bluuebunny/crossref_metadata_2025_split huggingface dataset:
The immunopathology of experimental allergic encephalomyelitis. II. Endothelial cell Ia increases prior to inflammatory cell infiltration.
Authors: Sobel R A , Blanchette B W , Bhan A K , Colvin R B 
Published: December 2022

Abstract
Experimental allergic encephalomyelitis (EAE) is a T cell-mediated neuroimmunologic disease model characterized by meningeal and parenchymal mononuclear cell infiltrates (see preceding companion paper). Here we report enhanced staining for Ia in the central nervous system (CNS) microvasculature endothelium in acute EAE in adult strain 13 guinea pigs (GP) sensitized with GP spinal cord homogenate (SC) or with GP myelin basic protein (MBP) in complete Freund's adjuvant (CFA). Cryostat sections of CNS and other tissues were stained with two monoclonal antibodies, 5S2 and 22C4, to GP Ia determinants, and with polyclonal antibody to factor VIII-related antigen (VIII-RA) as an endothelial cell marker. Morphometric techniques were employed on immunoperoxidase counterstained and coded sections to determine the frequency of Ia+ vessels and cells. Rare (approximately 10% of VIII-RA+) vascular endothelial cells were Ia+ in the CNS of normal and CFA-sensitized controls. SC- or MBP-sensitized strain 13 GP sacrificed on day 7, before the onset of neurologic signs (pre-clinical), had no detectable CNS mononuclear cell infiltrates, but had increased (approximately 30% of VIII-RA+) endothelial cell Ia staining over controls (p less than 0.001). The endothelial Ia staining persisted (approximately 35% of VIII-RA+) in vessels as the animals developed paralysis. There were no differences in endothelial cell Ia between SC- and MBP-induced disease. EAE-resistant strain 2 GP sensitized with SC/CFA had no neurologic signs, and had fewer inflammatory foci than strain 13 GP with EAE, but had similar numbers of Ia+ endothelial cells. No differences in endothelial cell Ia staining were found in non-CNS tissues among any GP groups. In EAE, increased endothelial cell Ia is a pre-inflammatory, target organ-specific alteration that persists during inflammation. The findings suggest that in vivo modulation of endothelial cell Ia may be part of the local immune response. Endothelial cells may play a significant role, in antigen presentation or in promoting T cell migration, in the in situ immune response in the CNS.
Identification and initial characterization of concanavalin A- and interferon-induced human suppressor factors: evidence for a human equivalent of murine soluble immune response suppressor (SIRS).
Authors: Schnaper H W , Pierce C W , Aune T M 
Published: December 2022

Abstract
Human suppressor T cells activated by leukocyte interferon have properties similar to murine suppressor cells activated by interferon or by concanavalin A. Murine suppressor cells release a soluble mediator, soluble immune response suppressor (SIRS), which accounts, at least in part, for suppressive activity in murine systems. To compare and contrast murine and human suppressor pathways, we evaluated the suppression of human polyclonal plaque-forming cell responses by concanavalin A, by leukocyte interferon, and by immune interferon, or by suppressor cells activated by these agents. In each instance, suppressive activity was prevented by levamisole, ascorbic acid, catalase, or 2-mercaptoethanol, agents known to interfere with murine SIRS activity. Furthermore, concanavalin A, immune interferon, and leukocyte interferon induced T lymphocytes to release 110,000 to 150,000 m.w. proteins which suppressed responses only when added early in the culture period. As with murine SIRS, suppression by each of these human factors was inhibited by 2-mercaptoethanol, ascorbic acid, catalase, or levamisole. The reaction of human suppressor factors with H2O2 (10(-6) M) activated suppressor factors so that they suppress responses when added late in the culture period. Human suppressor factors were protease- and acid (pH 2)-sensitive. The similarities between these human suppressor factors and murine SIRS show the existence of a human SIRS pathway.
Recombinant interferons increase macrophage Fc receptor capacity.
Authors: Fertsch D , Vogel S N 
Published: December 2022

Abstract
We utilized recombinant interferon preparations to confirm and extend our previous findings that biochemically purified preparations of interferon augment Fc receptor (FcR)-mediated functions. Five different recombinant human alpha-interferons (IFN) were tested and increased Fc-mediated phagocytosis and binding of opsonized erythrocytes with varying efficiencies. We found, however, that when the different alpha-IFN species were ranked with respect to their FcR-enhancing activity, their hierarchy differed from those reported for antiviral, antiproliferative, and NK cell-inducing activities. Recombinant murine gamma-IFN was also found to increase Fc-mediated phagocytosis, but was significantly more potent than either beta-IFN or recombinant alpha-IFN when compared on the basis of antiviral activity. A comparison of the amino acid sequences of the recombinant IFN may help define functional domains of the molecule.
A distinct "slow" cellular pathway involving soluble mediators for the T cell-instructed induction of monocyte tissue factor activity in an allogeneic immune response.
Authors: Helin H , Edgington T S 
Published: December 2022

Abstract
Allogeneic stimulation of human lymphoid cells initiates a collaborative cellular pathway that relatively rapidly induces in monocytes the synthesis and cell surface expression of tissue factor, the initiating cofactor of the extrinsic coagulation pathway. T cells are required for the monocyte procoagulant generation, because the addition of autologous or allogeneic T cells fully reconstitutes the activity in otherwise nonresponding highly purified monocytes. Despite a strict T cell requirement, only low T cell to monocyte ratios are necessary for maximal PCA response. Our results further demonstrate that the collaborative signal from allogeneically stimulated T cells to effector monocytes is transferred by a soluble mediator rather than direct cell to cell contact. Other aspects of the present study include the observation that among normal peripheral blood lymphoid cells, monocytes elicit the strongest allogeneic PCA response. This response is clearly exceeded by that induced upon stimulation with Daudi lymphoblastoid B cells. Our data demonstrate the existence of a second distinct cellular pathway that mediates the lymphoid procoagulant response. This pathway differs from the previously characterized response to bacterial LPS in respect to: a) kinetics of T cell triggering; b) mediation by a soluble product; c) lack of genetic restriction of T cell; monocyte collaboration; and d) deficient capacity for direct T cell induction of the monocyte PCA response.
Preparations of lymphotoxin induce resistance to their own cytotoxic effect.
Authors: Wallach D 
Published: December 2022

Abstract
Preparations of human lymphotoxins (LT) were effectively cytotoxic to HeLa cells when applied in the presence of cycloheximide (CHI). In the absence of CHI, however, they failed to cause any cell death. Moreover, LT applied in the absence of CHI induced resistance that was reflected in decreased vulnerability to subsequent incubation with LT in the presence of CHI. This induction of resistance to LT, in treating cells with preparations of LT, was quite rapid, reaching its maximal extent within 2 hr of LT application. It could also be observed in cells of other cultured human lines besides HeLa (SV80 and WISH), and the range of LT concentrations at which it was observed was similar to that at which death of cells was induced by LT in the presence of CHI. In fractionating LT preparations on DEAE cellulose, the resistance inducing activity appeared to co-purify with the cytotoxic activity, suggesting that both activities reside in the same molecule. We suggest that LT, or some lymphokines that are formed by lymphocytes concomitantly with the formation of LT, can induce cellular mechanisms that interfere with the cytotoxic activity of LT and that CHI makes the cell sensitive to the cytotoxicity of LT by reducing the activity of these protective mechanisms. This kind of negative feedback regulation in the function of LT might contribute to selectivity in their action.
A phosphatidylethanolamine-containing complex on human B cells that mediates rosette formation with mouse erythrocytes.
Authors: Zalewski P D , Valente L , Forbes I J 
Published: December 2022

Abstract
The maturation-associated human B cell rosette receptor (MER) for mouse erythrocytes has been solubilized from B cells by mild trypsinization. It specifically agglutinates mouse red cells. Material with hemagglutinating activity partitioned into the lipid-soluble phase of a Folch partition of the trypsin extract was sensitive to phospholipase C and alkali, and on two-dimensional thin layer chromatography, it co-migrated principally with phosphatidylethanolamine (PE). Phosphatidylcholine, the major lipid present, was inactive. The relationship of phospholipid structure to hemagglutinating activity has been described. PE in the crude trypsin extract was associated with unidentified glycoprotein and albumin. Material containing hemagglutinating lipid bound to a wheat germ lectin-Sepharose column and was released by N-acetylglucosamine, indicating that the PE was complexed with glycoprotein. When the crude trypsin extract or eluate from the lectin column was extracted with aqueous phenol, hemagglutinin in the aqueous phase no longer bound to wheat germ lectin-Sepharose; however, albumin was greatly enriched, indicating that some of the PE exists in a complex with albumin. The molar ratio of PE to albumin was approximately 200:1. After delipidation, this albumin (in molar excess) inhibited hemagglutination by PE in the same way as a recently described subclass of serum albumin. Studies with phospholipase-treated B cells were also consistent with PE being the MER. We conclude that MER is PE, existing in a complex containing glycoprotein and a subclass of albumin. The capacity to form rosettes can be transferred to nonrosetting Raji B cells by the complex, but not pure PE, indicating that the proteins may be involved in orienting PE correctly for it to function as the MER.
Circulating cellfree Fc gamma 2b/gamma 1 receptor in normal mouse serum: its detection and specificity.
Authors: Khayat D , Dux Z , Anavi R , Shlomo Y , Witz I P , Ran M 
Published: December 2022

Abstract
By using intact or Fab fragments of rat monoclonal antibodies against murine Fc gamma 2b/gamma 1 receptor, in a solid phase radioimmunoassay, we demonstrated the occurrence of circulating cellfree Fc gamma 2b/gamma 1 receptors (Cf-Fc gamma 2b/gamma 1R) in normal mouse serum. These Cf-Fc gamma 2b/gamma 1R were removed from serum by affinity chromatography by using Sepharose columns coupled with IgG but not by Sepharose coupled with F(ab')2 fragments. Furthermore, the material retained by and eluted from the Sepharose IgG column reacted with the monoclonal antibody; these results support a direct relationship between the antigenic and the functional Cf-Fc gamma 2b/gamma 1R that were detected in serum. This Cf-Fc gamma 2b/gamma 1R was found in all the 39 normal mouse sera that were tested. The results seemed to indicate that aging may be associated with increased levels of Cf-Fc gamma 2b/gamma 1R and that levels of circulating Fc gamma R may be under genetic regulation. By forming complexes with circulating IgG within the blood stream, such Cf-Fc gamma 2b/gamma 1R may modulate some of the functions in which the Fc portion of Ig is involved.
Purification and characterization of Rana pipiens brain Thy-1 glycoprotein.
Authors: Mansour M H , Cooper E L 
Published: December 2022

Abstract
The occurrence of Thy-1 antigens in Rana brain has been studied by the use of heterologous anti-Rana brain antisera raised in rabbit and BALB/c mouse (Thy-1.2) and AKR/J mouse (Thy-1.1) strains and by monoclonal anti-mouse Thy-1.1 and anti-mouse Thy-1.2 antibodies with the use of quantitative absorption assays. Three antigenic determinants were defined on Rana brain and referred to as: 1) the Rana-specific xenoantigen, 2) the Rana-mouse cross-reacting xenoantigen, and 3) the Thy-1.1 antigen. Thy-1 antigenic activities were solubilized from crude brain membranes in deoxycholate and followed by measuring the Rana-specific and the Thy-1.1 antigenic determinants. After solubilization, Rana brain Thy-1 antigens were purified by lentil lectin affinity chromatography and gel filtration on Sephadex G-200. A 605-fold and 400-fold enrichment in the Rana-specific and the Thy-1.1 antigenic activities with a yield of 25% and 17%, respectively, were obtained. Both antigenic activities were associated with a single glycoprotein of molecular size 3.1 nm and m.w. estimated at 27,000 by SDS-polyacrylamide gel electrophoresis. The serologic and biochemical properties of our purified Rana brain Thy-1 glycoprotein were very similar to those of the mammalian Thy-1 molecule, suggesting the conservation of the gene coding for Thy-1 during vertebrate evolution.
Effect of influenza virus infection on allergic sensitization to aerosolized ovalbumin in mice.
Authors: Sakamoto M , Ida S , Takishima T 
Published: December 2022

Abstract
An IgE antibody specific to ovalbumin was produced when C3H mice were first infected with influenza A virus before challenge with the aerosolized antigen. No antibody could be detected in those animals without preceding viral infection. Antigen inhalation immediately after virus infection could not induce the IgE antibody. A time lag of at least 2 days was required to sensitize the infected mice with inhaled antigen. The study revealed that allergic sensitization could be elicited only during the acute stage of the infection, but not in the convalescent stage. We concluded therefore that the inflammation of respiratory mucous membrane might allow inhaled antigens to penetrate the barrier, resulting in reaginic antibody production that has the capacity to serve as an allergic response.
Antigenic modulation induced by monoclonal antibodies: antibodies to measles virus hemagglutinin alters expression of other viral polypeptides in infected cells.
Authors: Fujinami R S , Norrby E , Oldstone M B 
Published: December 2022

Abstract
Polyclonal antibody to measles virus can have profound effects on external (outer plasma membrane) as well as internal (cytoplasmic) viral polypeptides expressed in infected cells. The process, termed "antibody-induced antigenic modulation," was further investigated by using monoclonal antibody to several viral polypeptides. Four monoclonal antibodies against the viral hemagglutinin had the ability to decrease the expression of the phosphoprotein, fusion, and membrane protein. A monoclonal antibody to the nucleocapsid protein did not cause these changes. The observed decreases were not due to preferential degradation of viral polypeptides as determined by pulse-chase experiments. Our results indicate that a specific signal to an epitope on the plasma membrane (monoclonal antibody measles virus hemagglutinin) can alter the expression of measles virus phosphoprotein and membrane protein, both polypeptides present in the cytoplasm of infected cells.
Neoplastic cells obtained from Hodgkin's disease function as accessory cells for mitogen-induced human T cell proliferative responses.
Authors: Fisher R I , Bates S E , Bostick-Bruton F , Tuteja N , Diehl V 
Published: December 2022

Abstract
Purified human peripheral blood T cells that have been depleted of Ia-bearing cells and adherent cells do not proliferate in response to concanavalin A. The addition of as few as 1% radiated L428 tumor cells restores the proliferative capacity of the T cells. The L428 cell line is a long-term tissue culture line of Reed-Sternberg cells obtained from a patient with Hodgkin's disease. The proliferation of the T cells plus the L428 cells follows the same kinetics and has the same response to varying doses of mitogen as either unfractionated mononuclear leukocytes or purified T cells plus allogeneic adherent cells. The L428 cells are 30 times more potent as accessory cells than allogeneic adherent cells. The accessory cell function of the L428 cells is not blocked in cultures containing anti-Ia antibody. Neither supernatant from the L428 cell cultures nor human IL 1 replaces the accessory cells. The ability of the L428 cells to restore the proliferative capacity of purified T cells isolated from patients with active Hodgkin's disease was also studied. Patients with early stages of the disease had normal proliferative responses in the presence of the L428 accessory cells. However, the proliferative response of the poor prognosis, advanced-stage patients was reduced as compared to age- and sex-matched controls, supporting a deficit in their T cell function. The L428 tumor cells share many properties such as accessory cell function, morphology, and cell surface markers with the dendritic cells described in animal and human systems.
Antigen-stimulated human B cell clones are committed to the production of a single class of antibody in vitro.
Authors: Yarchoan R , Engler R J , Barrow L A , Kurman C C , Nelson D L 
Published: December 2022

Abstract
We have investigated the isotype(s) of antibody produced in vitro by antigen-stimulated human B cell clones. An analysis of the class(es) of antibody produced in multiple replicate cultures containing a mean of less than one precursor B cell per well was consistent with the hypothesis that individual B cell precursors produced a single class of antibody. This result was obtained by using cells isolated from either the peripheral blood or tonsils. Thus, under the culture conditions utilized, no intraclonal isotype switching was detected.
Demonstration of activation-specific interactions among B lymphocyte membrane proteins by a photoreactive cross-linking agent.
Authors: Wolfert R L , Goodman M G , Weigle W O 
Published: December 2022

Abstract
The formation of plasma membrane protein complexes during B cell activation was examined by covalently stabilizing these complexes with a photolabile, cleavable, cross-linking reagent, dithiobisphenylazide (DTPA). Analysis by SDS polyacrylamide gel electrophoresis indicates that LPS induces a time-dependent rearrangement in membrane proteins of splenic B cells. These rearrangements were localized to the plasma membrane by examination of surface-labeled detergent lysates and purified plasma membrane preparations. DTPA-stabilized rearrangements could be detected as early as 15 min and were stable between 3 and 24 hr after mitogen addition. These changes are consistent with the formation of different functional protein complexes during B cell activation. LPS does not induce membrane protein rearrangement in thymocytes, nor does Con A do so in B cells. Therefore, the changes appear to be correlated with the transmission of a relevant activation signal. Activation of B cells with 8- bromoguanosine ( 8BrGuo ), an intracellular mitogen, did not result in protein rearrangement until 12 hr after mitogen addition, suggesting that initial stages of signal transduction by 8BrGuo and LPS follow separate pathways. A common "activated state" of the membrane is established by 12 hr. Inhibition of de novo protein synthesis by cycloheximide did not interfere with formation of new protein complexes during early stages of activation (15 min and 3 hr). These data indicate that covalent cross-linking with DTPA can be used to demonstrate activation-specific interactions among proteins on the surface membrane of B cells.
Anti-idiotype stimulation of antigen-specific antigen-independent antibody responses in vitro. II. Triggering of B lymphocytes by idiotype plus anti-idiotype in the absence of T lymphocytes.
Authors: Shenk R R , Weissberger H Z , Dickler H B 
Published: December 2022

Abstract
Antibodies specific for the idiotypes of B10 anti-(T,G)-A--L antibodies (anti-id) induced B lymphocytes to secrete anti-(T,G)-A--L antibodies in vitro in the absence of both antigen and T lymphocytes, provided either that the B lymphocytes were previously primed in vivo with (T,G)-A--L or that id specific for (T,G)-A--L was added to the cultures. These antigen- and T lymphocyte-independent responses were antigen specific and appeared not to require accessory cells. The results suggested that B lymphocyte activation occurred via the formation of id-anti-id complexes, and evidence was obtained that this activation involved two separate interactions between the B lymphocytes and the id-anti-id complexes. These studies document a previously undescribed regulatory function of anti-idiotype antibodies.
A population of resting IgM-IgD double-bearing lymphocytes in Peyer's patches: the major precursor cells for IgA plasma cells in the gut lamina propria.
Authors: Tseng J 
Published: December 2022

Abstract
The precursor cells in Peyer's patches and mesenteric lymph nodes responsible for repopulating IgA plasma cells in the gut lamina propria were identified by using cell separation and by using cell transfer in Ig allotype congeneic mice (CB-20 and BALB/cJ mice). It was found that the IgA precursor cells are mainly resting lymphoid cells bearing IgM and IgD on their surface. The IgA-bearing cells are also precursors; their repopulation efficiency, however, is remarkably low. The majority of the IgA precursor cells also bear complement receptors on their surface; this suggests that they are relatively mature B cells.
Cell-mediated cytotoxicity against allogeneic mutant H-2 antigens: restricted and nonrestricted responses.
Authors: Nakamura I 
Published: December 2022

Abstract
Two "gain and loss" type mutations of the H-2D region, the H- 2bm13 and H- 2bm14 , resulted in the expression of noncross-reactive CML determinants that are unique to each mutation, the Dbm13 gains and Dbm14 gains, respectively. According to the results of direct cytolytic and competitive inhibition assays of in vitro induced primary cytotoxic T lymphocytes, allogeneic responses specific for Dbm13 gains are generated by responders bearing the H-2b ( KbIbDb ) haplotype, but not by responders bearing the H- 2bm14 ( KbIbDbm14 ), KbIbDd , KbIbDk , or KbIb / qDq haplotype. Responses by the non-H-2b responders against Dbm13 are limited to those determinants shared by the Dbm13 and Db molecules. Because congenic mice differing only at the H-2D region are either responsive or nonresponsive to Dbm13 gains, the responsiveness is controlled by gene(s) in the H-2D region. F1 hybrid offspring of responsive (H-2b) and nonresponsive (non-H-2b) parents are invariably responsive, indicating genetic dominance of the responsiveness. In contrast to the response against Dbm13 gains, cytotoxicity specific for Dbm14 gains is generated by responders bearing the H-2b, H- 2bm13 , KbIbDd , KbIbDk , or KbIb / qDq haplotype. These data indicate the existence of two types of allogeneic MHC determinants; one, represented by Dbm14 gains, is the classic type capable of eliciting CML responses in mice of a wide range of H-2 haplotypes, whereas the other, exemplified by Dbm13 gains, elicits CTL responses only in mice of a few related haplotypes. It is proposed that recognition of Dbm13 gains is restricted by structures shared by Db and Dbm13 but missing from other D (or L, R, etc.) molecules, such as Dbm14 , Dd, Dk, and Dq. Availability of various restricting structures in self MHC molecules may thus influence the alloreactive CTL repertoire.