bluuebunny/crossref_metadata_2025_split huggingface dataset:
Human natural killer cell recognition of herpes simplex virus type 1 glycoproteins: specificity analysis with the use of monoclonal antibodies and antigenic variants.
Authors: Bishop G A , Marlin S D , Schwartz S A , Glorioso J C 
Published: December 2022

Abstract
The specificity of human natural killer (NK) cells for herpes simplex virus type 1 (HSV-1)-infected WISH cells was examined by using virus-specific antibodies to block NK killing and by using targets infected with virus variants that express antigenically altered cell surface glycoproteins. Fab fragments of human immunoglobulin (Ig) derived from an HSV-1 seropositive individual blocked NK activity against HSV-1-infected cells, whereas Fab fragments from a seronegative individual had no effect. Fab fragments of monoclonal antibodies specific for different epitopes of the HSV-1 glycoproteins gB and gC blocked NK activity, suggesting that NK cells interact directly with viral glycoproteins. In contrast, a control (HSV-unreactive) monoclonal antibody did not block NK activity. Further evidence that the blocking activity was associated with HSV glycoproteins was obtained by showing that: a) gC-specific antibodies did not decrease NK activity against cells infected with an HSV-1 mutant which does not insert gC into infected cell surface membranes; b) gB-specific antibodies did not reduce NK cytotoxicity against target cells infected with HSV-1 in the presence of 2-deoxy-D-glucose (2dG), which prevents cell surface expression of gB; c) HSV-1 glycoprotein-specific antibodies did not alter NK activity against uninfected cells or against K562, an NK-susceptible tumor cell line; and d) a monoclonal antibody reactive with a cell membrane glycolipid markedly reduced NK reactivity against K562 but had little effect on NK reactivity against HSV-1-infected cells, suggesting that NK cells recognize different determinants on the two types of target cells. Analysis of the fine specificity of NK cell recognition of HSV-1 glycoproteins was performed by using target cells infected with antigenic variants of HSV-1 referred to as monoclonal antibody-resistant (mar) mutants. mar mutants are altered in distinct epitopes of gB or gC, resulting in loss of recognition by the selecting virus-neutralizing monoclonal antibody. NK activity was reduced against cells infected with some, but not all, of these variants. Together, these findings demonstrated a positive correlation between expression of HSV-1 glycoproteins gB and gC and susceptibility of HSV-1-infected target cells to NK activity, implicating the viral glycoproteins as cell surface components recognized by NK cells. Moreover, mutations affecting glycoprotein epitopes defined by monoclonal antibodies also influenced the interaction between NK effector cells and HSV-1-infected target cells, suggesting that viral antigenic sites recognized by NK cells overlap with those recognized by anti-HSV-1 antibodies.
Roles of V antigen in promoting virulence and immunity in yersiniae.
Authors: Une T , Brubaker R R 
Published: December 2022

Abstract
It is established that yersiniae harboring an approximately 45-megadalton Vwa-plasmid can produce V and W antigens (Vwa+), and that sera containing anti-V provides passive protection to mice against Yersinia pestis. This observation was extended by the use of monospecific anti-V prepared by injecting rabbits with partially purified V, absorption of antisera with a Vwa- extract, and then separation of gamma-globulin by traditional processes of fractionation or by affinity chromatography. These preparations provided passive protection against 10 minimum lethal doses of virulent Y. pestis KIM, Yersinia pseudotuberculosis PB1, and Yersinia enterocolitica WA. Kinetics of elimination of these Vwa+ yersiniae from organs and blood of passively immunized mice closely resembled those of avirulent Vwa- mutants from normal mice. Injection into mice of sterile crude extracts of Y. pseudotuberculosis PB1 containing V promoted significant survival and retention of Vwa- mutants of Y. pestis, Y. pseudotuberculosis, and Y. enterocolitica. This effect was eliminated by the removal of V before injection by precipitation with monospecific antibody. These results indicate that V antigen per se is the major virulence factor mediated by Vwa-plasmids.
Alloimmune memory is absent in Hymeniacidon sinapium, a marine sponge.
Authors: Smith L C , Hildemann W H 
Published: December 2022

Abstract
The southern California sponge Hymeniacidon sinapium can recognize and reject transplanted allogeneic tissues. This species reveals a complex rejection response that involves cellular infiltration into the graft interface and a deposition at that site of a fibrous wall. The response then proceeds to a cytotoxic reaction in which the cells in the graft zone become necrotic and slough off, resulting in allogeneic tissue separation. The rate and intensity of this response varies with the genetic constitutions of the paired sponges and the temperature of the water. In experiments employing pre-sensitized second-set and unrelated third-party graftings, with changes in temperature, sensitization times, intervals before regrafting, and experimental sites, this species did not exhibit alloimmune memory (i.e., accelerated second-set rejection). When the allorejection described here for H. sinapium is taken in conjunction with rejection responses reported for other sponge species, it is apparent that sponges have two major methods for responding to allogeneic contacts: barrier formation or cytotoxicity. The rejection method seems to correspond with the presence or absence of immune memory, and may, in part, be correlated with habitat and frequency of contacts with "non-self." The development of the rudimentary immune system in metazoans is discussed in relation to the rejection of naturally transplanted tissues in addition to challenges from pathogens.
Inhibition of the T suppressor circuit of delayed-type hypersensitivity by interferon.
Authors: Knop J , Stremmer R , Taborski U , Freitag W , de Maeyer-Guignard J , Macher E 
Published: December 2022

Abstract
The effects of electrophoretically pure murine interferon (Mu-IFN-alpha beta) on the T suppressor pathway and on the T effector cell of delayed hypersensitivity (TDH) were investigated in BALB/c mice, in a 2,4-dinitrofluorobenzene (DNFB) contact-sensitivity model. Various T cell subpopulations, suppressor T cells of the afferent (Ts-aff) and efferent (Ts-eff) types, an auxiliary Ts (Ts-aux), as well as TDH were induced, and their function was assessed in transfer experiments. The results were as follows. At a dose of 5 X 10(3) U, IFN was shown to inhibit the Ts-aff response, when given to the donor animal shortly after induction of the Ts-aff subpopulation or when injected into the recipient 2 hr after spleen cell transfer. Pretreatment in vitro with IFN of the splenic cells to be transferred also abolished the Ts-aff response. Similar amounts of IFN were able to inhibit the generation of Ts-eff in the donor animals, whereas 10-fold-higher amounts were needed in vivo or in vitro to block the functional expression of Ts-eff in the recipient animal. Intravenous injection of IFN into recipients of Ts-eff on day 0 and 1 after sensitization inhibited the expression of the Ts-eff transferred 1 day before ear challenge. This suggests that the Ts-aux response required for the TDH suppression by Ts-eff is blocked by IFN. Secretion of a suppressor factor by Ts in vitro was not blocked by IFN. Treatment of the donor of suppressor factor-secreting Ts with IFN, however, blocked the induction of this Ts. The TDH were not sensitive to IFN even at amounts approximately 100 times higher than those used for the Ts inhibition in vivo as well as in vitro. These results demonstrate that low amounts of IFN may selectively block the suppressor pathway, because induction of these regulatory T cell subsets appears to be particularly sensitive to IFN. The exact mechanism of the IFN-mediated inhibition of Ts is not yet clear. The data suggest an important regulatory function of IFN in delayed-type hypersensitivity (DTH) reactions.
Lymphocyte changes during chronic administration of and withdrawal from corticosteroids: relation to Pneumocystis carinii pneumonia.
Authors: Walzer P D , LaBine M , Redington T J , Cushion M T 
Published: December 2022

Abstract
Corticosteroids were administered for up to 8 wk in adult Lewis rats to provoke Pneumocystis carinii pneumonia, and lymphocyte subsets were analyzed at different body sites with monoclonal antibodies by flow microfluorometry in a fluorescence activated cell sorter. The rats became chronically ill, debilitated, and exhibited marked involution of all lymphoid tissues. The lymphocytopenia was characterized in peripheral blood by a large fall in the frequency of T helper cells, and in the lungs by a fall in T helper (Th) cells and a rise in T suppressor (Ts) cells; at both sites there was reversal of the Th to Ts ratio. These changes were not found in the thymus, spleen, or bone marrow. When corticosteroids were withdrawn, the rats gained weight, cleared P. carinii from the lungs, and regenerated their lymphoid tissues. The lymphocyte subpopulations exhibited variation in their frequencies at different body sites, but gradually returned to baseline levels. Thus, in this model chronic corticosteroid administration results in profound generalized lymphocyte depletion and changes in the proportions of circulating and pulmonary T cell subsets. These abnormalities may be an important immunologic mechanism in the development of P. carinii pneumonia.
Anti-native DNA antibodies from autoimmune sera also bind to DNA in mitochondria.
Authors: Reimer G , Rubin R L , Kotzin B L , Tan E M 
Published: December 2022

Abstract
Sera from 20 patients with systemic lupus erythematosus (SLE), selected for elevated titers of antibody to native DNA (nDNA), were examined by indirect immunofluorescence (IF) on tissue culture Hep-2 and rabbit kidney cells. Twelve sera showed a particulate cytoplasmic staining, in addition to nuclear IF. Double IF staining by using a mouse monoclonal anti-nDNA and a human serum containing anti-mitochondrial antibody as probes showed that the cytoplasmic structures recognized by these 12 SLE sera were mitochondria. SLE sera showing mitochondrial staining had high anti-nDNA levels, as assessed by ELISA (3.5 +/- 1.9 O.D.), compared with those not showing this staining pattern (0.8 +/- 0.4 O.D.). Mitochondrial staining was abolished by DNase I pretreatment of the substrates. Liquid phase absorption of serum anti-nDNA with S1 nuclease-treated calf thymus DNA or purified mitochondrial DNA also removed staining. These findings demonstrate that anti-nDNA antibodies from patients with SLE bind to DNA in intact mitochondria. Therefore, mitochondrial IF staining on tissue culture cells in the presence of nuclear staining should be interpreted with caution, because the phenomenon could be entirely related to anti-native DNA. These observations might also provide new insights concerning the nature of immunogenic cellular components stimulating anti-DNA production.
IL 1 requirement for B cell activation revealed by use of adult serum.
Authors: Hoffmann M K , Mizel S B , Hirst J A 
Published: December 2022

Abstract
Fetal calf serum is an essential component of the culture medium developed by Mishell and Dutton for the immunization of murine spleen cells in vitro. Serum from adult donors (mouse, human, rabbit) does not support antibody synthesis in this system. This "deficiency" of adult serum can be overcome with IL 1. Adult serum in the presence of IL 1 is as effective in stimulating a B cell response against xenogeneic red cells as fetal calf serum. We attribute the capacity of fetal calf serum to support an immune response in the absence of exogenous IL 1 to serum factors that cause macrophages to release IL 1 endogenously. Our findings strengthen the notion that IL 1 plays an essential role in the process of B cell activation and suggests that the use of fetal calf serum should be avoided in studies concerned with the function of interleukin 1.
The interaction of lymphocyte membrane proteins with the lymphocyte cytoskeletal matrix.
Authors: Woda B A , Woodin M B 
Published: December 2022

Abstract
Lymphocyte membrane proteins are important in the transduction of signals across the plasma membrane. Visual and biophysical studies have shown that after ligand binding, membrane proteins may become immobile in the plane of the membrane and may cap. In intact cells, binding of cross-linking ligands to surface immunoglobulin converts it to a detergent-insoluble state (77% insoluble). This conversion is positively correlated with the transmission of a mitogenic signal. Class II histocompatibility proteins (Ia) and thy-1 remain predominantly detergent soluble (60 to 97% soluble). Insolubilized membrane proteins may be solubilized by incubating the detergent insoluble cytoskeletons with 0.34 M sucrose, 0.5 mM ATP, 0.5 mM dithiothreitol, 1 mM EDTA, or 3 X 10(-5) M DNAase I, 1 mM EDTA. To determine if the membrane-associated cytoskeleton contains the sufficient components for ligand-induced receptor insolubilization, experiments were done with a crude plasma membrane fraction. The results with whole cells or crude plasma membranes were comparable. These studies support the view that ligand-induced insolubilization of membrane proteins is due to their interaction with cytoskeletal structures.
H-40, an antigen controlled by an Igh-linked gene and recognized by cytotoxic T lymphocytes. II. Recognition of H-40 as a tumor antigen in leukemic animals.
Authors: Henderson L A , Ciavarra R , Riblet R , Forman J 
Published: December 2022

Abstract
C.B-20 (Ighb) but not (C.B-20 X BALB/c)F1 mice reject BCL1, a sIg+ tumor that spontaneously arose in an Igh congenic BALB/c (Igha) mouse. C.B-20 immune T cells from mice immunized with either BCL1 or BALB/c splenocytes adoptively transfer tumor protection to sublethally irradiated C.B-20 but not BALB/c or (BALB/c X C.B-20)F1 mice. These data suggest that BALB/c and BCL1 share an antigen, which if present in the host prevents the immune cells from eradicating the tumor. The antigen is controlled by H-40, a gene that maps to the C end of the Igh complex, telomeric to Tsu and in the region of Pre-1. The ability of H-40 to act as a tumor antigen for other BALB/c tumors inoculated into C.B-20 hosts was investigated. H-40 did not elicit rejection of P1798 (T lymphoma), Meth A (fibrosarcoma), or MOPC-315 (alpha, lambda myeloma) tumor cells. C.B-20 mice that previously rejected BCL1, however, showed partial resistance to a low challenge dose of the MOPC-104E (mu, lambda myeloma) tumor. These data suggest that H-40 has a differential degree of expression on BALB/c tumor cells. The ability of the adoptively transferred cells to confer protection against BCL1 is abrogated by pretreatment of the cells with anti-Lyt-1 or anti-Lyt-2 antibodies. However, an admixture of anti-Lyt-1- and anti-Lyt-2-treated cells provided protection. These data, together with the results detected by cytotoxic T lymphocyte (CTL) activity in vitro, indicate that H-40 can serve as a target antigen for tumor rejection by CTL in allogeneic hosts. The implications of the results for allogeneic bone marrow transplantation into leukemic individuals who benefit from a graft vs leukemia effect are discussed.
T-T cell interaction in the induction of delayed-type hypersensitivity (DTH) responses: vaccinia virus-reactive helper T cell activity involved in enhanced in vivo induction of DTH responses and its application to augmentation of tumor-specific DTH responses.
Authors: Takai Y , Kosugi A , Yoshioka T , Tomita S , Fujiwara H , Hamaoka T 
Published: December 2022

Abstract
The role of antigen-specific helper T cells in augmenting the in vivo development of delayed-type hypersensitivity (DTH) responses was investigated. C3H/HeN mice were inoculated i.p. with vaccinia virus to generate virus-reactive helper T cell activity. These vaccinia virus-primed or unprimed mice were subsequently immunized subcutaneously (s.c.) with either trinitrophenyl (TNP)-modified syngeneic spleen cells (TNP-self), vaccinia virus-infected spleen cells (virus-self), or cells modified with TNP subsequent to virus infection (virus-self-TNP). Seven days later, these mice were tested for anti-TNP DTH responses either by challenging them directly with TNP-self into footpads or by utilizing a local adoptive transfer system. The results demonstrated that vaccinia virus-primed mice failed to generate significant anti-TNP DTH responses when s.c. immunization was provided by either virus-self or TNP-self alone. In contrast, vaccinia virus-primed mice, but not unprimed mice, could generate augmented anti-TNP DTH responses when immunized with virus-self-TNP. Anti-vaccinia virus-reactive helper activity was successfully transferred into 600 R x-irradiated unprimed syngeneic mice by injecting i.v. spleen cells from virus-primed mice. These helper T cells were found to be antigen specific and were mediated by Thy-1+, Lyt-1+2- cells. DTH effector cells enhanced by helper T cells were also antigen specific and were of the Thy-1+, Lyt-1+2- phenotype. Furthermore, vaccinia virus-reactive helper T cell activity could be applied to augment the induction of tumor-specific DTH responses by immunization with vaccinia virus-infected syngeneic X5563 tumor cells. T-T cell interaction between Lyt-1+ helper T cells and Lyt-1+ DTH effector T cells is discussed in the light of the augmenting mechanism of in vivo anti-tumor-specific immune responses.
Analysis of the mode of antigen presentation required for triggering of T cell proliferation by using various azobenzenearsonate-tyrosine derivatives.
Authors: Tadakuma T , Yasuda T , Tamura A , Saito S , Tsumita T , Saito K 
Published: December 2022

Abstract
Various azobenzenearsonate-tyrosine (ABA-Tyr) derivatives were synthesized by modifying amino and carboxyl groups at the alpha-carbon of tyrosine, with preservation of most of the ABA-Tyr moiety (ABA plus hydroxyphenyl portion of tyrosine). These derivatives were tested for the ability to stimulate ABA-L-Tyr specific T cell lines derived from B10.BR and B10.S mice. ABA-acetyltyramine, ABA-hydroxyphenylpropionic acid (ABA-PPr), and ABA-propylphenol, which lack either the carboxyl or amino group or both, could not induce T cell proliferation. The lack of stimulation by these derivatives was not due to their cytotoxic effects. A similar pattern of proliferation was obtained on stimulating lymph node T cells from B10.BR and B10.S mice primed with ABA-L-Tyr. Some differences were observed, however, between B10.BR and B10.S mice. ABA-L-Tyr-specific T cells from B10.BR mice could not respond well to ABA-D-Tyr in contrast to B10.S T cells. Furthermore, B10.BR mice primed with ABA-acetyltyramine or ABA-PPr in complete Freund's adjuvant could not induce ABA-L-Tyr-reactive T cells, whereas T cells from B10.S mice primed with these derivatives could proliferate in the presence of ABA-L-Tyr. The differences between B10.BR and B10.S mice were further investigated by using (B10.S X B10.BR)F1 mice. T cells from ABA-L-Tyr-immunized F1 mice responded poorly to ABA-D-Tyr when presented with B10.BR antigen-presenting cells (APC), but responded well when presented with B10.S APC. Similarly, T cells from ABA-PPr-primed F1 mice did not proliferate to ABA-L-Tyr in the presence of B10.BR APC, but could proliferate in the presence of B10.S APC. Our results clearly indicate that the presence of charged groups at the alpha-carbon of tyrosine plays a critical role in the triggering of ABA-L-Tyr-specific T cell proliferation. The significance of these results is discussed.
Hybridoma anti-DNA autoantibodies from patients with rheumatoid arthritis and systemic lupus erythematosus demonstrate similar nucleic acid binding characteristics.
Authors: Rauch J , Massicotte H , Tannenbaum H 
Published: December 2022

Abstract
Hybridoma anti-DNA antibodies have been generated from the fusion of the GM 4672 lymphoblastoid line with peripheral blood lymphocytes from four normal subjects, nine patients with rheumatoid arthritis (RA), and 13 patients with systemic lupus erythematosus (SLE). A total of 441 hybridoma clones were obtained, of which 37 secreted anti-DNA autoantibodies. The nucleic acid binding characteristics of the anti-DNA antibodies produced by two hybridomas from normal subjects, nine hybridomas from RA patients, and 18 hybridomas from SLE patients are reported. The hybridoma anti-DNA antibodies from all three groups showed similar antigen-binding characteristics for denatured DNA (dDNA), native DNA (nDNA), poly(I), poly(dT), and cardiolipin, by both direct binding and competitive binding analyses. One difference noted between normal-derived anti-DNA antibodies and autoimmune-derived antibodies was the inability of the former to react with z-DNA. However, this requires further substantiation with larger numbers of normal-derived clones. The broad overlap of reactivity to nucleic acid antigens among individual anti-DNA autoantibodies found in two clinically different autoimmune diseases, namely RA and SLE, suggests that the pathogenicity of anti-DNA autoantibodies may bear no relationship to their nucleic acid antigen-binding characteristics.
Differences in T15 expression of primary and secondary anti-PC responses with T cells from T15+ and T15- donors.
Authors: Smyk S K , McNamara M K , Gleason K S , Kohler H 
Published: December 2022

Abstract
The expression of T15 idiotype dominance with T cells from T15- mice was investigated. It was found that T15 dominance in the T-dependent response to phosphorylcholine (PC) could be generated by unprimed BALB/c B cells with T cells from T15+ and xid T15- mice. T15 dominance was also expressed when T15 neonatally suppressed BALB/c were used as T cell donors. With PC-primed B cells, however, T15 dominance was not established until 3 wk after adoptive co-transfer with T helper cells from xid NBF1 mice. To further study the different efficiencies of T cells for T15 dominance, limiting dilution analysis was performed. The data demonstrate that T15-specific T cell populations in BALB/c mice and NBF1 male mice differ in their precursor frequencies. In BALB/c mice, a frequent set of T15/M167-recognizing T helper cells is present; a corresponding frequent set of cells is absent in NBF1 males. This difference is likely to be one of the reasons why dominance is not immediately established after transfer of T cells from xid mice.