bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cloning of murine splenic T lymphocytes and natural killer (NK) cells on filter paper discs: detection of a novel NK/T phenotype
Authors: Sarzotti Marcella , Kumar Vinay , Bennett Michael , Kelsoe Garnett 
Published: March 2007

AbstractDiscrete colonies of splenocytes were grown on filter paper discs in the presence of concanavalin A and interleukin 2. Phenotypic analysis of the colonies indicated that the majority expressed the Thy‐1.2 marker and 72% of these co‐expressed the CD3 molecule. Of the colonies 20%–25% were NK 1.1+ and they developed regardless of the presence of Con A in the culture medium, a property of the NK lineage. In addition, Thy‐1.2+ colonies developed when splenocytes from scid mice, which lack mature T and B cells, were grown both in the presence and absence of concanavalin A. These results demonstrate that colonies of murine splenic T lymphocytes and NK cells could be successfully grown on filter paper discs and phenotypically characterized. With this colonies technique, it was possible to identify a novel subset of NK 1.1+ colonies that co‐expresses CD3 and shares growth properties with T cell colonies.
Rescue of thymocytes and T cell hybridomas from glucocorticoid‐induced apoptosis by stimulation via the T cell receptor/CD3 complex: a possible in vitro model for positive selection of the T cell repertoire
Authors: Iwata M. , Hanaoka S. , Sato Kazuki 
Published: March 2007

AbstractPositive and negative selection events are involved in determining useful T cell clones to mature in the thymus. Accumulating evidence suggests that immature self‐reactive thymocytes undergo apoptotic death (negative selection) upon stimulation via the T cell receptors (TcR). A similar phenomenon of activation‐induced death has been reported in T cell hybridomas. On the other hand, little is known about the mechanism of the positive selection. Apoptosis in rodent thymocytes or T cell hybridomas is also known to be induced by glucocorticoids in vitro at concentrations within the physiologic range. We report here that the TcR/CD3‐mediated stimulation and glucocorticoids mutually inhibit the apoptosis in T cell hybridomas. The production of interleukin 2 by the rescued cells indicated that the TcR/CD3‐mediated signal was transduced into the cells. Thymocytes were also rescued from glucocorticoid‐induced apoptosis by the stimulation with antibodies to TcR/CD3 molecules. The rescue of thymocytes, however, was observed only at a narrow concentration range of each of the antibodies, suggesting that the proper stimulation via the TcR/CD3 is required for the rescue. If thymocytes in situ are differentially stimulated according to the affinity of the TcR towards self, only the thymocytes whose TcR have proper affinity towards self may be rescued from glucocorticoid‐induced apoptosis. Therefore, we propose a hypothesis that the positive selection of the T cell repertoire is based on the inhibition of glucocorticoid‐induced apoptosis in immature thymocytes bearing TcR with proper affinity for self by the TcR‐mediated signals in situ. Furthermore, the selection may be influenced by the peak level of glucocorticoid concentration, since the proper concentration range of the anti‐TcR/CD3 antibody for the rescue was variable depending on the glucocorticoid concentration.
The “adjuvant effect” of the polymorphic B‐G antigens of the chicken major histocompatibility complex analyzed using purified molecules incorporated in liposomes
Authors: Salomonsen Jan , Eriksson Håkan , Skj⊘dt Karsten , Lundgreen Tina , Simonsen Morten , Kaufman Jim 
Published: March 2007

AbstractThe polymorphic B‐G region of the chicken major histocompatibility complex has previously been shown to mediate an “adjuvant effect” on the humoral response to other erythrocyte alloantigens. We demonstrate here that B‐G molecules purified with monoclonal antibodies exert this adjuvant effect on the production of alloantibodies to chicken class I (B‐F) molecules, when the two are in the same liposome. The adjuvant effect may in part be mediated by antibodies, since the antibody response to B‐G molecules occurs much faster than the response to B‐F molecules, and conditions in which antibodies to B‐G are present increase the speed of the response to B‐F molecules. We also found that the presence of B‐G molecules in separate liposomes results in a lack of response to B‐F molecules. In the light of this and other data, we consider the possible roles for the polymorphic B‐G molecules, particularly for the generation of B cell diversity, in the immune systems of birds and other animals.
Functional dichotomy of CD4+ T helper lymphocytes in asymptomatic human immunodeficiency virus infection
Authors: Clerici Mario , Shearer Gene M. , Via Charles S. , Lucey Daniel R. , Roilides Emmanuel , Pizzo Philip A. 
Published: March 2007

AbstractThe majority of asymptomatic, human immune deficiency virus seropositive (HIV+) individuals exhibit a defect in CD4+ T helper cell (Th) function that is selective for responses to recall antigens, but not to HLA alloantigens. The CD4‐dependent Th response to HLA alloantigens (Allo) can be mediated by two distinct Th pathways: self‐restricted CD4+ Th that recognize allogeneic determinants processed and presented by autologous or self accessory or antigen‐presenting cells (sAC); and allo‐restricted, CD4+ Th that recognize allogeneic determinants directly on allogeneic accessory or antigen‐presenting cells (aAC). In contrast, the Th response to recall antigens requires CD4+ Th and sAC and is therefore limited to the major histocompatibility complex (MHC) self‐restricted pathway. Peripheral blood leukocytes from 56 asymptomatic HIV+ patients that exhibited a selective defect in CD4+ Th function were analyzed to determine whether the Th response to Allo was entirely functional, or whether one of the CD4‐mediated components of the Allo Th response was also defective. By depletion of AC and/or CD8+ Th subsets (to analyze CD4+ Th function), we demonstrated that HIV+ patients who were selectively deficient in Th function to recall antigens were also unresponsive to Allo presented by autologous AC (HLA self‐restricted Th pathway), but retained Allo Th activity presented by allogeneic AC (allo‐restricted CD4+ Th pathway). These findings indicate that the CD4+ Th defect seen in the majority of asymptomatic, HIV+ individuals is not limited to recall antigens, but also extends to the component of the response to HLA alloantigens that involves the self‐restricted, CD4+ Th pathway. Thus, the Th defect observed in asymptomatic, HIV+ patients does not involve a CD4+ Th defect per se, but is limited to the HLA self‐restricted component of Th function.
Human interleukin 7 is a B cell growth factor for activated B cells
Authors: Joshi Pratibha C. , Choi Yong Sung 
Published: March 2007

AbstractWe investigated the capacity of human interleukin (IL) 7 to induce proliferation of B cells. Purified tonsillar B cells were cultured in the presence of IL7 with Staphylococcus aureus Cowan I (SAC) or anti‐μ beads as co‐mitogens. IL 7 supported a dose‐dependent proliferation of anti‐μ‐activated B cells but did not significantly support proliferation of SAC‐activated B cells. When B cells were separated on Percoll gradient into small (60%‐80%) and large (50%–60%) B cells and then cultured with anti‐μ beads, IL7 acted on both cell populations equally well. IL7 and BCGF (low molecular weight) were synergistic in their proliferative action on anti‐μ‐activated B cells in a 5‐day culture. On the other hand, synergistic effect of IL 7 on activated B cells was not evident in the presence of any other factor recombinant [(r)IL 1β, rIL2, rIL3, rIL4, rIL5, rIL6, recombinant tumor necrosis factor‐α, recombinant lymphotoxin, recombinant granulocyte‐monocyte colony‐stimulating factor and recombinant interferon‐γ] we tested. IL7 did not induce IgG secretion by activated B cells.
Granzyme A and perforin as markers for rejection in cardiac transplantation
Authors: Griffiths Gillian M. , Namikawa Reiko , Billingham Margaret , Weissman Irving , Mueller Christoph , Liu Chau‐Ching , Young John Ding‐E 
Published: March 2007

AbstractThe use of granzyme A and perforin as markers for rejection after cardiac transplantation has been investigated. Using in situ hybridization we have detected lymphocytes expressing granzyme A and perforin RNA that are infiltrating the donor heart after transplantation.A total of 29 different biopsies from 17 different patients who had undergone cardiac transplantation were examined. Twelve biopsies classified by conventional histological criteria as showing evidence of rejection were found to contain lymphocytes expressing granzyme A and perforin. Seven biopsies classified as showing no histological evidence of rejection infiltrating lymphocytes were found not to be expressing granzyme A or perforin. However, in 10 other biopsies from 5 different patients that had been classified as showing no evidence of rejection by the conventional grading system, lymphocytes expressing granzyme A and perforin were detected. In six of these cases the patient was found to have undergone a subsequent rejection episode. In the other four cases the biopsies were either taken at a very early stage after transplantation and the high doses of immunosuppression used routinely at that stage are likely to have averted any rejection episodes, or it was not possible to follow subsequent rejection episodes. These results, which are statistically significant (p = 0.06), demonstrate that granzyme A‐ and perforin‐expressing lymphocytes can be identified in rejecting biopsies before histological damage is seen. The identification of perforin and granzyme A expression in vivo suggest a possible role for these proteins in the cytolysis that occurs during transplantation rejection. Furthermore, the data presented here suggest that it may be possible to use granzyme A and perforin as early predictive markers of transplantation rejection.
Chronic experimental autoimmune encephalomyelitis induced by the 89‐101 myelin basic protein peptide in B10RIII (H2r) mice
Authors: Jansson Liselotte , Holmdahl Rikard , Olsson Tomas , Höjeberg Bo 
Published: March 2007

AbstractDevelopment of experimental allergic encephalomyelitis (EAE) in the SJL (H‐2s) mice is associated with a T cell‐dependent autoimmune response to the C‐terminal part of the myelin basic protein (MBP). In this study the influence of both H‐2 and non‐H‐2 genetic background on EAE induced with the MBP89‐101 peptide is described. Analysis of different H‐2q haplotype strains, B10G, B10Q, SWR and NFR/N, showed that the B10 background is relatively resistant to disease induction. Both SWR and NFR/N were susceptible to EAE showing that the H‐2q haplotype is permissive for EAE development induced with MBP89‐101 and that the T cell receptor (TcR) haplotype or complement C5 deficiency exert no significant influence on disease susceptibility. In a series of H‐2‐congenic strains on the B10 background only B10RIII (H‐2r) mice were susceptible to EAE. The B10RIII mice developed a severe EAE with early onset and chronic progressive or relapsing course of disease. In addition, B10RIII mice treated with Freund's complete adjuvant and pertussis toxin alone showed an early monophasic disease. The clinical observations were confirmed by immunohistopathologic analysis of the central nervous system. In these studies, we also applied antibodies to different TcR Vβ elements which showed no specific limitation of the used TcR among infiltrating T cells in the target tissue in any of the strains. It is concluded that an MBP peptide‐specific disease can be induced in three different haplotypes and it is possible that shared structures between the As, Aq and Ar molecules are of importance for the trigger of encephalitogenic T cells with different TcR Velements. The presently described chronic EAE model induced in the B10RIII mice will be of value as a model for multiple sclerosis.
Phorbol ester responsiveness of murine Ly‐1‐lineage B cells from normal and viable motheaten mutant mice
Authors: Kolber Donna L. , Rothstein Thomas L. , Shultz Leonard D. 
Published: March 2007

AbstractSimultaneous analysis of stimulated cells for surface phenotype and DNA content by flow cytometry was used to delineate the characteristics of murine lymphocytes that respond to phorbol esters. Peritoneal cells that expressed high‐density sIgM, Ly‐1, Mac‐1 and high‐density Pgp‐1, were preferentially stimulated to enter the S + G2/M phases of the cell cycle by the protein kinase C agonist, phorbol 12‐myristate 13‐acetate (PMA). Since these phenotypic characteristics correspond well with those of Ly‐1‐lineage B cells, non‐peritoneal sources of Ly‐1+ B cells were examined to test the relative role of lineage and environment in determining phorbol ester responsiveness. Splenic sIgM+ lymphocytes from adult mev/mev mice, and Ly‐1+ splenic B cells from neonatal normal mice, were stimulated to enter the S + G2/M phases by PMA, although not to the same extent as peritoneal Ly‐1+ B cells. These results suggest that responsiveness to phorbol ester, acting alone, is characteristic of murine Ly‐1‐lineage B cells regardless of tissue of origin; however, a role for environmental influences has not been completely ruled out.
Unusual phenotype of intestinal intraepithelial lymphocytes in the rat: predominance of T cell receptor α/β+/CD2− cells and high expression of the RT6 alloantigen
Authors: Fangmann Josef , Schwinzer Reinhard , Wonigeit Kurt 
Published: March 2007

AbstractThe phenotype of intraepithelial lymphocytes (IEL) from the small intestine of adult rats was studied by flow cytometry. Using appropriate monoclonal antibodies the expression patterns of the T cell receptor α/β (TcR2), CD2, the alloantigen RT6 and several other T cell antigens were analyzed. The vast majority of rat IEL expressed TcR 2 which is in contrast with data reported for the mouse. The comparison of IEL with lymph node cells revealed major phenotypic differences. Whereas CD2 was present on virtually all lymph node T cells it was found on only < 5% of IEL. The T cell‐specific differentiation antigen RT6 present on only a fraction of lymph node cells was found on about 99% of IEL demonstrating uniform expression with an approximately tenfold higher density. Identity of the detected molecule with RT6 was proven by using congenic controls and by the demonstration of phosphatidylinositol linkage to the IEL membrane. About 86% of IEL expressed CD8 but a substantial proportion of these cells co‐expressed the CD4 molecule (34%). Two‐color analysis revealed that the CD4+CD8+ double‐positive subset completely lacked CD45RB suggesting that they represent memory cells. In the CD4−CD8+TcR2+ subset there was a remarkable heterogeneity of CD5 expression. A substantial number of these cells did not express CD5 despite high density of TcR 2. Phenotypic peculiarities found on all or most IEL such as the lack of CD2 and the increased expression of RT6 indicate that the intestinal epithelial environment exerts strong effects on the development and maturation of these cells.
Staphylococcal enterotoxin B as a potent suppressant of T cell proliferative responses in rats
Authors: Ben‐Nun Avraham 
Published: March 2007

AbstractThe staphylococcal toxins are well known as stimulators of powerful T lymphocyte proliferative responses. Staphylococcal enterotoxin B (SEB) was found, in both humans and mice, to preferentially stimulate T cells bearing particular Vβ gene products as part of their functional T cell receptor α/β. In contrast to this reported stimulatory activity we demonstrate here that SEB is a poor stimulant of T lymphocyte proliferative responses in Lewis rats. Moreover, under appropriate conditions, SEB can serve as a powerful suppressant of Lewis rat T lymphocytes, capable of abolishing their antigen‐specific or mitogen‐stimulated proliferative responses. Suppression of mitogen‐induced proliferative responses of rat T cell clones was effective in the presence of syngeneic or allogeneic accessory cells and similar to its stimulatory characteristics, SEB suppressed high proportions of rat T lymphocyte subsets. These data suggest that in certain circumstances SEB can be considered a “supersuppressogen” as well as a “superantigen”. Whether SEB will be “superantigen” or “supersuppressogen” is likely to depend on the TcR elements of the lymphocytes as well as on the MHC molecules presenting SEB.
Contribution of the VH11 gene family to mitogen‐responsive B cell repertoire in C57BL/6 mice
Authors: Kaushik Azad , Bona Constantin , Reininger Luc , Jaton Jean‐Claude , Kelsoe Garnett 
Published: March 2007

AbstractThe contribution of VH11 gene family to the development of the primary B cell repertoire has been studied by analyzing 1.8 × 104 mitogen induced B lymphocyte colonies. The data demonstrate that VH11 family is predominantly expressed among neonatal splenic as well as adult peritoneal B cell colonies, both rich in Ly‐1+ B cells. VH11 gene family expression among B splenocytes decreases during ontogeny and VH11 family pairs stochastically with different Vx families among mitogen‐activated neonatal B cell colonies, which are representative of an antigen unselected B cell repertoire. Thus, an increased VH11 expression among peritoneal and neonatal B cells points towards its biased expression among Ly‐1+ B lymphocytes. The restricted V gene rearrangements and VH11‐Vx9 pairing observed among anti‐bromelain‐treated mouse red blood cells autoantibodies are likely to be an outcome of both intrinsic gene recombination processes per se as well as selection by an autoantigen and/or local selective environmental factors.
Interleukin 2‐dependent activation of tumor‐specific cytotoxic T lymphocytes in vivo
Authors: Ley Victoria , Langlade‐Demoyen Pierre , Kourilsky Philippe , Larsson‐Sciard Eva‐Lotta 
Published: March 2007

AbstractWe have quantitatively studied the effect of interleukin (IL) 2 on the cytotoxic T lymphocyte (CTL) response to tumor cells in vivo. Mastocytoma P815 was transfected with murine IL 2 cDNA (P815‐IL 2) and injected into syngeneic mice. The anti‐tumor response was analyzed and compared with the response induced by the non‐transfected cells. P815 parental cells are highly tumorigenic, causing death within 20‐30 days. In contrast, IL 2‐transfected cells were totally rejected. Co‐injection of IL 2‐secreting and parental cells resulted in the inhibition of growth of both type of tumors. In addition, the response induced by IL 2‐secreting cells protected the mice against a subsequent challenge with P815. Long‐term memory persisted in treated mice 3 months after tumor rejection. Frequencies of CTL precursors and CTL specific for P815 increased as a result of IL 2 secretion by the target cells. Estimates of CTL frequency at days 8 and 12 after injection were 2 to 3 times higher in mice inoculated with P815‐IL 2 cells, and this correlated with tumor rejection.
Platelet‐induced expression of FcγRIII (CD16) on human monocytes
Authors: Phillips Joseph H. , Chang Chiwen , Lanier Lewis L. 
Published: March 2007

AbstractMonocytes constitutively express Fc receptor (FcR) for IgG type I (CD64) and type II (CD32), but not type III (CD 16). Prior studies have indicated that in vitro culture of monocytes results in spontaneous induction of CD16, but this phenomenon has been variable and the mechanism unexplained. Here, we demonstrate that activated platelets are responsible for induction of CD16 on monocytes, as a consequence of TGF‐β release. Local release of TGF‐β by activated platelets at sites of tissue damage may induce CD16 on infiltrating or resident monocytes that in turn facilitate the function of these effector cells. The FcR on these CD16+ monocytes is functionally competent, and enables the monocytes to kill murine anti‐CD16 hybridoma cells. CD16 expressed on platelet‐activated monocytes is structurally similar to the transmembraneanchored CD16‐II polypeptide expressed on natural killer (NK) cells. However, whereas CD16‐II on NK cells is co‐associated with CD3ζ, we were unable to detect CD3 ζ transcript or protein in monocytes. Transcripts for the γ subunit of the high‐affinity IgE FcR (FcϵRI‐γ) were detected in monocytes, and presumably γ proteins are co‐associated with CD16‐II in these cells. Nucleotide sequence analysis of FcϵRI‐γ cDNA derived from both NK cells and cultured monocytes indicated identity with the structure previously cloned from basophils. Since CD16+ monocytes can kill anti‐CD16 hybridoma cell targets in the absence of CD3 ζ, these results indicate that CD3 ζ is not essential for signal transduction in CD16‐II‐mediated cytotoxicity.
Studies on the human T cell receptor α/β variable region genes. I. Identification of 7 additional Vα subfamilies and 14 Jα gene segments
Authors: Roman‐Roman Sergio , Ferradini Laurent , Azocar José , Genevée Catherine , Hercend Thierry , Triebel Frédéric 
Published: March 2007

AbstractThe anchored‐polymerase chain reaction has been used to study further the diversity of the human T cell receptor α chain. The analysis of 308 cDNA transcripts from human peripheral lymphocytes hybridizing with a Cα probe led to the identification of a series of additional Vα and Jα gene segments. The sequences of seven Vα gene segments which individually define a novel Vα subfamily (termed Vαw23 to Vαw29) are reported. The sequences of some previously described Vα1, Vα2, Vα5, Vα7 and Vα22 gene segments are also extended. In addition, we report 14 novel Jα gene segment sequences. Taken together, these data indicate that the contribution of the α chain combinatorial diversity to the human T cell receptor α/β variability has not yet been fully appreciated.
Relative frequencies of secondary B cells activated by cognate vs. other mechanisms
Authors: Johnson Julia G. , Jemmerson Ronald 
Published: March 2007

AbstractThree distinct mechanisms for the activation of secondary B cells to antibody‐forming cells have been examined in splenic fragment cultures. The clonal response to a protein antigen [cytochrome c (cyt)] was quantified in terms of both the number of B cells activated and the amount of antibody produced by each clone. The vast majority of memory B cells required surface immunoglobulin (sIg) receptor‐mediated uptake of antigen followed by cognate interactions with an antigen‐specific T helper cell. Nevertheless, a significant number (as many as 12%) could be activated via soluble factor‐mediated bystander activation, involving occupation of neither the sIg receptor nor class II major histocompatibility complex (MHC) molecules. This pathway, however, was relatively inefficient in that individual clones secreted less than half as much antibody as clones activated as a result of cognate collaboration with a T helper cell. A similar number of secondary B cells were activated following nonspecific uptake of high concentrations of antigen for which splenic fragment T cells had been primed [i. e., hemocyanin (Hy)], independent of sIg receptor occupancy. Antibody levels were similar to those in cultures where B cells were activated in a cognate manner with sIg receptor occupancy. When Hy‐stimulated fragment cultures were supplemented with polymerized cyt, the frequency of activation via this latter pathway increased fourfold, despite the fact that no cyt‐primed T cells were present. This observation supports the idea that receptor‐mediated uptake of antigen serves not just to focus antigen but also provides an important signal in activating B cells. Bystander B cell activation, however, was not enhanced by providing a sIg cross‐linking signal with polymerized cyt. The lower level of antibody production by B cells activated in a bystander fashion and the inability to enhance their frequency of activation with sIg receptor occupancy suggest that there is indeed a fundamental difference between soluble factor‐mediated bystander activation and activation via T cell determinant‐mediated cognate T helper‐B cell interactions, perhaps involving signaling through class II MHC molecules.