-1+2- T cells. This response is specific to the immunizing tumor and appears 5 to 7 days after reexposure to the tumor in vivo. Proliferation also requires the presence of a population of adherent cells. In fact, adherent peritoneal exudate cells pulsed with tumor membrane fragments derived from S1509a cells can stimulate proliferation. Proliferation is blocked by the addition of anti-I-Ak monoclonal antibody to the culture medium without complement or by treatment of the responder population with anti-I-Ak and complement. In vitro responsiveness is also inhibited by the presence of tumor-specific suppressor T cells in vivo. These observations suggest in vitro proliferation may provide a potential means of defining tumor antigens and cell-surface structures involved in tumor immunity.
Evidence for thymic regulation of autoimmunity in BXSB mice: acceleration of disease by neonatal thymectomy.
Authors: Smith H R , Chused T M , Smathers P A , Steinberg A D 
Published: December 2022

Abstract
BXSB mice spontaneously develop an autoimmune syndrome characterized by autoantibody production, immune complex renal disease, and lymphadenopathy containing B cells. The male BSXB mouse has a rapid onset of disease that is determined by defective stem cells. Although the B cell hyperactivity has been traced to the stem cell, previous studies did not evaluate the T cells of BXSB mice with regard to a role in modifying their natural history. The present study was carried out in an attempt to determine whether or not thymic regulation played a role in modulating the stem-B cell abnormalities in BXSB mice. It was found that neonatal thymectomy led to a marked increase in autoantibody production (anti-RBC, anti-DNA), a dramatic increase in lymphadenopathy, and worsening of renal disease. Flow cytometric analysis of the lymph node cells from intact and thymectomized mice demonstrated a loss of Lyt-2+ cells from the thymectomized mice and an increased proportion of Ly-1+, Thy-1.2- cells. These results indicate that although the B cell hyperactivity of BXSB mice is determined by a marrow stem cell defect, thymic regulation normally serves to dampen that B cell hyperactivity; neonatal thymectomy reduces the thymic regulation of autoimmunity in the BXSB males and leads to excessive B cell numbers and function.
Constitutive production of a factor supporting B lymphocyte differentiation by a T cell hybridoma.
Authors: Elkins K , Cambier J C 
Published: December 2022

Abstract
To investigate the role of soluble T cell products during B cell differentiation more fully, we have produced T cell hybridomas by the fusion of normal helper T cells with the T cell lymphoma BW5147. In this report we describe the production of one such hybrid, 14G3, the subclone 14G3.1F2, and the functional activity of the constitutive product. The hybrid supernatant acts exclusively in antigen-nonspecific, but antigen-dependent, promotion of B cell differentiation. It is optimally effective in the presence of small amounts of EL4 supernatant. It does not itself contain any detectable IL 2 or BCGF or interferon activity, however. 14G3.1F2 activity is probably an important component of the conventional TRF preparations produced by mixed lymphocyte populations, and will be useful in further dissection of the contributions of different soluble T cell products to B cell differentiation.
Identification of human natural killer soluble cytotoxic factors (NKCF) derived from NK-enriched lymphocyte populations: specificity of generation and killing.
Authors: Farram E , Targan S R 
Published: December 2022

Abstract
Activated natural killer (NK) cells were induced by stimulation of normal peripheral blood lymphocytes with a B cell line for 5 days or by interferon activation for 1 hr. They were enriched for large granular lymphocytes (LGL) by separation on Percoll density gradients. Supernatants were obtained from incubation mixtures of LGL and NK-sensitive target cells (MOLT-4 or K562). Although some lysis could be detected at 16 hr, optimal NK-sensitive target cell lysis by this supernatant was evident after 40 hr incubation by using a microcytotoxicity assay and trypan blue exclusion. Supernatants derived by co-culture of NK targets with either NK-depleted cell populations or NK cells alone were not cytolytically active. Target cell requirements for both the generation and cytotoxic activity of NKCF were specific. That is, only the NK-sensitive target cells MOLT-4 and K562, and not the NK-resistant cells YAC-1, EL4, IM9, and Raji, could induce release of, or be lysed by, NKCF. Furthermore, the requirement for both Ca2+ and Mg2+ in the generation of NKCF suggests that both target cell binding and initiation of programming for lysis are required for its release. NKCF lytic potential was stable for 2 mo at -20 degrees C and partially stable at 60 degrees C. NKCF activity could be substantially removed by prior absorption on the NK-sensitive target cells, K562 or MOLT-4, but not Raji or IM9 (resistant) cells. Therefore, it appears that the specificity of this cellfree lytic factor depends on its recognition of, or its being recognized by, appropriate target cells. The properties of NKCF will enable the study of the mechanism involved in the lethal hit of NK cell-mediated cytotoxicity.
Activation of the classical pathway of human complement by a human monoclonal IgE, IgE(DES).
Authors: Saint-Remy J M , Magnusson C G , Masson P L 
Published: December 2022

Abstract
Activation of the classical pathway of human complement by monoclonal IgE from patient DES was demonstrated by using IgE(DES) coupled to latex particles. This material depleted human serum of C1 and C4 hemolytic activities. In addition, C3bi was deposited in a calcium-dependent way onto the insolubilized IgE as shown by the agglutination of latex by conglutinin. The alternative pathway was also activated. These anticomplementary activities were dose and time dependent. Moreover, we confirmed that another monoclonal IgE, IgE(PS), activated the alternative pathway exclusively. Particular attention was paid to exclude contamination by other immunoglobulins or C-reactive protein, generation of artifacts due to the chemical coupling, and the presence of proteolytic enzymes in the IgE(DES) preparation. Moreover, evidence is also presented against the involvement of IgG or IgM anti-IgE autoantibodies that could activate the classical pathway after their binding to insolubilized IgE(DES). Although one cannot exclude the possibility that IgE(DES) or IgE(PS) are abnormal proteins, these findings suggest the existence of an isotypic or allotypic variation of IgE.
Arachidonic acid metabolism in the murine eosinophil. III. Effect of nonsteroid anti-inflammatory drugs on lymphokine-directed eosinophil migration in vivo.
Authors: Rand T H , Clanton J A , Colley D G 
Published: December 2022

Abstract
In vitro studies of murine eosinophils indicated that lymphokine-stimulated metabolism of arachidonic acid by a lipoxygenase pathway was required for a migration response. In this study we tested the effects of drugs that affect arachidonic acid metabolism on lymphokine-dependent eosinophil accumulation in vivo by the use of 111In-labeled eosinophils. Indomethacin at different dosages either stimulated (1 mg/kg) or partially inhibited (5 to 25 mg/kg) eosinophil accumulation. Aspirin had no significant effects in doses up to 50 mg/kg. BW755C, a drug that inhibits both cyclooxygenase and lipoxygenase, dramatically inhibited eosinophil accumulation at 25 to 125 mg/kg. Pretreatment in vitro of 111In-labeled eosinophils with some drugs known to inhibit lipoxygenase reduced their subsequent accumulation at a lymphokine-injected site in vivo, but the high concentrations required for inhibition suggested that the effects of the drugs were at least partially reversible. Pretreatment with indomethacin did not inhibit the ability of 111In-labeled eosinophils to accumulate at the site of lymphokine injection in vivo. It may be anticipated from these results that drugs inhibiting lipoxygenase will have critical effects on manifestations of immunologic reactions that recruit eosinophils.
Antibodies reactive with liposomal phospholipids are produced during experimental Trypanosoma rhodesiense infections in rabbits.
Authors: Richards R L , Aronson J , Schoenbechler M , Diggs C L , Alving C R 
Published: December 2022

Abstract
Antibodies against phospholipids appeared spontaneously during the course of experimental Trypanosoma rhodesiense infections in rabbits. These antibodies were observed in rabbits infected either with a lethal strain or with a strain newly discovered to give a spontaneous self-cure. Serum antibodies reacting with liposomes containing dimyristoyl phosphatidylcholine (DMPC), phosphatidylinositol (Pl), phosphatidylinositol phosphate (PlP), or cardiolipin were detected at 3 to 4 wk by complement-mediated release of trapped marker from liposomes. Antibodies were also detected against a trypanosomal lipid fraction (TrF2) that contained Pl as a major constituent. The antibody activities against DMPC, Pl, or TrF2 all reacted (or cross-reacted) with DMPC, and were removed from the serum by adsorbing with liposomes containing DMPC as the only phospholipid. Phosphocholine inhibited the antibodies reactive with liposomes containing either DMPC or DMPC and Pl as phospholipids. Antibodies against PlP, however, reacted only with liposomes containing PlP and were not removed by adsorbing with liposomes lacking PlP. We conclude that anti-phospholipid antibodies appear during the course of trypanosomal infections that either undergo apparent self-cure or are lethal, and at least two anti-phospholipid antibody specificities can be detected.
Transformation of murine LMTK- cells with purified HLA class I genes. I. Modification of conformation of murine beta 2-microglobulin upon its association with HLA heavy chains.
Authors: Lemonnier F A , Le Bouteiller P P , Malissen B , Golstein P , Malissen M , Mishal Z , Caillol D H , Jordan B R , Kourilsky F M 
Published: December 2022

Abstract
Murine LMTK- cells were unexpectedly found to cross-react with a murine anti-human beta 2-microglobulin (beta 2-m)monoclonal antibody (m.Ab) after transformation with cosmid clones containing different purified HLA class I genes. The same cross-reactivity was observed with CTP 34 B4 (murine x human) somatic hybrid cells, which express class I molecules constituted of human HLA heavy chains and murine beta 2-m. Inhibition studies of the complement-dependent cytolysis mediated by the cross-reacting m.Ab indicated that isolated murine beta 2-m does not express the cross-reacting determinant, suggesting that its expression by the transformed cells reflects conformational modification of murine beta 2-m upon its association with HLA heavy chains. These results illustrate one of the possible post-translational mechanisms through which the antigenicity of a polypeptide chain can be modified. They might provide a serologic marker of the third domain of HLA class I heavy chains. Finally, because quantitative differences of reactivity with the anti-human beta 2-m m.Ab were observed, depending on the HLA class I genes used for transformation, these results individualize two families of HLA class I heavy chains responsible for different conformational modifications of murine beta 2-m.
Recombinant interferon-gamma increases HLA-DR synthesis and expression.
Authors: Basham T Y , Merigan T C 
Published: December 2022

Abstract
It has been shown that all three classes of interferons enhance the expression of the major histocompatibility class I antigens (HLA-A,B,C;H-2) on a wide variety of cell types (1-10). However, their effect on the expression of the class II antigens (HLA-DR, Ia), which play a major part in cellular interactions that initiate an immune response, is more controversial. The predominate findings have been that the interferons specifically increase the synthesis and expression of only the class I antigens (3, 4, 6, 8, 10, 11). We report here that recombinant interferon-gamma (IFN-gamma) increases the synthesis and expression of the HLA-DR (la-like) antigens as well as beta 2-microglobulin (beta 2-m), a low m.w. subunit of HLA, on human melanoma cells. No increase in HLA-DR was detected on these melanoma cells with leukocyte interferon (IFN-alpha) at doses 400 times higher than the maximum dose of IFN-gamma. These findings were extended to show that pure IFN-gamma also increases the expression of the HLA-DR antigens on normal peripheral blood monocytes, whereas recombinant IFN-alpha at a similar dose had little effect on the expression of this surface antigen. These findings suggest a specialized role for IFN-gamma in immune regulation in comparison with IFN-alpha.
Depletion of human NK cells with monoclonal antibodies allows the generation of cytotoxic T lymphocytes without NK-like cells in mixed cultures.
Authors: Strassmann G , Bach F H , Zarling J M 
Published: December 2022

Abstract
In vitro stimulation of human mononuclear cells with x-irradiated autologous lymphoblastoid cell line (LCL) or allogeneic normal cells in mixed leukocyte cultures (MLC) was previously shown to result in the generation of OKT3+ OKT8+ cytotoxic T lymphocytes (CTL) lytic for allogeneic and autologous LCLs and also of natural killer- (NK) like cells that are OKT3- and primarily OKT8- and are lytic for HLA- NK-sensitive K562 cells. The origin of the NK-like cells was not previously known because, although the majority of fresh human NK cells react with monoclonal antibodies OKM1 and B73.1, lymphocytes bearing these markers are not detected several days after the onset of MLC, when NK-like cells are present. In this study, experiments were undertaken to determine whether NK-like cells generated after stimulation with x-irradiated pooled allogeneic normal cells (poolx) or with autologous LCL are derived from cells expressing antigens reactive with monoclonal antibodies OKM1 or B73.1, which react with fresh NK cells. Mononuclear cells, depleted of monocytes, were stained with OKM1 or B73.1 and fluorescein-labeled goat anti-mouse IgG. Lymphocytes depleted of OKM1+ or B73.1+ cells, by fluorescence-activated cell sorting, and lymphocytes that were stained but not sorted were stimulated for 7 days with either poolx or autologous LCL. The generation of NK-like activity was decreased at least 90% after depletion of cells reactive with OKM1 or B73.1, whereas the generation of CTL against autologous and allogeneic LCL was minimally affected. These findings show that NK-like cells generated in MLC are derived from cells that express the phenotype of fresh NK cells (OKM1+ or B73.1+) and that CTL can be generated in cultures in which relatively little NK-like activity is concomitantly detected, by depleting NK cells with monoclonal antibodies before stimulation.
Inhibition of ongoing myeloma IgE synthesis in vitro by activated human T cells.
Authors: Hassner A , Saxon A 
Published: December 2022

Abstract
The ability of activated T cells to suppress ongoing IgE synthesis in vitro was assessed using U266--a human myeloma cell line spontaneously producing IgE. T cells were able to inhibit U266 IgE synthesis in the presence of 10 micrograms/ml of Con A by 41.8% (p less than 0.01). T cells preincubated with 10 or 50 micrograms/ml of Con A and washed extensively were still able to inhibit U266 IgE synthesis in the absence of Con A by 41 and 46% (p less than 0.05 and p less than 0.02, respectively). The decrease in IgE measured was due to inhibition of newly formed IgE by U266, as shown by control experiments with cycloheximide. The inhibition was not due to the simple depletion of nutrient growth factors by the activated T cells, as it did not occur with MOLT-4, T cells that are very active metabolically; nor could it be reversed with medium containing IL 2 and B cell growth factors. Culture supernatants of Con A-activated T cells were also able to suppress IgE synthesis by U266 (21%; p less than 0.01), which suggests that upon appropriate activation, T cells secrete material(s) with inhibitory properties for IgE synthesis. Activation of T cells by mixed lymphocyte culture using puromycin-treated lymphoblastoid cell lines as stimulators also generated T cells that had suppressive activity for IgE synthesis. T cells activated with Con A and subsequently incubated with IgE demonstrated a diminished ability to suppress IgE synthesis. This observation is in agreement with the finding that patients with high levels of IgE may lack isotype-specific suppressor T cells for spontaneous IgE secretion. However, T cells from such patients have so far shown variable loss of IgE suppressive function. These results suggest that human IgE synthesis is susceptible to inhibition at a very differentiated stage, and this may be important in expression of allergic diseases.