bluuebunny/crossref_metadata_2025_split huggingface dataset:
Human memory T lymphocytes express increased levels of three cell adhesion molecules (LFA-3, CD2, and LFA-1) and three other molecules (UCHL1, CDw29, and Pgp-1) and have enhanced IFN-gamma production.
Authors: Sanders M E , Makgoba M W , Sharrow S O , Stephany D , Springer T A , Young H A , Shaw S 
Published: December 2022

Abstract
Studies of cell-surface molecules involved in human T cell interaction reveal that differential expression of each of three adhesion molecules (LFA-3, CD2, and LFA-1) subdivides human peripheral blood T cells into major subpopulations. Systematic analysis of the relationship between expression of these and other markers of T cell subsets demonstrates a single major subset of human peripheral blood T lymphocytes distinguished by enhanced expression of LFA-3, CD2, LFA-1, and three other markers (CDw29 [4B4], UCHL1, and Pgp-1). Large differences in relative expression are observed for UCHL1 (29-fold) and LFA-3 (greater than 8-fold), and smaller differences (2- to 4-fold) are seen for CDw29, CD2, LFA-1, and Pgp-1. Bimodal distribution of LFA-3 is found on both CD4+ cells and on CD8+ cells as well as on B lymphocytes (CD19+). Neonatal T cells (CD3+) are comprised almost exclusively of the subset expressing low LFA-3, CD2, LFA-1, CDw29, and UCHL1. Activation of cord peripheral blood mononuclear leukocytes with PHA leads to uniform enhanced expression of each of these molecules on CD3+ cells. Functional analyses of these T cell subsets were performed after sorting of adult T cells based on differential LFA-3 expression. Only the LFA-3+ subset proliferated in response to the Ag tetanus toxoid, even though the LFA-3- subset proliferated more strongly to PHA. Furthermore, the LFA-3+ subset made greater than fivefold more IFN-gamma than the LFA-3- subset in response to PHA, despite the fact that both subsets made equivalent amounts of IL-2. This phenotypic and functional analysis of resting and activated newborn and adult T cells indicates that human memory T cells express enhanced levels of LFA-3, CD2, LFA-1, UCHL1, CDw29, and Pgp-1; we speculate that the increase in expression of T cell adhesion molecules LFA-3, CD2, and LFA-1 on memory cells is functionally important in their enhanced responsiveness.
Immunogenic and antigenic epitopes of Ig. XXV. Monoclonal antibodies that differentiate the Mcg+/Mcg- and Oz+/Oz- C region isotypes of human lambda L chains.
Authors: Walker M R , Solomon A , Weiss D T , Deutsch H F , Jefferis R 
Published: December 2022

Abstract
The C region of human lambda L chains is specified by multiple C lambda genes of which three--C lambda 1, C lambda 2, and C lambda 3--encode for the isotypes designated Mcg+, Kern- Oz-, and Kern- Oz+, respectively. The Mcg, Kern, and Oz factors have been characterized by sequence differences involving specific C lambda amino acid residues. They have also been recognized serologically by polyclonal antisera but, with rare exception, these reagents are no longer available. We have obtained two murine anti-human lambda-chain mAb, 14G1 and 14D1, that recognize antigenic determinants specific for the C lambda isotypes Mcg and Oz, respectively. These antisera have been used to classify as Mcg+/Mcg- or Oz+/Oz- monoclonal lambda-chains (Bence Jones proteins) and intact Ig lambda proteins. There was complete concordance between the chemical and serologic assignment of lambda-chains as Mcg+/Mcg- or as Oz+/Oz-; no single protein expressed both isotypes. There was no evident association between the C region isotype Mcg or Oz and the V region subgroup of the protein tested. However, our finding that four of seven amyloid-associated lambda VI Bence Jones proteins were Oz+ suggests a predominant expression of the C lambda 3 gene product among proteins of this uncommon V lambda subgroup.
Eosinophil granule major basic protein regulates generation of classical and alternative-amplification pathway C3 convertases in vitro.
Authors: Weiler J M , Gleich G J 
Published: December 2022

Abstract
Eosinophil major basic protein (MBP), a highly charged polycation, forms the core of the eosinophil granule and mediates tissue damage in allergic disease. Purified MBP was studied for capacity to regulate the generation of classical and alternative-amplification pathway C3 convertases because previous studies have shown that other polycations (protamine, poly-L-lysine) and polyanions (heparin) may play important roles in regulating C activation. MBP inhibited the generation of EAC1,4b,2a and EAC4b,3b,Bb,P but appeared to inhibit the generation of classical pathway convertase more than the alternative amplification pathway convertase at a given dose. Dose-response curves with MBP were steeper than curves seen with polyanion (heparin). MBP did not lyse cellular intermediates at concentrations that caused almost total inhibition of convertase generation. One mechanism of inhibition of convertase generation may have been through an action on C3b, because preincubation of MBP with an EAC4b,3b cellular intermediate interfered with the ability of this cellular intermediate to be lysed. Furthermore, MBP prevented consumption of B in a reaction mixture that contained factors B, D, and C3b, also suggesting an action on C3b. Reduced and alkylated MBP (A-MBP) was compared with native MBP, which possesses two reactive sulfhydryl groups, to determine whether charge alone is responsible for blocking convertase generation; native MBP rapidly associates and is relatively insoluble at neutral and alkaline pH whereas A-MBP remains soluble. A-MBP impaired convertase generation, did not appear to remain bound to cellular intermediates and did not suppress B consumption in the fluid phase assay. This suggests that the ability of MBP to regulate C activation is complex and not entirely through its net charge. Finally, although heparin or MBP alone may prevent C activation, when these substances were present at the same time there was no effect on C activation suggesting that charge neutralization may abrogate the effects of these charged substances on C activation. Taken together, these studies suggest that MBP at physiologic concentrations may regulate in vivo C activation at the tissue level.
CD3-negative lymphokine-activated cytotoxic cells express the CD3 epsilon gene.
Authors: Biassoni R , Ferrini S , Prigione I , Moretta A , Long E O 
Published: December 2022

Abstract
The expression of genes encoding different polypeptide chains of the TCR-CD3 complex was analyzed in a panel of cloned MHC-unrestricted cytotoxic cells. The clones were derived from CD3+ and CD3- human PBL. After expansion in rIL-2, all clones were able to lyse the NK-sensitive target cell line K562. In contrast, lysis of fresh tumor cells was achieved almost exclusively by CD3- clones. To test whether a known TCR-CD3 complex may be involved in MHC-unrestricted cytotoxicity, total RNA from nine CD3+ and 11 CD3- clones was isolated and hybridized with DNA probes for the TCR alpha-, beta-, and gamma-chains and for the CD3 gamma-, delta-, and epsilon-chains. TCR gamma transcripts were present at high levels in CD3+CD4- CD8- clones but were undetectable in all CD3- clones. Lysis of fresh tumor cells is an activity which can be independent of the TCR alpha beta and TCR gamma complexes because the CD3- clones did not express these TCR genes. Interestingly, all CD3- clones expressed CD3 epsilon transcripts, but not CD3 gamma- or delta-transcripts. CD3- lymphokine-activated cytotoxic cells may therefore be derived from immature T cells which do not yet express a complete CD3 complex. The CD3 epsilon chain, if expressed in CD3- cells in association with other molecules, could be involved in the activation and lytic function of these MHC-unrestricted cytotoxic cells.
Adherence induces selective mRNA expression of monocyte mediators and proto-oncogenes.
Authors: Haskill S , Johnson C , Eierman D , Becker S , Warren K 
Published: December 2022

Abstract
Adherence is an important regulatory signal for several monokines and the proto-oncogenes c-fms and c-fos in human peripheral blood monocytes. Although there is little if any constitutive expression of the IL-1 beta, TNF-alpha and CSF-1 genes in freshly isolated monocytes, adherence is sufficient to induce high steady-state levels of mRNA for TNF and c-fos and more slowly that of CSF-1. Expression of mRNA for the CSF-1R gene, c-fms, was transiently down-regulated by 4 h. In contrast, the induction of high levels of IL-1 beta mRNA were achieved independent of culture conditions. Although all of these genes could be induced by adherence, actual secretion of the mediators required the exposure to a second signal derived from LPS. Thus adherence rapidly primes monocytes for a variety of inflammatory responses, the magnitude of which depends on the nature of a second "activating" signal. It is likely that some of these products act locally as paracrine or autocrine factors to further regulate the phenotype of the differentiating macrophage.
CD4 is involved in a post-binding event in the cytolytic reaction mediated by human CD4+ cytotoxic T lymphocyte clones.
Authors: Blanchard D , Van Els C , Aubry J P , de Vries J E , Spits H 
Published: December 2022

Abstract
CTL lyse their target cells in discrete phases. First, the CTL bind to the target cell in a Mg2+-dependent manner followed by a Ca2+-dependent cytolytic phase. In the present study, we investigated the role of CD4 in the different phases of the cytolytic reaction mediated by human CD4+ class II MHC-specific CTL clones by using a single cell assay. It was found that the anti-CD4+ mAb OKT4A, which blocks cytotoxic reactions by CD4+ CTL clones as measured with a 51Cr release assay, only marginally affects the formation of conjugates. It appeared that OKT4A more strongly blocked the post-binding phase of the cytolytic reaction. In contrast, anti-leukocyte function-associated mAb strongly blocked the formation of conjugates but not the subsequent lytic phase. As was found previously with CD8+ CTL clones, anti-TCR mAb generally did not affect the formation of conjugates. One exception was noted. The activity of a CD4+ CTL clone, HY-640, could not be blocked by OKT4A, but was affected by an anti-TCR mAb. This anti-TCR mAb could partly reduce the formation of conjugates between HY-640 cells and their specific target cells. These results suggest that this clone has a high affinity TCR, which can contribute to the formation of conjugates. Although preincubation of the CTL clones with OKT4A only marginally affects the number of conjugates upon subsequent mixture with target cells, it was observed that incubation at 37 degrees C of preformed conjugates with OKT4A markedly reduced the number of conjugates. This dissociation of preformed conjugates was optimal only after 2 h of incubation. In contrast, an anti-leukocyte function-associated mAb induced a much more rapid dissociation of preformed conjugates.
The requirement for surface Ig signaling as a prerequisite for T cell:B cell interactions. A possible role for desialylation.
Authors: Kearse K P , Cassatt D R , Kaplan A M , Cohen D A 
Published: December 2022

Abstract
Models for T cell:B cell collaboration suggest that activated B cells process and present Ag to Th cells which subsequently induce B cell proliferation and differentiation. In contrast to activated B cells, resting B cells have generally been shown to be less efficient APC. If this model of T:B collaboration is physiologically correct, then resting B cells must undergo a phenotypic change that permits effective interaction with T cells. In this report, the requirement for rapid signaling through surface Ig on resting B cells for the induction of T:B interaction was investigated with an in vitro clustering assay. Resting splenic B cells were unable to form specific conjugates with T cell clones, unless the B cells were first treated with neuraminidase to remove sialic acid. In contrast, LPS-activated B cells were able to form conjugates without prior treatment. The ability of antibody against LFA-1 or L3T4 to inhibit cluster formation depended on the state of B cell activation in that anti-LFA-1 and anti-L3T4 mAb inhibited cluster formation by neuraminidase-treated resting B cells, but not by LPS-activated B cells. In addition, Ag-specific B cells which were isolated by their capacity to bind specific Ag were able to form clusters without any additional treatment. Moreover, treatment of resting splenic B cells with anti-mu-antibody induced clustering potential in B cells in as little as 10 min, suggesting that signaling through surface Ig was sufficient to induce this phenotypic change in B cells. Furthermore, activation of protein kinase C and Ca2+ mobilization were shown to be involved in that PMA and ionomycin treatment were also able to induce clustering potential in resting B cells. The rapid induction of clustering potential in resting B cells after signaling through surface Ig may represent a fundamental change in B cell physiology which occurs after recognition of specific Ag and may be required for effective cognate recognition between resting hapten-specific B cells and carrier-specific T cells. The potential role of desialylation for the induction of T:B interaction is discussed.
Recognition of hepatitis B surface antigen by human T lymphocytes. Proliferative and cytotoxic responses to a major antigenic determinant defined by synthetic peptides.
Authors: Celis E , Ou D , Otvos L 
Published: December 2022

Abstract
The antigenic sites for human T lymphocytes on hepatitis B surface Ag (HBsAg) were studied by using synthetic oligopeptides. T cell lines of the helper/inducer class, which were isolated from hepatitis B vaccine recipients, were found to react strongly and in an Ag-specific way with peptides corresponding to a sequence of 10 to 30 amino acids near the amino terminus of the HBsAg molecule. Cells with surface expression of the antigenic determinant contained in these synthetic peptides induced both proliferative and cytotoxic responses in the hepatitis B-specific T cells. The results indicate that amino acid residues 24-27 of HBsAg could be directly involved in this T cell determinant. Inhibition studies with mAb to MHC class II Ag and target cells from various HLA-typed individuals suggest that some T cell responses to this determinant of HBsAg might be restricted by the DPw4 molecule. However, the possibility exists that more than one of the MHC class II molecules could be involved as restricting elements of T cell responses to this synthetic peptide. In vivo experiments with synthetic peptides such as those described here are needed to demonstrate the possibility of enhancing HBsAg immune responses in some individuals.
Evidence that leukocyte function-associated antigen-1 is involved in recirculation and homing of human lymphocytes via high endothelial venules.
Authors: Pals S T , den Otter A , Miedema F , Kabel P , Keizer G D , Scheper R J , Meijer C J 
Published: December 2022

Abstract
We report the results of mAb inhibition studies of human lymphocyte-high endothelial venule interaction in vitro. These studies in which T cells from both normal donors and from a LFA-1-deficient patient were used indicate that in addition to a system of organ-specific 90-kDa "homing" receptors on lymphocytes, LFA-1 is also involved in lymphocyte recirculation and homing.
Analysis of the suppression of IL-1 alpha and IL-1 beta production in human peripheral blood mononuclear adherent cells by a glucocorticoid hormone.
Authors: Lew W , Oppenheim J J , Matsushima K 
Published: December 2022

Abstract
The suppression of IL-1 production in human adherent PBMC by a glucocorticoid hormone was studied. From 10(-5) to 10(-8) M glucocorticoid hormone (prednisolone) inhibited both IL-1 alpha and IL-1 beta production by LPS-stimulated adherent human PBMC in a dose-dependent fashion, as assayed by Western blotting of cell-associated IL-1 and a thymocyte comitogenic bioassay. IL-1 alpha and -beta mRNA levels were concomitantly suppressed by glucocorticoid treatment, as determined by Northern blotting analysis. These data suggest that the suppression of IL-1 activity by glucocorticoids is consistently associated with decreased levels of IL-1 proteins and mRNA expression and therefore presumably regulated at the transcriptional level.
Adoptive protection against Plasmodium chabaudi adami malaria in athymic nude mice by a cloned T cell line.
Authors: Brake D A , Long C A , Weidanz W P 
Published: December 2022

Abstract
T cell-dependent, cell-mediated immune mechanisms have been shown to contribute to resistance against malaria. Because the identity of plasmodial Ag responsible for the activation of these protective immune responses remains unknown, a major step in isolating these potential immunizing agents will be the development of adequate screening procedures designed to identify important T cell Ag. This study focused on the isolation of protective T cell clones that may play a pivotal role in this process. A T cell clone designated CTR2.1 and two subclones derived from it adoptively transferred protection to athymic nude mice infected with Plasmodium chabaudi adami, a murine malarial parasite known to be recognized by protective thymus-dependent immune mechanisms. The protective T cell clone displayed a L3T4+, Lyt-2- surface phenotype and secreted both IFN-gamma and IL-2 after stimulation with solubilized parasites in vitro. This is the first report of results demonstrating a cloned T cell line capable of providing adoptive protection against malaria in vivo. More importantly, CTR2.1 and other protective T cell clones may provide for the identification of plasmodial antigenic epitopes recognized by important cell-mediated immune mechanisms during acute malarial infection.
Regulation of the Ig kappa-chain enhancer by the adenovirus E1A gene products. Repression in lymphoid cells, activation in fibroblasts.
Authors: Bergman Y , Shavit D 
Published: December 2022

Abstract
Proteins encoded by early region 1A (E1A) regulate transcription of viral and cellular genes. The mechanism of this trans-activation is not understood, but is of considerable interest as an example of transcription regulation through a cellular intermediate. We have therefore studied the effect of E1A products on the activity of the kappa L chain gene promoter and enhancer. By using transient and stable transfections into lymphoid and nonlymphoid cells, we found that the E1A proteins have a pleiotropic effect on the regulation of the mouse kappa-chain gene enhancer. In lymphoid cells the E1A products repress kappa-chain enhancer, whereas in fibroblasts, the kappa-chain enhancer is activated by the E1A products whether the E1A gene is in an extrachromosomal location or stably integrated in the genome. Furthermore, a functional kappa-chain promoter, containing the octanucleotide and "TATA" sequences is needed in order to be transcribed in E1A-producing cells. This ability of E1A products to negatively and positively regulate kappa-chain transcription may reflect a more general phenomenon in which a given cellular protein could participate in a variety of different cellular controls.
Macrophage migration in fibrin gel matrices. II. Effects of clotting factor XIII, fibronectin, and glycosaminoglycan content on cell migration.
Authors: Lanir N , Ciano P S , Van de Water L , McDonagh J , Dvorak A M , Dvorak H F 
Published: December 2022

Abstract
We investigated the migration of oil-induced, guinea pig peritoneal macrophages in three-dimensional fibrin matrices, with particular attention to variables which modified fibrin gel structure and/or its adhesive properties for cells. The variables studied were fibrin concentration, gel cross-linking, and fibronectin and glycosaminoglycan content. Macrophage migration was an inverse linear function of fibrinogen concentration. Little or no fibrinolysis accompanied macrophage migration; rather, macrophages migrated through fibrin gels by an active process associated with marked distortions of cell shape and specialized plasma membrane contacts with fibrin strands. Fibrin matrices prepared from fibrinogen that had been depleted of clotting factor XIII and/or fibronectin provided a superior matrix for macrophage migration. Both the number of migrating cells and distance of migration were reduced when the gel matrix included fibronectin and was cross-linked by factor XIII. A hexapeptide containing the fibronectin cell-binding RGDS sequence reversed this migration inhibition, suggesting that fibronectin immobilized by cross-linking to fibrin may have bound macrophages and restricted cell migration. Hyaluronic acid, heparin, and heparan sulfate inhibited macrophage migration in cross-linked fibrin-fibronectin gels over a range of concentrations. These data are relevant to an understanding of macrophage migration in vivo where cross-linked fibrin-fibronectin gels containing variable amounts of glycosaminoglycans are deposited in tissues in immunologic reactions and in many other types of pathology.
Mast cell-dependent amplification of an immunologically nonspecific inflammatory response. Mast cells are required for the full expression of cutaneous acute inflammation induced by phorbol 12-myristate 13-acetate.
Authors: Wershil B K , Murakami T , Galli S J 
Published: December 2022

Abstract
Mast cells clearly are critical for the expression of some IgE-dependent responses, but their roles in other forms of inflammation are uncertain. We previously described a new model system for defining the unique contribution of mast cells to biologic responses in vivo, genetically mast cell-deficient WBB6F1-W/Wv mice that have undergone selective local repair of their mast cell deficiency by the injection of IL-3-dependent cultured mast cells derived from the congenic normal (WBB6F1-+/+) mice. Using this approach, we analyzed the contribution of mast cells to the acute inflammation induced by the epicutaneous application of PMA. Even though PMA can activate a wide variety of cell types that may contribute to acute inflammation, we found that mast cells were required for the full expression of the tissue swelling and leukocyte infiltration associated with the response to the agent in vivo. Thus, in WBB6F1-W/Wv mice selectively reconstituted with dermal mast cells by intradermal injection of cultured WBB6F1-+/+ mast cells into the left ear only, PMA induced approximately twice the tissue swelling and neutrophil infiltration in the mast cell-reconstituted left ears as in the contralateral control ears. This represents the first use of W/Wv mice locally reconstituted with mast cells to confirm the hypothesis that mast cells can represent an important amplification mechanism in acute inflammatory responses of nonimmunologic origin. It also defines a model system that may be generally useful for investigating mast cell-dependent and -independent aspects of acute inflammatory responses.