bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nutritionally variant streptococcal serotype I antigen. Characterization as a lipid-substituted poly(ribitol phosphate).
Authors: George M , van de Rijn I 
Published: December 2022

Abstract
Initial characterization of the nutritionally variant streptococcal serotype I amphipathic polymer indicated an estimated m.w. of 360,000 for the aggregated form of the molecule, whereas the dissociated form had an estimated m.w. of 38,000 based on dextran m.w. standards. In addition, SDS-PAGE indicated an amphiphile with a stepladder appearance made up of several components with m.w. larger than the major electrophoresis components of LPS or lipoteichoic acid. Chemically, the serotype I amphiphile appeared to be a lipid-substituted poly(ribitol phosphate) with galactose and alanine substitution on the ribitol phosphate backbone. This report represents the first characterization of a bacterial amphiphile with a chemical composition and structure as proposed here. As is the case with other bacterial amphiphiles, the nutritionally variant streptococcal serotype I amphiphile was found both intra- and extracellularly. Finally, immunofluorescence studies demonstrated that the amphiphile was expressed on the cell surface.
Studies on the capacity of B cells as well as T cells to serve as accessory cells for the activation of herpes simplex virus-specific cytolytic T cells.
Authors: Grammer S F , Ishioka G Y , Chesnut R W 
Published: December 2022

Abstract
Experiments were conducted in an effort to determine the ability of B and T lymphocytes to serve as APC for the activation of HSV-primed splenic T cells to become class I-restricted, HSV-specific CTL. The results showed that both freshly isolated splenic B cells as well as LPS and dextran sulfate (L/D)-activated B cells were effective at stimulating the generation of CTL during a 5-day in vitro culture. There was no requirement for the addition of exogenous IL-2 to the culture and, since murine B cells do not appear to express either membrane or secreted IL-1, this lymphokine appears to either not be required for the activation of virus-specific CTL or to be provided by the T cells themselves. When normal B cells were separated into fractions enriched for resting vs activated cells and then tested for their ability to stimulate the generation of HSV-specific CTL, it was found that while the activated B cells were quite effective at stimulating the generation of CTL, resting B cells were ineffective at carrying out this function. In contrast to normal B cells, normal T cells were unable to act as APC. However, Con A-activated T lymphoblasts were equivalent to L/D B cells in their ability to mediate the generation of CTL activity. L/D B cells that had been pulsed with HSV and then incubated at 37 degrees C for greater than 1 h could be fixed with paraformaldehyde and were still able to function as APC. The finding that L/D B cells, that had been fixed at 1 h or less after exposure to HSV, were unable to function as APC suggested that either active Ag "processing" steps may be required for the presentation of Ag in the context of class I molecules or that there is a requirement for the synthesis of viral protein Ag before presentation.
Exposure of mice to live Pseudomonas aeruginosa generates protective cell-mediated immunity in the absence of an antibody response.
Authors: Markham R B , Powderly W G 
Published: December 2022

Abstract
In previous studies we have elicited T cell-mediated protective immunity to the extra-cellular Gram-negative bacterium Pseudomonas aeruginosa by administering P. aeruginosa polysaccharide Ag and the anti-mitotic agent vinblastine sulfate to BALB/c mice. The current studies indicate that T cells which inhibit the growth of P. aeruginosa in vitro and protect granulocytopenic mice from P. aeruginosa infection can be generated by exposure of BALB/c mice to as few as 10(2) live bacteria without simultaneous administration of vinblastine. The in vitro inhibition of bacterial growth and mouse protection are P. aeruginosa immunotype specific. Exposure to 10(6) live bacteria is required to elicit a detectable antibody response. These findings indicate a potential role for T cells in resistance to P. aeruginosa infection in the large majority of individuals who lack anti-P. aeruginosa antibody.
Immunosuppression during viral oncogenesis. IV. Generation of soluble virus-induced immunologic suppressor molecules.
Authors: Strayer D S , Korber K , Dombrowski J 
Published: December 2022

Abstract
We describe herein functional attributes and generation of immunologic suppressor activity elaborated in response to oncogenic virus infection. Malignant rabbit fibroma virus-induced immunologic suppressor factor (VISF) is a T cell product produced in peak quantities by spleen cells taken from infected rabbits 7 days after infection in vivo. Its production does not appear to require macrophage participation. VISF is highly labile, 3.5 to 12 kDa, and capable of suppressing both B and T lymphocytic responses. Indomethacin and the cyclic nucleotides cAMP and cGMP inhibit its generation. VISF activity is neither antigen nor species specific. It suppresses murine and leporine immune responses to antigens unrelated to the inducing virus. Comparable suppressor activity may be induced by infecting an apparently non-functional rabbit T lymphoma line, RL-5, with malignant rabbit fibroma virus. VISF is principally a suppressor-inducer factor: in vitro, lymphocytes exposed to VISF do not show decreased immunologic responsiveness until 4 days of culture. VISF induces T suppressor cell activity when normal spleen cells are exposed briefly to VISF. Thus, immunosuppressive consequences of malignant fibroma virus infection are partially mediated by a small, non-specific T cell-derived suppressor lymphokine with unique functional characteristics. Non-specific immunologic dysfunction that often attends virus infections may reflect the activity of such factors in humans as well.
Induction of glial cell MHC antigen expression in neurotropic coronavirus infections. Characterization of the H-2-inducing soluble factor elaborated by infected brain cells.
Authors: Suzumura A , Lavi E , Bhat S , Murasko D , Weiss S R , Silberberg D H 
Published: December 2022

Abstract
Neurotropic coronavirus (mouse hepatitis virus strain A59) infection induces major histocompatibility complex class I (H-2) surface antigens on oligodendrocytes and astrocytes, cells that do not normally express detectable MHC antigens on their surface. The induction on MHC antigen expression potentially allows immunocytes to interact with infected glial cells and may play a critical role in the development of virus-induced, immune-mediated demyelination in the central nervous system, a possible model of human multiple sclerosis. In this study, we characterized the soluble factor involved in MHC antigen induction, quantitated induction of MHC antigens, and analyzed the central nervous system cell type involved in the production of the factor. The H-2-inducing factor, most likely produced by astrocytes, was found to be nondialyzable, heat- and trypsin-sensitive, but resistant to treatment at pH 2.0. The m.w. of the factor was estimated as 50 to 100 kDa. Studies on fractionation by ultrafiltration and sucrose density gradient along with antibody-blocking experiments indicate that the factor is not interferon or virus particles.
Cell surface expression of the amino-terminal domain of A kappa alpha. Recognition of an isolated MHC antigenic structure by allospecific T cells but not alloantibodies.
Authors: McCluskey J , Munitz T , Boyd L , Germain R N , Coligan J E , Singer A , Margulies D H 
Published: December 2022

Abstract
To evaluate the relationship between structure and function of the alpha 1 and beta 1 domains of class II MHC molecules, a strategy has been developed whereby isolated alpha 1 or beta 1 domains can be expressed on the surface of transfected mouse L cells as a part of a hybrid class II/class I molecule. The construction and expression of a chimeric class II/class I gene encoding the first two exons of A kappa alpha linked to the C2, TM and cytoplasmic exons of H-2Dd (A kappa alpha 1/DdC2) are described. High levels of A kappa alpha 1/DdC2 protein were detected on transfected L cells with a DdC2-specific mAb. An anti-Ia xenoantiserum specifically bound to A kappa alpha 1/DdC2-transfected L cells, although 12 different mAb reactive against I-A kappa alpha and an anti-Ia kappa alloantiserum did not bind these cells. However, alloreactive Ia kappa-specific CTL lines were able specifically to lyse cells expressing the hybrid A kappa alpha 1/DdC2 molecule. This indicates that the isolated A kappa alpha 1 domain preserves some of the structure of the native molecule and demonstrates the recognition by T cells of domain-specific A alpha allodeterminants.
H-2 antigen expression and sensitivity of BL6 melanoma cells to natural killer cell cytotoxicity.
Authors: Gorelik E , Gunji Y , Herberman R B 
Published: December 2022

Abstract
The sensitivity of H-2b-high and H-2b-low variants of BL6 melanoma to the cytotoxic action of NK and lymphokine-activated killer cells was investigated. BL6 mouse melanoma cells lack detectable H-2Kb and had low levels of expression of H-2Db Ag. The BL6T2 variant cells, obtained after treatment of BL6 cells with mutagen N-methyl-N-nitro-N'-nitro-soguanidine, had relatively high levels of expression of class I H-2b Ag. Poly(I:C)-stimulated spleen cells of nude mice were highly cytotoxic for BL6T2, whereas H-2b-low BL6 cells were less sensitive to NK activity in an 18-h 51Cr-release assay. Similar results were obtained after 4-h incubation of radio-labeled tumor cells with IL-2-activated effector cells. In contrast, both lines were equally sensitive to lysis by purified granules derived from rat large granular lymphocytes (LGL) or by macrophages. By using various clones selected from BL6 or BL6T2 cells, it was found that BL6 or BL6T2 clones with low H-2b Ag expression were less sensitive to lysis by NK cells than H-2b-high clones. After IFN treatment of either BL6 or BL6T2, the target cells became more resistant to lysis by either NK cells or by purified LGL granules. IFN-treated BL6 cells had substantially increased expression of H-2b Ag and in this respect became similar to untreated BL6T2. However, IFN-treated BL6 cells were more resistant than BL6T2 cells to lysis by NK cells and LGL granules, suggesting that augmentation of H-2b Ag expression and NK resistance could be two independent IFN-induced effects. With a cold target inhibition assay, it was found that BL6T2 or its H-2 positive clones were highly competitive and inhibited the cytotoxic activity of NK and lymphokine-activated killer cells against radiolabeled YAC-1 and BL6T2, whereas BL6 cells or H-2-negative clones of BL6T2 and BL6 lines showed poor competitive ability. Thus, our data indicate that the NK resistance of H-2-low BL6 cells may be due to a paucity of NK recognizable determinants. N-Methyl-N-nitro-N'-nitroguanidine treatment of BL6 melanoma cells was associated with an increase in class I H-2b Ag expression and NK sensitivity, suggesting the involvement of class I MHC Ag in the sensitivity of tumor cells to NK cell-mediated cytotoxicity.
Activation of human T4 cells by cross-linking class I MHC molecules.
Authors: Geppert T D , Wacholtz M C , Davis L S , Lipsky P E 
Published: December 2022

Abstract
These studies examined whether cross-linking class I MHC molecules results in functional or biochemical responses in human T4 cells. The initial studies demonstrated that cross-linking class I MHC molecules either by culturing highly purified T4 cells with immobilized mAb to class I MHC Ag or reacting the T4 cells with mAb to class I MHC Ag and then cross-linking the mAb with goat antimouse Ig (GaMIg) enhanced T4 cell proliferation induced by an immobilized mAb to CD3, OKT3. More-over, immobilized but not soluble mAb to class I MHC Ag enhanced T4 cell proliferation induced by the combination of two mAb to CD2, OKT11, and D66.2. Finally, T4 cells reacted with mAb to CD3 and class I MHC Ag proliferated in the presence of IL-2 when cross-linked with GaMIg more vigorously than T4 cells reacted with either mAb alone. Cross-linking class I MHC molecules was also found to stimulate T4 cells directly. T4 cells reacted with mAb to class I MHC Ag or beta 2 microglobulin and cross-linked with GaMIg proliferated vigorously in the presence of IL-2 or PMA. In addition, it was demonstrated that cross-linking class I MHC molecules by culturing T4 cells with immobilized mAb to class I MHC Ag induced T4 cell proliferation in the presence of IL-2. T4 cell proliferation in the presence of IL-2 and PMA could also be induced by reacting the cells with specific mAb to polymorphic determinants on class I MHC molecules and cross-linking with GaMIg. Cross-linking mAb to CD4 or CD11a did not have a similar functional effect on T4 cells. Finally it was demonstrated that adding GaMIg to T4 cells reacted with mAb to class I MHC Ag but not CD11a resulted in an increase in intracellular calcium concentration. The data demonstrate that cross-linking class I MHC molecules results in the generation of at least one activation signal, a rise in intracellular calcium concentration, and, thereby, stimulates human T4 cells.
Selective adhesion of mast cells to tracheal epithelial cells in vitro.
Authors: Varsano S , Lazarus S C , Gold W M , Nadel J A 
Published: December 2022

Abstract
In allergic and nonallergic lung diseases, if intraluminal mast cells adhere to airway epithelium, inflammatory mediators released from activated mast cells may reach high local concentrations and thus greatly affect airway function. To determine whether mast cells adhere to airway epithelial cells, radiolabeled or unlabeled dog mastocytoma cells were incubated with cultured dog tracheal epithelial cells, with extracellular matrix substrates, and with cryostat-cut sections of dog trachea. Mast cells adhered well to cultured epithelial cells (35 +/- 13% adhesion, mean +/- 1 SD, n = 23) but adhered poorly to types I and IV collagen or to fibronectin (less than 7.5% mean adhesion in all cases). Similarly, in tracheal tissue sections, mast cells adhered preferentially to epithelial cells in surface epithelium or in submucosal glands but not to basal membrane or connective tissue. Adhesion to cultured epithelial cells was a characteristics of a subpopulation of mast cells, could persist for more than 48 h, did not require energy or the presence of divalent cations, and was not mediated by a known family of leukocyte-associated adhesion glycoproteins. Adhesion was completely abolished by pretreatment of mast cells with pronase E or proteinase K but not with trypsin (up to 10 micrograms/ml at 37 degrees C for 20 min each). In contrast, pretreatment of cultured epithelial cells with any of these proteinases had no effect on adhesion. It is concluded that dog mastocytoma mast cells adhere to dog tracheal epithelial cells and do so selectively. It is suggested that mast cell adhesion to airway epithelium may play a role in the effectiveness of mast cell-epithelial cell interactions, and thus, in certain lung diseases, airway function may be affected by intraluminal mast cells more than is currently appreciated.
Suppression of simian immunodeficiency virus replication in vitro by CD8+ lymphocytes.
Authors: Kannagi M , Chalifoux L V , Lord C I , Letvin N L 
Published: December 2022

Abstract
The AIDS-like disease in rhesus monkeys induced by the simian immunodeficiency virus (SIV) has been used as a model to explore the nature of the T lymphocyte response after infection with viruses of the human immunodeficiency virus family. Activated CD8+ lymphocytes are present in increased numbers in the paracortex of lymph nodes of SIV-infected rhesus monkeys with a lymphadenopathy syndrome. We demonstrate that SIV is more readily isolated from CD8+ lymphocyte-depleted PBL of SIV-infected animals than from their unfractionated PBL. Rather than reflecting the fact that the CD8+ lymphocyte-depleted cell populations are simply enriched for CD4+ lymphocytes, this indicates that CD8+ cells themselves are critical in this regulatory interaction. In fact, CD8+ lymphocytes from SIV-infected but not uninfected rhesus monkeys can block SIV replication in vitro in PBL populations. A T lymphocyte population that blocks replication of viruses of the HIV family may contribute to containing the progression of AIDS.
Phosphorylation of intracellular precursors of human IL-1.
Authors: Kobayashi Y , Appella E , Yamada M , Copeland T D , Oppenheim J J , Matsushima K 
Published: December 2022

Abstract
The human IL-1 molecules (IL-1 alpha and IL-1 beta) are post-translationally cleaved from 31-kDa precursor to 18-kDa biologically active molecules. During the course of studies of post-translational modifications of human IL-1, we have observed that although LPS induced the production of both intracellular IL-1 alpha and IL-1 beta in human monocytes, [32P]orthophosphate labeling of these cells revealed that intracellular precursor of IL-1 alpha (pre-IL-1 alpha) to be phosphorylated at least 10-fold more than intracellular pre-IL-1 beta. However, no 32P-incorporation could be detected in the 18-kDa processed IL-1 alpha and IL-1 beta. Analysis by TLC revealed that the major phosphorylation site occurred at serine residue(s). The 32P was incorporated into multiply cleaved precursors of IL-1 alpha, which appeared in the absence of protease inhibitors. Since the smallest Mr pre-IL-1 alpha that was labeled with 32P was 22 kDa, the phosphorylated serine residue is presumably located adjacent to a sequence of four basic amino acids located in the 4-kDa region at the amino terminus of the 22-kDa precursor of IL-1 alpha. This serine residue might also be a major phosphorylation site for a cAMP-dependent protein kinase. This hypothesis was substantiated by the demonstration that a synthetic peptide analogue of this region (residue 84 to 112) could be similarly phosphorylated in vitro by a cAMP-dependent protein kinase. Furthermore, a truncated pre-IL-1 alpha (residue 64 to 271) and a "fusion" protein containing staphylococcal protein A and an amino-terminal half-portion of pre-IL-1 alpha (residue 1 to 112), but not mature IL-1 alpha (residue 113 to 271), could also be phosphorylated by cAMP-dependent protein kinase. There is no comparable amino acid sequence in IL-1 beta which could be expected to be phosphorylated by a cAMP-dependent protein kinase. The physiologic relevance of phosphorylation of pre-IL-1 alpha was investigated. The data showed that phosphorylation of truncated pre-IL-1 alpha greatly enhanced its susceptibility to digestion by trypsin and promoted the conversion of pre-IL-1 alpha to the more biologically active IL-1. Although the precise role of the rather selective phosphorylation of pre-IL-1 alpha is not known, our findings do suggest that the phosphorylation of serine close to dibasic/tetrabasic amino acid sequence functions to facilitate the processing and/or release of IL-1 alpha.
IL-2-dependent expansion of CD3+ large granular lymphocytes expressing T cell receptor-gamma delta. Evidence for a functional receptor by anti-CD3 activation of cytolysis.
Authors: Colamonici O R , Ang S , Quinones R , Henkart P , Heikkila R , Gress R , Felix C , Kirsch I , Longo D , Marti G 
Published: December 2022

Abstract
The nature and function of the TCR on PBL of a patient with a chronic CD3+ large granular (LGL) proliferation was studied. Fresh peripheral blood from this individual was comprised of 80% lymphocytes, 65 to 75% of which were CD3+, CD8+, Leu-7+ LGL. Of these LGL, 72% initially expressed the TCR-alpha beta heterodimer, whereas 21% did not. Cytotoxicity directed against MHC-unrestricted targets was minimal. After several days of exposure to rIL-2, cytotoxic activity was greatly enhanced, correlating with a disappearance of CD3+ cells expressing the alpha beta heterodimer. Twelve days after rIL-2 exposure, the LGL expressed only TCR-gamma delta heterodimer in association with CD3 and alpha beta heterodimer expression could no longer be detected. The TCR/CD3 complex on these cells was demonstrated to be functional as anti-CD3 elicited an increase in cytoplasmic free calcium concentration, stimulated cytolytic activity, and stimulated granule enzyme secretion from the LGL.
Inhibition of allergic reactions with monoclonal antibody to the high affinity IgE receptor.
Authors: Kitani S , Kraft D , Fischler C , Mergenhagen S E , Siraganian R P 
Published: December 2022

Abstract
A mAb that reacts with the high affinity IgE-R on the rat basophilic leukemia cells (RBL-2H3) was used to inhibit allergic reactions. In vitro, the intact mAb BA3 and its Fab fragment inhibited radiolabeled IgE binding to the RBL-2H3 cells. The mAb binds to the IgE-R with a higher affinity than does IgE. Whereas the intact mAb released histamine from the RBL-2H3 cells, the Fab was inactive. The addition of the Fab fragments to RBL-2H3 inhibited the IgE-mediated histamine release reaction. The Fab fragments also inhibited in vivo passive cutaneous reactions in rats when injected intradermally either before or after IgE. The injection of the mAb Fab i.v. before the injection of the IgE into the skin sites also inhibited reactions, although it was less effective. The results demonstrate that anti-R antibodies can be used as a model for inhibiting immediate hypersensitivity reactions.
Immunosuppressive lymphokine derived from natural suppressor cells.
Authors: Hertel-Wulff B , Strober S 
Published: December 2022

Abstract
Cloned natural suppressor (NS) cells derived from spleens of total lymphoid irradiated BALB/c mice were incubated with the phorbol ester, PMA, and calcimycin for 4 h. After thorough washing, the induced NS cells were incubated in serum-free medium for 24 h and the supernatants were collected. The supernatants suppressed the MLR between normal adult responder and stimulator spleen cells. There was no Ag specificity or H-2 haplotype restriction of the MLR suppression. The supernatants did not inhibit [3H]thymidine incorporation per se, because they did not suppress mitogen stimulation of spleen cells. Protease digestion of the supernatants removed the suppressive activity, and dialysis studies indicated that the molecular size of the suppressive factor was larger than 50,000 Da and smaller than 100,000 Da. The suppressive activity was stable at 56 degrees C, pH 2, for 1 h. Thus, NS cell clones can be induced to secrete an immunosuppressive lymphokine, NS factor.