bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stimulation of human neutrophilic granulocyte chemotaxis by monoclonal antibodies.
Authors: Laskin D L , Rovera G 
Published: December 2022

Abstract
Two mouse monoclonal antibodies, L12.2 and S5.22, were developed that are specific for human neutrophilic granulocytes and produce a twofold to threefold stimulation of n-formyl-methionine-leucyl-phenylalanine (FMLP)-induced chemotaxis. Stimulation of chemotaxis by the antibodies is specific for FMLP and is concentration dependent. L12.2 appears to be more potent in stimulating chemotaxis and is isotypically distinct from S5.22. In addition, although L12.2 reacts only with mature peripheral blood granulocytes, S5.22 reacts with leukemic cells of both myeloid and monocytic origin and with immature granulocyte precursor cells. This suggests that L12.2 interacts with an antigen that appears late in the differentiation pathway, whereas S5.22 binds to an antigen that is present throughout the myeloid lineage. By means of the under-agarose and Boyden chamber techniques, L12.2, but not S5.22, by itself was also found to be a potent granulocyte chemoattractant. Cells in a gradient of L12.2 display polarized and oriented morphology. L12.2 alone, but not S5.22, also stimulates granulocyte phagocytosis and induces superoxide anion production. Neither L12.2 nor S5.22 affected the release of myeloperoxidase or lysozyme from granulocytes either alone or in combination with FMLP, C5a, or the tumor promoter, 12-O-tetradecanoyl-phorbol-13-acetate (TPA). These results suggest that L12.2 interacts with a single antigenic determinant on granulocytes that is involved in chemotaxis, phagocytosis, and superoxide anion release.
Rejection of ticks from guinea pigs by anti-hapten-antibody-mediated degranulation of basophils at cutaneous basophil hypersensitivity sites: role of mediators other than histamine.
Authors: Brown S J , Askenase P W 
Published: December 2022

Abstract
Previous studies have established that recruitment of basophils to sites of tick feeding in guinea pigs is required to effect immune resistance. In the current study, actively sensitized guinea pigs treated three times daily with H-1 (mepyramine) and H-2 (cimetidine) histamine receptor antagonists, during the challenge tick infestation period, expressed normal resistance to Amblyomma americanum larvae. Similarly, naive guinea pigs treated with anti-histamines four times daily, beginning 7 days before transfer of immune serum and tick challenge and continuing through the tick infestation period, also expressed normal antibody-mediated resistance to A. americanum. These results indicated that histamine was not an important basophil mediator of the resistance response. Ticks allowed to feed on tissue rich in basophils that were induced by sensitization and subsequent local challenge with non-tick protein antigen, keyhole limpet hemocyanin (KLH), expressed normal yield. Ticks that fed on similar tissue rich in basophils induced by sensitization and challenge with KLH, in which the basophils expressed anti-picryl specificity due to systemic passive transfer of anti-picryl antibodies, were rejected when basophils were induced to degranulate by i.v. challenge with picryl antigen at 6 hr (29% rejection), 12 hr (18% rejection), 24 hr (22% rejection), and 48 hr (37% rejection) post-tick attachment. However, basophil degranulation at 18, 72 and 96 hr post-tick attachment had no adverse effect on tick feeding. These hosts were protected from systemic anaphylaxis by treatment with the anti-histamine mepyramine. Release of histamine occurred at tick feeding sites, but vasoactive effects were blocked by mepyramine treatment as evidenced by a lack of increased vascular permeability (bluing) at these sites compared with non-tick-infested tissues, or to cutaneous basophil hypersensitivity (CBH) sites of animals not protected with mepyramine. These results indicate that local recruitment and subsequent degranulation of basophils via immune mechanisms dependent on non-tick antigens can lead to tick rejection, and that basophil-derived mediators other than histamine are involved in this immune resistance response to A. americanum ticks. The identity of the crucial basophil mediator(s) is not known. The significant susceptibility of ticks to basophil-mediator release at 6 to 12 hr and 24 to 48 hr post-attachment coincides with the tick attaching and fast-feeding phases, respectively, suggesting that these phases of tick parasitism are particularly susceptible to the effect of basophil mediators other than histamine.
Filarial parasite-specific T cell lines: induction of IgE synthesis.
Authors: Nutman T B , Volkman D J , Hussain R , Fauci A S , Ottesen E A 
Published: December 2022

Abstract
The development of T lymphocyte lines and clones of defined specificity has provided an important method for investigating T cell recognition of foreign antigens as well as T cell influence on B cell activity. We described previously a parasite-specific T cell line (TCL) derived from a patient with a naturally acquired filarial infection and elevated levels of serum IgE. The TCL is composed of Leu-3+ helper cells and is maintained independent of exogenous growth factors. In the present study, we used these T cells to investigate their immunoregulatory function on the in vitro IgE response. These parasite-specific T cells can provide isotype-specific help for antigen-induced IgE production by B cells in vitro. Autologous T cells profoundly suppress IgE production in a concentration-dependent manner. Furthermore, soluble factors generated from these filarial-specific TCL after antigen stimulation are able to induce the production of IgE in normal human cells not already synthesizing measurable amounts of IgE in vitro. Partial physicochemical characterization of this factor has shown that it is heat labile, has an m.w. between 10,000 and 30,000 M(r), and is a mannose-rich glycoprotein.
Induction of neutralizing antibody in mice against poliovirus type II with monoclonal anti-idiotypic antibody.
Authors: Uytdehaag F G , Osterhaus A D 
Published: December 2022

Abstract
Syngeneic monoclonal anti-idiotope antibody Ab2,2-17C3SCC was raised against an idiotope on a protective monoclonal antibody with specificity for poliovirus type II. Ab2,2-17C3SCC detects a paratope-related interspecies IdX. Ab2,2-17C3SCC purified from supernatant fluids of hybridoma cells by protein A-Sepharose was injected into 4- to 6-wk-old BALB/c mice. The sera of the mice were screened for the expression of antibodies bearing the corresponding idiotope. Immunization of mice with Ab2,2-17C3SCC induced antibodies of complementary specificity. Furthermore, micro VN tests suggest that Ab2,2-17C3SCC can substitute for antigen in the induction of anti-polio neutralizing antibodies, and hence can function as a monoclonal anti-idiotypic vaccine.
Identification of several cell surface proteins of non-T, non-B acute lymphoblastic leukemia by using monoclonal antibodies.
Authors: Quackenbush E J , Letarte M 
Published: December 2022

Abstract
Monoclonal antibodies (MAb) were produced by immunization of BALB/c mice with cells from a non-T, non-B acute lymphoblastic leukemia (ALL) cell line. Nine distinct antigens (groups I to IX) were defined by these monoclonal antibodies, some of which appear to be associated with specific stages of cellular differentiation. The number of molecules of each MAb reactive with the ALL cell line, measured in a quantitative cellular radioimmunoassay, varied from 0.6 X 10(5) to 11 X 10(5) molecules/cell, indicating that the antigens identified represent major constituents of the cell surface. The biochemical nature of the antigens was examined on the ALL cell line by antibody affinity chromatography and/or immunoprecipitation and SDS-polyacrylamide gel electrophoresis. Groups I through III are composed of previously described antigens: HLA class I, HLA class II molecules, and CALLA, the common ALL antigen. The other MAb define antigens previously undescribed on non-T, non-B ALL cells. Group IV antigen is a polypeptide of apparent m.w. 95,000 distinct from CALLA. It is expressed on some ALL samples and on the vascular endothelial cells of several tissues. Group V antigen is a single polypeptide chain of m.w. 94,000, also distinct from CALLA and expressed by lymphocytes, thymocytes, acute myelogenous leukemia (AML) cells, and ALL cells. Group VI is a molecular complex composed of two noncovalently associated polypeptides of apparent m.w. 125,000 and 87,000 and appears to be restricted to ALL, AML, macrophages, and hematopoietic precursor cells. Group VII is a glycoprotein of apparent m.w. 85,000, which, within the thymus, is primarily restricted to the medullary area. It is also present on AML, bone marrow cells, and mature T and B lymphocytes. Group VIII is a disulfide-linked complex of apparent m.w. greater than 120,000 under nonreducing conditions. It is resolved into three major polypeptides of apparent m.w. 57,000, 47,000, and 41,000 under reducing conditions. This complex is found in greatest amounts on the non-T, non-B ALL cell line but is also present on AML, ALL, and on subpopulations of normal bone marrow and tonsil cells. Group IX antigen is a single polypeptide chain of apparent m.w. 51,000 on the ALL cell line. This antigen is expressed strongly on ALL and AML samples and on normal bone marrow; much lower antigenic density is found on thymus and tonsil cells. The antigens described here with a series of MAb produced in a single fusion represent a unique array of cell surface molecules of non-T, non-B ALL cells.(ABSTRACT TRUNCATED AT 400 WORDS)
Specific effect of anti-transferrin antibodies on natural killer cells directed against tumor cells. Evidence for the transferrin receptor being one of the target structures recognized by NK cells.
Authors: Alarcón B , Fresno M 
Published: December 2022

Abstract
Treatment of PBL or Percoll-isolated LGL with anti-transferrin antibodies plus complement reduced their natural killing activity against K-562 cells between 30 and 70%. The same antibodies inhibited natural cytotoxicity when added directly to the assay. Similar depletion or inhibition of NK cytotoxicity was observed when using HeLa cells as targets. The decrease or inhibition by transferrin antibodies was less marked when IFN-treated PBL or LGL as effector cells were used. The inhibition of anti-transferrin antibodies seems to be located at the level of the effector cell population. When PBL but not target K-562 cells were pretreated with anti-transferrin antibodies and were washed before use in the assay, cytotoxicity was decreased by 50%. In addition, about 80% of the LGL positively selected on anti-transferrin plates stained with Leu-11. Furthermore, no reduction by anti-transferrin antibodies plus complement treatment of PBL or LGL, or inhibition by antibodies alone, was observed when the cells were tested against HSV-1-infected cells. Membrane extracts from LGL inhibited NK cytotoxicity against K-562 or HeLa cells. Moreover, the inhibitory component of this extract was removed by anti-transferrin IgG but not by control IgG. These results are in agreement with the recent hypothesis that NK cells recognize the transferrin receptor in tumor target cells, because both the transferrin receptor and anti-transferrin antibodies may share a similar structure that interacts with the NK cells.
Functional heterogeneity in allospecific cytotoxic T lymphocyte clones. II. Development of syngeneic cytotoxicity in the absence of specific antigenic stimulation.
Authors: Claesson M H , Miller R G 
Published: December 2022

Abstract
Two out of four long-term murine allospecific cytotoxic T lymphocyte (CTL) clones tested could develop high levels of cytotoxicity against syngeneic target cells when cultured under appropriate conditions. All CTL clones maintained strict allospecificity so long as they were cultured with both appropriate allogeneic stimulator cells and growth factor (supernatant from secondary mixed lymphocyte cultures). In two of the clones, syngeneic reactivity rapidly developed when the allogeneic stimulator cells were replaced with syngeneic or third party stimulator cells, and when the supernatant from EL4 thymoma cells stimulated with phorbol ester was used as growth factor. In addition to killing the appropriate allogeneic target, clones with syngeneic reactivity could kill both syngeneic C57BL/6 targets and H-2-congenic BALB.B targets but not third party unrelated targets, suggesting that the self structure recognized was coded for within the major histocompatibility complex. Such clones did not kill the natural killer (NK) target YAC. The results obtained from cold target inhibition and from subcloning at limiting dilution of clones with syngeneic reactivity suggested that both allogeneic and syngeneic reactivity could be expressed by the same individual cell in the CTL clone. The specificity for syngeneic H-2 as opposed to third party H-2 and NK-sensitive target cells, and the observation that both allospecific and syngeneic killing could be partially blocked by anti-Lyt-2 antibody treatment of the CTL, strongly suggested that different recognition structures are involved in CTL-mediated syngeneic cytotoxicity and NK cytotoxicity.
Induction of proliferation in vitro of resting human natural killer cells: expression of surface activation antigens.
Authors: London L , Perussia B , Trinchieri G 
Published: December 2022

Abstract
In this report, we show that resting human peripheral blood NK cells, positively enriched with antibody B73.1, can be induced to proliferate in vitro in short-term cultures, and newly express membrane activation antigens. B73.1+ NK cells, cultured for 6 days in the presence of conditioned medium containing IL 2 and irradiated B lymphoblastoid cells, show significant [3H]TdR incorporation beginning on day 4. At that time, a large proportion of the cells express HLA-DR and 4F2 antigens, and transferrin and IL 2 receptors, all detectable at high density by indirect immunofluorescence with the use of monoclonal antibodies. These cells maintain their ability to lyse target cells spontaneously or in the presence of antibodies. By two-color immunofluorescence and cell cycle analysis combined with indirect immunofluorescence, we demonstrate directly that the activation antigens are expressed on all NK (B73.1+) cells in the S/G2/M phases of the cell cycle, and on only a proportion of those in the G0/G1 phases.
Modulation of human natural killer cell function by L-leucine methyl ester: monocyte-dependent depletion from human peripheral blood mononuclear cells.
Authors: Thiele D L , Lipsky P E 
Published: December 2022

Abstract
L-leucine methyl ester (Leu-OMe) causes lysosomal disruption and death of human monocytes (M phi). In addition, Leu-OMe removed natural killer cell (NK) activity from human peripheral mononuclear cells (PBM). Thus, a brief preincubation of PBM with Leu-OMe (greater than 1 mM) caused irreversible loss of NK function as assessed by the lysis of K562 targets. By contrast, a variety of other amino acid methyl esters, including L-glutamic dimethyl ester, L-valine methyl ester, and L-isoleucine methyl ester caused reversible inhibition of NK activity in a manner that was similar to other lysosomotropic agents such as chloroquine and ammonium chloride, but did not cause irreversible loss of all NK function. Leu-OMe appeared to cause actual removal of NK effector cells from PBM, because K562 target binding cells, Leu-11b+ lymphocytes, and OKM1+ lymphocytes were depleted. If M phi were removed from PBM before the incubation, Leu-OMe caused only reversible inhibition of NK function in a manner similar to that observed with other amino acid methyl esters. Upon the addition of freshly isolated M phi, polymorphonuclear leukocytes, or sonicates of these cells to M phi-depleted lymphocyte populations, irreversible ablation of NK function was again observed as a result of Leu-OMe exposure. After in vitro culture, M phi lost their susceptibility to Leu-OMe toxicity and the ability to mediate the irreversible deletion of NK cells resulting from Leu-OMe incubation. These results indicate that in the absence of M phi, Leu-OMe and a variety of other amino acid methyl esters are reversible inhibitors of NK function. However, Leu-OMe is unique in that it can interact with M phi or granulocytes to effect an irreversible loss of NK activity from human peripheral blood lymphocytes.
Leu-11+ lymphocytes with natural killer (NK) activity are precursors of recombinant interleukin 2 (rIL 2)-induced activated killer (AK) cells.
Authors: Itoh K , Tilden A B , Kumagai K , Balch C M 
Published: December 2022

Abstract
Precursors of activated killer (AK) cells cytotoxic for human noncultured metastatic melanoma and colon carcinoma were characterized. These cells required 3 days incubation with recombinant interleukin 2 (rIL 2) and DNA synthesis for the induction of AK activity. Both negative and positive cell purification methods were used to identify the subpopulation of cells containing AK precursors. By complement-mediated cell depletion studies, AK precursors were largely present in the Leu-11+ fraction, and to a much lesser extent in the Leu-7+ and Leu-2a+ fractions; they were absent in Leu-3a+ and Leu-4+ cells. Lymphocyte subpopulations were then purified with a cell sorter to positively select for the subset containing AK precursors. Leu-11+ cells had the highest level of AK activity and proliferative response when cultured for 3 days with rIL 2 as well as the highest level of NK activity before culture. Leu-7+ cells had neither AK activity nor a proliferative response when cultured with rIL 2, although they still possessed high NK activity. The same levels of AK and NK activity were found in Leu-2a+ and Leu-2a- fractions, but both activities were absent among Leu-4+ and Leu-3a+ cells. Further fractionation with a two-step sorting technique showed that the highest AK activity resided in the Leu-7-Leu-11+ cell fraction. Morphologically, this subfraction was granular lymphocytes. Titration experiments or rIL 2-responsive cells showed that the number of cells required to achieve a comparable level of rIL 2 proliferative response were as follows: 35 X 10(3) cells from unseparated PBL, 10 X 10(3) cells from Leu-11+ cells, 3.3 X 10(3) from Leu-7-Leu-11+ cells, and 640 X 10(3) cells from Leu-7+ cells. These results indicate that the lymphocyte subpopulation that proliferates in the presence of rIL 2 and then develops AK activity was a subpopulation of Leu-11+ granular lymphocytes, which also possessed the highest NK activity. These Leu-11+ cells lacked the antigens defined by the Leu-7, Leu-3a, or Leu-4 antibodies. Although Leu-7+ cells did not respond to rIL 2 by themselves, they may play a role in the induction of AK activity.
Antibody localization in the glomerular basement membrane may precede in situ immune deposit formation in rat glomeruli.
Authors: Agodoa L Y , Gauthier V J , Mannik M 
Published: December 2022

Abstract
The administration of cationized antibodies, specific to human serum albumin, into the renal artery of rats caused transient presence of IgG in glomeruli by immunofluorescence microscopy. Intravenous infusion of appropriate doses of antigen after the injection of cationized antibodies resulted in immune deposit formation in glomeruli that persisted through 96 hr. By electron microscopy, these deposits were located in the subepithelial area. The injection of large doses of antigen produced immune deposits which were present in glomeruli for only a few hours, presumably due to formation of only small-latticed immune complexes. The presented data indicate that cationic antibodies bound to the fixed negative charges of the glomerular basement membrane can interact with circulating antigen to form immune deposits in glomeruli. This mechanism may be important because anionic antigens have been shown to induce the synthesis of cationic antibodies.
Lipopolysaccharide-treated RAW 264.7 cells produce a mediator that inhibits lipoprotein lipase in 3T3-L1 cells.
Authors: Mahoney J R , Beutler B A , Le Trang N , Vine W , Ikeda Y , Kawakami M , Cerami A 
Published: December 2022

Abstract
RAW 264.7 cells upon stimulation with lipopolysaccharide secrete a protein mediator(s) that suppresses lipoprotein lipase activity in differentiated 3T3-L1 cells. The mediator(s), which is absent from unstimulated culture supernatants, is nondialyzable and thermolabile. Preliminary characterization suggests that this mediator(s) may be the same as that previously found in medium from lipopolysaccharide-treated thioglycollate-elicited mouse peritoneal macrophage cultures.
Regulation of secretory component by glucocorticoids in primary cultures of rat hepatocytes.
Authors: Wira C R , Colby E M 
Published: December 2022

Abstract
The present study examined the effects of steroid hormones on the production of secretory component (SC) by rat hepatocytes in cell culture. When hepatocytes were incubated in the presence of cortisol (10(-6) M), the levels of SC in media increased significantly after 2 days of incubation. This response was dose-dependent and specific for glucocorticoids because progesterone, dihydrotestosterone, and estradiol had no effect. When estradiol was added to the incubation media along with dexamethasone, a known potent synthetic glucocorticoid, it diminished the glucocorticoid response. The addition of cycloheximide to incubation media significantly decreased the effect of dexamethasone on SC accumulation. These findings suggest that glucocorticoid regulation of hepatocyte SC most likely involves stimulation of its synthesis. In addition, our results suggest that endogenous glucocorticoids may play a role in enhancing the clearance of IgA from blood into bile in the intact animal.
2-Chloroadenosine: a selective lethal effect to mouse macrophages and its mechanism.
Authors: Saito T , Yamaguchi J 
Published: December 2022

Abstract
In our studies on the effects of purine compounds on immune responses in vitro, we found that 2-chloroadenosine (2-Cl Ado) exhibited a potent lethal effect on a viability of mouse adherent cells derived from the peritoneal cavity. The lethal effect was specific for adherent peritoneal cells (PC) (macrophages) and was prevented by exogenous addition of adenosine (Ado) or coformycin, a potent inhibitor of adenosine deaminase. A rapid decrease of intracellular ATP content (26% of control) in adherent PC was observed soon after 1 hr exposure to 2-Cl Ado (0.1 mM), and this decrease of ATP was comparable with that of monoiodoacetate (MIA, 0.1 mM)- or NaN3 (5 mM)-treated adherent PC. The ATP decrease by 2-Cl Ado was restored to 88 or 90% of control value by 1 hr addition of Ado or coformycin, respectively. Polymorphonuclear cells and lymphocytes to which 2-Cl Ado did not exhibit the lethal effect did not cause a significant ATP decrease of the cells. Therefore, the data suggested that the reason for the lethal effect on adherent PC treated with 2-Cl Ado could be attributed to a rapid decrease of ATP content at an early time. We assume that 2-Cl Ado competes with intracellular Ado in macrophages and then causes the adenosine starvation resulting in the ATP decrease.