bluuebunny/crossref_metadata_2025_split huggingface dataset:
Splenic B cells function as immunogenic antigenpresenting cells for the induction of effector T cells
Authors: Tzehoval Esther , De Baetselier Patrick , Ron Yacov , Tartakovsky Boris , Feldman Michael , Segal Shraga 
Published: February 2007

AbstractPrevious studies performed in our laboratory have revealed that an ordered, sequential, tricellular interaction is obligatory for the antigen‐driven induction of a specific effector memory T cell. Thus, it was found that antigen‐pulsed peritoneal macrophages signal, in spleen cells, the generation of antigen‐specific initiator lymphocytes. These lymphocytes, following injection to syngeneic recipients, recruit, in the draining lymph nodes, “virgin” antigen‐reactive T lymphocytes. Although the nature of the first and last cell in the interacting sequence was well characterized, the identity of the intermediary initiator splenic cell was obscure. Studies were carried out to characterize the nature of the splenic initiator cells. It was found that spleen cells from nu/nu, adult thymectomized and neonatal thymectomized, or spleen cells from normal donors which had been subjected to cytolysis using anti‐Thy‐1.2 antibodies in the presence of complement, did generate, following interaction with keyhole limpet hemocyanin (KLH)‐fed macrophages, specific initiator cells. Carrageenan impairment of spleen macrophages did not affect the generation of initiator cells, nor did the depletion of dendritic cells from the spleen. On the other hand highly enriched B cell, but not highly enriched T cell populations, when seeded on KLH‐pulsed macrophages, generated antigen‐specific initiators, which, in vivo, recruited antigen‐reactive T cells. It thus appeared that B lymphocytes can function as intermediary obligatory antigen‐presenting cells and actively transfer immunogenic signals from peritoneal antigen‐presenting cells to T lymphocytes. These findings may therefore suggest that antigen‐specific B cells do not function solely as antibody‐producing cells, but, once activated by macrophages, may control the induction and differentiation of some antigen‐reactive T cell subsets. Thus, one can view the B cell as an important regulatory cell of both cellular and humoral immune functions. The significance of this observation with regard to Ir gene control at the level of B lymphocytes is discussed.
The preparation of mouse VH fragments and the characterization of heterologous anti‐mouse VH antibodies
Authors: Karjalainen Klaus 
Published: February 2007

AbstractVH fragments were prepared from several mouse IgM molecules by cyanylation. In all cases VH fragments were purified to homogeneity by using Ig light chain affinity columns. Several different anti‐VH antisera were prepared in rabbits and the specificities of these antibodies were studied. Two patterns of cross‐reactivities were observed: (a) some anti‐VH antibodies reacted only with closely related VH molecules, e.g., anti‐VH HPC52 anti bodies reacted only with VH of phosphorylcholine‐binding myeloma or hybridoma protesin, and concrodantly, stained about 4% of mouse spleen B cells; (b) on the other hand, antisera‐like anti‐VH 104E and 8916 antibodies were very cross‐reactive. Binding assays showed that both of these anti‐VH antibodies reacted with 50–60% of mouse immunoglobulins, and thus the pool of these antibodies reacted with about 95% of mouse VH regions. Concordantly, anti‐VH 104E antibodies stained in the fluorescence‐activated cell sorter (FACS) analysis more than 50% of mouse spleen B cells.Cross‐reactive anti‐VH antibodies (“anti‐framework”) did not stain T cells nor did they immunoprecipitate VH‐like molecules which were synthesized by T cells.
Electron microscopy of the complement protein C1q from the bullfrog, Rana catesbeiana
Authors: Slayter Henry S. , Alexander Richard J. , Steiner Lisa A. 
Published: February 2007

AbstractThe complement protein C1q, isolated from bullfrog (Rana catesbeiana) serum, was found by electron microscopy to resemble human C1q; peripheral globular units, probably six in number, are connected by thin strands to a hollow stem‐like central structure. The dimensions of frog and human C1q were also found to be very similar. These results are consistent with earlier observations that frog and human C1q are similar, although not identical, in overall size, subunit structure, amino acid composition, and functional properties. Evidently this protein, which binds to antigen‐antibody complexes and to C1r and C1s, thereby forming a physical link between the immune and complement systems, has been highly conserved in evolution.
The genetic basis of antibody production: A single heavy chain variable region gene encodes all molecules bearing the dominant anti‐arsonate idiotype in the strain A mouse
Authors: Siekevitz Miriam , Huang Shu Ying , Gefter Malcolm L. 
Published: February 2007

AbstractA nucleic acid probe specific for heavy chains bearing the cross‐reactive idiotype (Id) associated with the anti‐p‐azophenylarsonate response of strain A mice has been prepared. Analysis of arsonate‐binding Id+ hybridoma cell lines has revealed that all of them contain the same germ‐line VH gene rearranged to the JH2 segment. An Id+ hybridoma which is unable to bind arsonate utilized the same VH gene, but it has apparently rearranged to the JH4 segment. Id− cell lines contain other rearranged VH genes. Analysis of DNA of strain A mice revealed that there is apparently only one germ line gene that can give rise to Id+ heavy chains. Since the Id is expressed as a large collection (> 50) of related but nonidentical heavy chain sequences, we conclude that their diversity is the result of a somatic mutation process. Analysis of a single hybridoma cell line (45–59) reveals that somatic mutation can operate on an Id‐encoding gene and result in an antigen‐binding molecule that has lost all of its Id determinants. Further analysis of the genome of strain A mice has revealed the presence of germ‐line genes differing from the Id‐encoding gene by at least 8 base pairs. These genes, however, apparently do not contribute to the anti‐arsonate Id response.
Temperature and cellular regulation of spontaneous cytotoxicity in the shark
Authors: Pettey Carolyn L. , McKinney E. Churchill 
Published: February 2007

AbstractSpontaneous cytolytic activity of shark peripheral blood leukocytes is observed only during periods of decreased environmental temperature (< 23°C). The effector cell is adherent to glass and is phagocytic. Leukocytes tested during warmer periods (26–31°C) exhibit no spontaneous activity; however, glass‐adherent cells isolated from those fish are cytotoxic in vitro, indicating that the effector cell is present at all temperatures. During warmer temperatures, nonadherent cells added to adherent cells were shown to inhibit spontaneous cytotoxicity. This inhibition requires viable cells in contact with the spontaneous cytotoxic population. Thus decreased environmental temperature correlated with spontaneous cytotoxicity, and appears to affect a regulatory cell that is glass nonadherent. In addition, the cytotoxic effector cell is more active at 23°C than 30°C in vitro. These data show that by the time of emergence of the nurse shark, a temperature‐dependent mechanism had evolved for cellular regulation of at least one immune function, spontaneous cytotoxicity.
Regulation of plasminogen activator secretion, interferon induction and proliferation in murine macrophages
Authors: Neumann Christine , Sorg Clemens 
Published: February 2007

AbstractThe purpose of this work was to study the interrelationship of proliferation and secretion of plasminogen activator (PA) and interferon (IFN) by murine macrophages. For induction of macrophage proliferation and secretion of PA, concanavalin A (Con A) was used. Secretion of IFN was induced by polyinosinic polycytidylic acid complex. The glucocorticoid dexamethasone acetate (DA) (10−6 − 109 M) inhibited Con A‐stimulated secretion of PA and synthesis of DNA as evaluated by incorporation of [3H]thymidine. DA did not inhibit IFN induction. Preincubating macrophages with DA for 45 h reduced basal proliferation and secretion of PA but did not reduce responsiveness to Con A. Also retinoic acid, a modulator of carcinogenesis was used in inhibition studies because of its known antagonistic effects on lymphocyte mitogenesis. In macrophages a biphasic effect of retinoic acid (1 × 10−5 − 5 × 10−5M) was found: (a) inhibition of DNA synthesis and secretion of PA during the first 45 h of incubation, and (b) enhancement of DNA synthesis (but not PA secretion) after 72 h. Secretion of IFN was not affected. It is suggested that secretion of PA but not IFN is linked to cell cycle traverse of macrophages.
A monoclonal anti‐HLA antibody recognizes a mouse tumor‐associated antigen
Authors: Evan Gerard I. , Lennox Edwin S. , Alderson Thomas , Croft Lorraine 
Published: February 2007

AbstractThe monoclonal antibody W6/32.1 recognizes a public determinant on the HLA‐A, B and C antigens of all tested human haplotypes. Though the antibody does not bind to normal mouse cells of any H‐2 haplotype, it does show an unexpected specificity for the T cell leukemia line MBL‐2 from a C57BL/6 mouse. It is shown that the murine antigen recognized by W6/32.1 is on an H‐2‐like molecule which also carries the determinant recognized by the monoclonal antibody B22‐249R1, specific for the H‐2Db antigen. Unlike B22‐249R1, however, W6/32.1 does not bind to normal H‐2b lymphocytes, nor to a variety of tumor cell lines of the H‐2b haplotype. This crossreaction is specific to W6/32.1, and is not shared by other monoclonal antibodies of similar anti‐HLA specificities. Moreover, the affinity of W6/32.1 for its human antigen is substantially higher than for its mouse antigen. We conclude that W6/32.1 fortuitously recognizes a novel determinant on the H‐2Db antigen of MBL‐2, rather than an extensive region of structural homology shared between HLA and H‐2. Thus for cells of the H‐2b allotype this determinant is detected only on MBL‐2, and by definition is thus an example of a tumor‐associated antigen.
Alteration of immunologic function through early ontogenetic experiences Selective inactivation of T15‐positive B cells in neonatal mice is related to receptor avidity and is independent of thymus function
Authors: Etlinger Howard M. , Heusser Christoph H. 
Published: February 2007

AbstractThe immunologic effects initiated by injecting neonatal mice with phosphorylcholine (PC)‐protein conjugates were analyzed. Pretreated nude or thymus‐bearing mice produced greater proportions of low‐avidity, TEPC 15‐negative antibody than control animals when challenged as adults with thymus‐dependent (TD) or ‐independent (TI) PC‐conjugated antigen. Furthermore, pretreatment had a greater inhibitory effect on responses elicited by TD compared with TI antigen. These results demonstrate that exposure of neonatal mice to PC‐protein conjugates results in the selective inactivation of higher avidity, T15‐positive, PC‐reactive B cells; this process is independent of thymic function and the duration of hyporesponsiveness is linked to the relative T dependency of the challenge antigen.
Intra‐H‐2 and T cell requirements for the induction of maximal positive and negative allogeneic effects in vitro
Authors: Rolink Anton G. , Van Der Meer Walter , Melief Cornelis J. M. , Gleichmann Ernst 
Published: February 2007

AbstractCultures of T cell‐depleted mouse spleen cells (B cells) were reconstituted with either allogeneic or syngeneic untreated T cells. The primary (day 4) antibody‐forming cell responses to sheep red blood cells were then compared. In almost all combinations and regardless the nature of the H‐2 incompatibility between the T and B cells tested, small numbers of untreated allogeneic T cells provided better help [positive allogeneic effect (AE)] than the same numbers of syngeneic T cells; only in the combination in which B10.A(2R) T cells were added to B10.A(4R) B cells (differing at I‐B, I‐J, and S), no AE at all appeared. A strong positive AE was induced when the incompatibility included or consisted of I‐A. A strong positive AE was also induced across an I‐E difference, provided the B cells expressed the Eα molecule on the cell surface and did not differ at K/D. A negative AE only occurred when the H‐2 incompatibility on the B cells included or consisted of a difference at the K and/or D locus.In contrast to untreated T cells, anti‐Lyt‐1 plus complement‐treated T cells induced neither a positive nor a negative AE. T cells treated with anti‐Lyt‐2 plus complement, too, were incapable of inducing a negative AE; instead, addition of anti‐Lyt‐2‐treated T cells to B cells that differed either at all of H‐2, at K plus I‐A, or at I‐a alone consistently led to the induction of a strong positive AE. Only a syngeneic‐like response was induced, however, when anti‐Lyt‐2 and complement‐treated T cells were added to B cells differing solely at the K locus.
Immune responses to xanthan gum I. The characteristics of lymphocyte activation by xanthan gum
Authors: Ishizaka Shigeaki , Sugawara Isamu , Hasuma Tadayoshi , Morisawa Seiji , Möller Göran 
Published: February 2007

AbstractXanthan gum (XG), a microbial polysaccharide produced extracellularly by fermentation of Xanthomonas campestris, has unique physical properties. We studied the effects of XG on murine lymphocytes in vitro and found that XG induced both a significant increase of DNA synthesis in mouse splenic B cells and thymocytes as well as polyclonal IgM and IgG antibody responses in B cells. XG‐activated thymocytes, however, did not display helper or suppressor functions. XG was almost as effective in inducing polyclonal antibody responses as lipopolysaccharide (LPS) in murine systems. Hamster spleen cells, however, were weakly triggered to nonspecific antibody production by XG but they were not triggered at all by LPS. Spleen cells from normal neonatal mice and from adult CBA/N mice, a strain which possesses an X‐linked defect affecting B cell differentiation, responded relatively well to XG and LPS, suggesting that XG can stimulate immature B cells as well as LPS does. It was found that XG activated B cells in the relative absence of T cells and macrophages. Spleen cells from LPS‐nonresponder C3H/HeJ mice and seven other mouse strains were stimulated to polyclonal antibody production by XG. In contrast, spleen cells from C57BL/10 mice were unresponsive or only slightly responsive to XG, but fully responsive to LPS.
Antibody response of mice following neonatal treatment with a monoclonal anti‐receptor antibody. Evidence for B cell tolerance and T suppressor cells specific for different idiotopic determinants
Authors: Cerny Jan , Cronkhite Richard , Heusser Christoph 
Published: February 2007

AbstractBALB/c mice were injected neonatally with monoclonal antibody against a T15 idiotope, MaId5‐4, and the immune potential of splenic lymphocytes against phosphorylcholine (PC) was studied by stimulation with S. pneumoniae R36a (Pn) in vitro. The total number of PC‐specific plaque‐forming cells (PFC) and the proportion of PFC expressing the MaId5‐4 idiotope (Id+ PFC), as well as two other distinct (nonhomologous) idiotypes of the T15 family recognized by monoclonal antibodies AB1‐2 and B36‐82, was determined by plaque assay against PC‐coupled red blood cells. The magnitude of the total PFC response of splenocytes from age‐matched normal and MaId5‐4‐suppressed mice was comparable but all three Id(s) which were expressed on > 70% PFC from normal splenocytes were below detection level in splenocytes from suppressed mice. Depletion of T cells lowered the total PFC response to a comparable degree in both mice. Normal B cells (BN) stimulated by Pn expressed all three Id(s) much like the normal splenocytes. B cells from MaId5‐4‐suppressed mice (Bs) always failed to express MaId5‐4 but they occasionally did express the B36‐82 or Ab1‐2. The reciprocal mixing of B and T cells followed by Pn stimulation revealed that both normal T cells (TN) and T cells from MaId5‐4‐suppressed mice (Ts) provided equal help to either BN or Bs in regard to total PFC number. Ts consistently inhibited the expression of MaId5‐4 in BN cultures, but only rarely the expression of Ab1‐2 and B36‐82. Bs cocultured with TN never expressed MaId5‐4 but they sometimes did express one or both of the other two Id. These results show that neonatal application of a monoclonal anti‐Id suppresses the expression of the Id determinant which is recognized by the antibody, as well as other determinants. The mechanism of the suppression of the target Id (MaId5‐4) involves both B cell tolerance and active suppression. The mechanism of cosuppression (idiotopes AB1‐2 and B36‐82) is variable, apparently involving a B cell tolerance, lack of Id‐specific help, and/or active suppression.
Human large granular lymphocytes contain an esterase activity usually considered as specific for the myeloid series
Authors: Heumann Didier , Colombatti Marco , Mach Jean‐Pierre 
Published: February 2007

AbstractA cytochemical marker such as alpha‐naphthyl acetate esterase (ANAE) has been found useful for the morphological identification of the subset of T lymphocytes having receptors for Fcμ (TM cells). ANAE reaction on TM cells gives a typical pattern of one to four positive spots, whereas this pattern is not found on T cells with receptors for Fcγ (TG cells). ANAE is abundant in monocytes but not detectable in granulocytes. Herein another type of esterase activity, naphthol‐AS‐D chloroacetate esterase (NCAE), is described; it is known to be abundant in granulocytes and was found to give a specific pattern of reactivity with the subpopulation of large granular lymphocytes (LGL). This pattern of fine granular staining was observed not only on LGL present in the TG cell subpopulation but also in LGL present in the non‐T, non‐B cells.Fractions of peripheral blood mononuclear cells which were ènriched up to 80% in LGL by Percoll discontinuous density gradient gave a similar percentage of specific NCAE pattern. In addition, among the different fractions from Percoll gradient, there was a good correlation (r = 0.94) between the number of NCAE‐positive cells and the natural killer activity against the natural killer susceptible K562 target cells. It will be important to determine whether or not this enzymatic activity plays a role in the cytotoxic activities of LGL.
H‐2D products do not affect lysis of Kk target cells by Kk‐specific cytotoxic T cells
Authors: Teh Hung‐Sia , Romaniuk Roman , Von Boehmer Harald 
Published: February 2007

AbstractAntigens coded by the major histocompatibility complex (MHC) stimulate a large number of cytotoxic T lymphocyte (CTL) precursors. Matzinger and Bevan have suggested that the high alloreactivity is a result of the formation of interaction antigens between MHC and non‐MHC‐coded antigens. Previous work by Langhorne and Fischer Lindahl did not support this hypothesis. In this report we describe an improved culture system to show that the recognition of Kk target cells by Kk‐specific clones is also unaffected by H‐2D products. Using such a culture system, which controls for the induction of nonspecific CTL by interleukin 2 (T cell growth factor), we were also able to confirm the original conclusion of Langhorne and Fischer Lindahl that polymorphic minor histocompatibility antigens do not significantly contribute to putative “interaction antigens” formed by MHC and other antigens.
Immunoglobulin C gene expression. IV. Alternative control of IgG1‐producing cells by helper cell‐derived B cell‐specific growth or maturation factors
Authors: Coutinho Antonio , Pettersson Sven , Ruuth Erik , Forni Luciana 
Published: February 2007

AbstractThe influence of helper cell‐derived B cell‐specific growth or maturation factors in the membrane expression and secretion of IgG1 and IgG3 isotypes among lipopolysaccharide‐activated B cell blasts was studied in mass cultures and in single clones. The results demonstrate that helper cells regulate IgG1 expression by two alternative modes: growth‐promoting factors expand membrane IgG1‐bearing nonsecretory activated B cells, while maturation factors induce terminal differentiation to high‐rate secretion of IgG1 in previously switched cells.Apart from the isotype specificity in the maturation‐inducing signals for activated B lymphocytes, the present experiments demonstrate that isotype control by helper cells is intimately connected to the control of proliferation vs. terminal maturation in proliferating B cell populations.
Homologies between cell interaction molecules controlled by major histocompatibility complex‐ and Igh‐V‐linked genes that T cells use for communication; both molecules undergo “adaptive” differentiation in the thymus
Authors: Yamauchi Katsumi , Flood Patrick M. , Singer Alfred , Gershon Richard K. 
Published: February 2007

AbstractWe have previously described two types of immunoregulatory interactions between T cell subsets; in one an Ly‐1; I‐J+ inducer cell makes a soluble product (Ly‐1 T suppressor inducer factor, TsiF) that is also I‐J+ and which activates the effector cells of a suppressor circuit. Under normal circumstances the Ly‐1 TsiF activity is restricted by Igh‐V‐linked genetic polymorphisms. However, we now find the genotype of the inducer cell does not control this restriction. The inducer cell acquires a new Igh‐V‐linked self repertoire if it (“adaptively”) differentiates in an appropriate F1 radiation chimera or in an F1 thymus graft in a homozygous nude mouse. Conversely, cells from F1 mice cannot acquire this “dual” self repertoire if the host in which they differentiate does not express the relevant selecting structure(s).A previously demonstrated H‐2‐restricted suppressor factor (Ly‐2 T suppressor factor) has also been examined and it is shown that this molecule is subject to the same differentiation constraints as is the Igh‐V‐linked restricted factor except, or course, in this case H‐2‐linked genes are the “restricting” elements. Thus, Igh‐V restrictions are related to major histocompatibility complex (MHC) restrictions in the parameter that has been termed “adaptive” differentiation.The results also imply that the I‐J‐marked Igh‐V‐linked self recognition molecule(s) has a variable and constant region, since the adaptively differentiated molecules that show a new self recognition specificity retain the genetic I‐J polymorphism of the mice that supplied the bone marrow precursor cells and not the one of the thymus in which they differentiated.It may be considered surprising to find a structure in the thymus that acts to select MHC‐positive molecules that see Igh‐V‐linked structures as self. The F1 into parent experiments make it unlikely that the thymus is passively armed by circulating molecules that might act as the selecting elements. Since there is such a striking parallelism in the “adaptive” differentiation of cells that recognize Igh‐V and MHC as self, one must consider the possibility that Igh‐linked gene products are expressed by cells in the thymus and function there to select for those Ly‐1 TsiF producer cells that can recognize these Igh‐V‐linked cell interaction structures as self.