bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mechanism of systemic immune suppression by UV irradiation in vivo. II. The UV effects on number and morphology of epidermal Langerhans cells and the UV-induced suppression of contact hypersensitivity have different wavelength dependencies.
Authors: Noonan F P , Bucana C , Sauder D N , De Fabo E C 
Published: December 2022

Abstract
We previously reported that broad band UV radiation or narrow bands of UV (Hbw 3 nm) of wavelengths 250 to 320 nm cause a systemic suppression of contact hypersensitivity (CHS) in mice, observed when the contact sensitizer is applied to a nonirradiated site. To determine if this effect is associated with UV-induced alterations in epidermal Langerhans cell (LC) numbers and morphology, we performed the following study. LC were identified by ATPase staining of EDTA-separated epidermal sheets. Electron microscope studies confirmed that this method was a satisfactory indicator of the presence of LC; we found no evidence for LC which did not stain for ATPase in either irradiated or unirradiated epidermis. Mice were irradiated on the back with narrow band UV of peak wavelength 270, 290, or 320 nm. The irradiated skin was excised 24 hr later and was stained as described. The number of LC with ATPase staining dendrites and the number of nondendritic LC were enumerated. We found that UV radiation of 270 or 290 nm caused 1) an alteration in LC morphology (loss of dendrites) and 2) a decrease in the total number of epidermal LC. Both effects occurred in a dose-dependent fashion. Previously, these same wavelengths of narrow band UV, but at higher doses, had been shown to cause systemic suppression of CHS. In this study, the doses of 270 or 290 nm UV that resulted in the decreased LC numbers and alterations in LC morphology described above were insufficient to cause systemic suppression of CHS. The converse was found if the irradiating waveband of UV had a peak at 320 nm. A dose of 320 nm UV that caused 50% systemic suppression of CHS had no effect on either the number or the morphology of LC at the site of irradiation. In addition, the number and morphology of LC were unaffected in the ventral epidermis (site of contact sensitization) of mice that had been previously irradiated on the back with a systemically suppressive dose of UV. We conclude: (a) UV-induced alterations in the number and morphology of LC at the site of irradiation are not necessary for the generation of systemic suppression of CHS by UV radiation; this indicates that the initial UV-absorbing event triggering systemic suppression is neither a loss of, nor morphologic alterations to, LC at the irradiation site. (b) A systemic effect of UV radiation on the number and morphology of LC at the unirradiated site of contact sensitization does not occur, and thus is not responsible for the UV-induced systemic suppression of CHS by UV radiation.
Recipient contributions to serial passive transfer of experimental allergic encephalomyelitis.
Authors: Wegmann K W , Hinrichs D J 
Published: December 2022

Abstract
EAE can be adoptively transferred into normal recipients by the transfer of BP-specific EAE effector cells. After cell transfer, a series of ill-defined events occur in the recipient that culminate in the development of paralysis associated with neural tissue damage. We investigated the subsequent recipient response to the adoptively transferred disease and examined the role that recipient lymphocytes play in the development of adoptively transferred EAE. Recipient involvement was assessed by the transfer of EAE through a series of normal F1 animals as recipients and at the endpoint of the experiment, determining the MHC restriction pattern of the BP-sensitive cells present. The serial transfer of EAE from BP-CFA-sensitized LEW----(LEW X F-344)F1----(LEW X P2)F1, and from BP-CFA sensitized LEW----(LEW X F344)F1----(LEW X F-344)F1, resulted in the development of BP-sensitive cells in the spleens of the secondary recipients that were able to transfer disease into normal LEW recipients. To test directly for the development of host-derived BP-sensitive cells that might arise in the F1 animal, the serial transfer of EAE from LEW----(LEW X ACI)F1----(LEW X ACI)F1 was performed. When BP-sensitive cells obtained from the secondary (LEW X ACI)F1 recipient animal were transferred into either normal LEW and ACI, or irradiated LEW and ACI animals as final recipients, transfer of disease was successful only into the LEW parental. These results suggest that the development of passive EAE is due solely to the transferred BP-sensitive cells originating from the actively immunized donor, and that no host-derived lymphocytes are recruited into the pool of EAE effector precursor cells found in the spleen of animals after the development of adoptively transferred EAE.
A rat monoclonal antibody that binds specifically to mouse T lymphoblasts and inhibits IL 2 receptor functions: a putative anti-IL 2 receptor antibody.
Authors: Osawa H , Diamantstein T 
Published: December 2022

Abstract
To obtain an anti-interleukin 2 (IL 2) receptor antibody, we immunized rats with phorbol myristate acetate-pulsed mouse T lymphoblasts. The spleen cells of the rats were fused with rat myeloma cells. Several stable clones of hybridoma cells were obtained that produced monoclonal antibodies (mAb) reacting specifically with mouse T lymphoblasts. One of these mAb, AMT-13, showed characteristics of a putative anti-IL 2 receptor antibody. As tested by FACS analysis, the mAb AMT-13 binds to murine T lymphoblasts or to IL 2-dependent T cell lines, but not to B lymphoblasts, thymocytes, splenocytes, lymph node cells, or bone marrow cells. The mAb AMT-13 inhibited in a species-specific and dose-dependent manner: i) the capacity of mouse T lymphoblasts to absorb IL 2 activity, and ii) the capacity of mouse T lymphoblasts to proliferate in response to IL 2. The function of T lymphoblasts of rat origin was not affected by the mAb AMT-13. The time course of the acquisition by mitogen-stimulated spleen cells of the capacity to absorb IL 2 activity was paralleled by that of their capacity to bind the mAb AMT-13. Preliminary biochemical analysis of the antigen recognized by AMT-13 revealed a major component with an apparent m.w. of 50,000 to 60,000. According to these data, the mAb AMT-13 seems to be directed against an antigenic determinant of the murine IL 2 receptor molecule.
Expression of antigens of the 'T200' family of glycoproteins on hemopoietic stem cells: evidence that thymocyte cell lineage antigens are represented on 'T200'.
Authors: Ralph S J , Berridge M V 
Published: December 2022

Abstract
A panel of monoclonal antibodies has been used to investigate the presence of antigens of the 'T200' family of cell surface glycoproteins on hemopoietic stem cells. As measured by spleen colony inhibition using CBA bone marrow, stem cells were shown to be antigenically heterogeneous with respect to 'T200' family antigens; greater than 60% loss of spleen colonies was observed with 74/8 and 30F11 monoclonal antibodies and with Ly5.1 alloantiserum, whereas little effect was observed with 30G12. Two of four monoclonal antibodies with specificity for B220 showed significant inhibition of spleen colony formation. Monoclonal antibodies against Mac-1, another family of cell surface glycoproteins, had little effect on stem cells. In general, a similar pattern of spleen colony inhibition was observed in CBA, BALB/c, and C57/BL/6 mice. Spleen colony inhibition did not correlate with antibody isotype or with antibody binding to thymocytes, B lymphocytes, macrophages, or platelets as determined by indirect radioimmunoassay. Cell lineage antigens held in common between thymocytes and stem cells were shown to be wholly represented on the T200 glycoprotein. Thus, the anti-stem cell activity in anti-thymocyte serum (ATS) was absorbed by BW5147 T200+ cells but not by a T200- variant. The results show that some antigens of the 'T200' family of cell surface glycoproteins defined with monoclonal antibodies are expressed on stem cells and that other T200 antigens represented in ATS but not as yet identified with monoclonal antibodies show T lineage restriction.
Stabilization of the amplification convertase of complement by monoclonal antibodies directed against human factor B.
Authors: Daha M R , Deelder A M , Van Es L A 
Published: December 2022

Abstract
Three IgM mouse monoclonal antibodies (MoAb), 5B5-A, 2D2-B, and 5B12-A, were prepared by fusion of spleen cells from mice immunized with human B with the SP 2/0 myeloma cell line. They were assessed for their effect on cell-bound and fluid-phase amplification convertases of complement (C) with purified proteins in vitro. 5B5-A and 2D2-B were similar in their effects on cell-bound preformed C3bBb in that they bound to cell-bound C3bBb, stabilized the C3bBb convertase, and rendered the C3bBb convertase relatively resistant to the plasma protein H. These two MoAb were also able to enhance C3 consumption in vitro in reaction mixtures containing C3b, C3, B, and D. At the same time, they presumably stabilized the C3 convertase and caused relative sparing of B hemolytic activity in the reaction mixtures. In contrast, 5B12-A, which also bound to Bb and C3bBb, did not induce any stabilization, but rather caused accelerated decay of cell-bound C3bBb. These results indicate that MoAb against B can have C3NeF-like activity. On the other hand, not all MoAb against B have stabilizing activity on the C3bBb convertase.
Cathepsin G in human mononuclear phagocytes: comparisons between monocytes and U937 monocyte-like cells.
Authors: Senior R M , Campbell E J 
Published: December 2022

Abstract
Previous studies demonstrating that a continuous line of human monocyte-like cells (U937) and human monocytes contain elastase probably identical to human neutrophil elastase suggested the possibility that mononuclear phagocytes share other proteinases with neutrophils. The present work establishes that U937 cells contain cathepsin G, an enzyme heretofore found only in neutrophils. U937 cells contain approximately 10 micrograms of cathepsin G-like activity per 10(7) cells, about 25% of the cathepsin G activity in human neutrophils. Normal monocytes have minimal cathepsin G-like activity (approximately 0.1 microgram per 10(7) cells). The cathepsin G-like activity of U937 cells appears to be due to an enzyme that is the same as cathepsin G by several criteria: 1) it is a serine proteinase with activity like cathepsin G against a synthetic chymotrypsin substrate, succinyl-ala-ala-pro-phe-p-nitroanilide; 2) the proteolytic fragments it releases from fibronectin match those released by cathepsin G; 3) like cathepsin G, it can be purified by sequential Trasylol-Sepharose affinity chromatography and carboxymethyl-Sephadex ion exchange chromatography; 4) its amino acid composition and migration on SDS-polyacrylamide gel electrophoresis are indistinguishable from cathepsin G; and 5) it binds with antiserum raised to cathepsin G. The presence of cathepsin G in U937 cells, in much higher concentration than in normal monocytes, indicates either that the content of cathepsin G in monocytes decreases markedly during monocyte differentiation or that U937 cells differ from normal immature monocytes with respect to synthesis of this neutral proteinase.
Phagocytosis inhibits the expression of tissue transglutaminase in mouse peritoneal macrophages.
Authors: Mehta K , Murtaugh M P , Juliano R L , Davies P J 
Published: December 2022

Abstract
Culture of mouse peritoneal macrophages in serum-containing medium produces a rapid and marked induction of tissue transglutaminase. Concurrent endocytosis of a variety of particles via specific and nonspecific routes suppresses or completely abolishes the induction of the enzyme. The suppression is dose-dependent and is reversible. The rate of recovery from the inhibitory effect, however, depends on the nature of the particles internalized. The inhibitory effect is due to the inhibition of the synthesis of tissue transglutaminase.
Monocyte suppression of antigen-specific lymphocyte responses in diffuse cutaneous leishmaniasis patients from the Dominican Republic.
Authors: Petersen E A , Neva F A , Barral A , Correa-Coronas R , Bogaert-Diaz H , Martinez D , Ward F E 
Published: December 2022

Abstract
Patients from the Dominican Republic with diffuse cutaneous leishmaniasis showed in vivo and in vitro anergy to leishmanial antigen. Relatives of these DCL patients living in the same endemic area frequently showed skin test and lymphocyte reactivity to leishmanial antigens. This further supports the concept of specific anergy in patients with diffuse cutaneous leishmaniasis. Adherent suppressor cells modulate the antigen-specific lymphocyte proliferative response. Suppressor cells could also be isolated by Percoll gradient centrifugation. Co-culturing of lymphocytes and monocytes from HLA-identical leishmanin responders and nonresponders also identified the suppressor cell as a monocyte. In one patient, this suppression disappeared when clinical cure had been accomplished.
The reactions of monoclonal antibodies with structural proteins of mumps virus.
Authors: Orvell C 
Published: December 2022

Abstract
Mouse hybridomas producing antibodies against structural proteins of mumps virus were established by fusion of FO or SP 2/0 myeloma cells with spleen cells from BALB/c mice immunized with purified preparations of egg-grown mumps virus. Ascites fluids collected after i.p. inoculation of mice were characterized by different serologic tests. By immune precipitation tests with [35S]methionine-labeled mumps virus polypeptides, 17 clones were found to produce antibodies against the nucleocapsid protein (NP), 11 against the polymerase (P) protein, 10 against the membrane (M) protein, 12 against the fusion (F) protein, and 24 against the hemagglutinin-neuraminidase (HN) protein. Competitive binding enzyme-linked immunosorbent assay (ELISA) tests were performed to determine the reactivity of the monoclonal antibodies with different antigenic sites of each structural component. The monoclonal antibodies directed against the NP, P, and M proteins identified a minimum of 10, 10, and 9 separate antigenic sites, respectively. The 12 clones directed against F were directed against a minimum of eight separate antigenic determinants. These antibodies did not neutralize the infectivity of the virus either in the absence or presence of anti-gamma-globulin. Only low capacity to block hemolysis (HL) activity of the virus was detected in clones directed against three of the eight antigenic sites. Based on their serologic reactivity, the 24 clones directed against the HN protein could be divided into four groups. The first group of clones could not inhibit any biologic activity of the protein. The second group consisted of two clones that blocked HL but did not block hemagglutination (HA) or neuraminidase (NA) activity. The third group, which included five clones, blocked HA, NA, and HL activity of the virus and had high neutralizing capacity. These clones were directed against three distinct antigenic sites. Two of the clones directed against one antigenic site could block NA activity only when a large substrate, fetuin, was used, but not when a small substrate, neuraminlactose, was used in the test. The fourth group included five clones that could block NA but not HA activity of the virus. These clones could neutralize the infectivity of the virus and had high capacity to block HL activity. In blocking experiments, all these antibodies reacted with one antigenic site. The reaction of all clones was tested in ELISA with four different strains of mumps virus. Each strain had unique antigenic sites. Variations were found in four, three, and three different antigenic sites of the NP, P, and HN proteins, respectively.
Soluble factors produced during an immune response regulate Ia antigen expression by murine adenocarcinoma and fibrosarcoma cells.
Authors: Callahan G N 
Published: December 2022

Abstract
LT-85 is an alveologenic adenocarcinoma of C3Hf/HeN mice. Comparisons of the in vitro and in vivo surface properties of these cells revealed that under normal conditions, they expressed I-A and I-E antigens iv vivo only. By using clonally derived cells, it was established that this phenomenon was not due to the selection of an Ia antigen-positive tumor cell subpopulation, but resulted from phenotypic conversion of Ia antigen-negative tumor cells. These tumor cells and 1053 cells (a fibrosarcoma of C3H/HeN MTV- mice) could, however, be induced to express I-A, I-E, and much higher levels of H-2 antigens in vitro by co-culturing them with spleen cells from LT-85 tumor-bearing C3H/HeN MTV- mice. In vitro induction of Ia and H-2 antigens did not result from contaminating splenocytes or from antigen transfer, because splenocytes from BALB/c (H-2d) mice immunized with A/J (H-2k/d) cells were able to induce the expression of Iak antigens by both tumor cell lines. It was found that this phenomenon was neither H-2-restricted nor antigen-specific. The results clearly indicated, however, that an immune response was required to generate phenotypic conversion of the tumor cells, both in vivo and in vitro. It was further found that soluble, rather than cellular, factors produced during an immune response induced the expression of Ia antigens by LT-85 and 1053 tumor cells. In contrast to what has been reported about the induction of Ia antigens on macrophages and normal epithelial and endothelial cells, the induction of Ia antigens on LT-85 and 1053 cells did not appear to require T cells, and did not involve gamma-interferon. These findings demonstrate that some tumor cells are capable of altering their MHC antigen phenotype in response to factors produced during an immune response in vivo or in vitro. Because of the involvement of Ia antigens in several aspects of immune phenomena, the ability of tumor cells to differentially express Ia antigens in response to environmental factors may have profound effects on host-tumor interactions. Furthermore, the differences seen in the phenotypes of tumor cells grown in vitro and in vivo suggest that in vitro methodologies of tumor cell characterization may not present a complete picture of the natural state of the tumor cell surface.
Genetic control of the induction of cytolytic T lymphocyte responses to AKR/Gross viral leukemias. I. H-2-encoded dominant gene control.
Authors: Green W R 
Published: December 2022

Abstract
Previously, a system was devised whereby H-2-restricted cytotoxic T lymphocytes could be raised that were specific for tumors induced by endogenous AKR/Gross murine leukemia virus and that displayed the Gross cell surface antigen (GCSA). The generation of such anti-AKR/Gross virus CTL required in vivo priming with allogeneic (H-2 and/or non-H-2 incompatible) GCSA+ tumor cells, followed by in vitro restimulation with H-2-compatible GCSA+ tumor cells. The prototype responder strain of mice was C57BL/6, which is of the H-2b type and which has a low incidence of spontaneous virus-induced leukemia ("low leukemic"). Present experimentation indicates that there is H-2-encoded control of the ability to mount an anti-AKR/Gross virus CTL response. In addition to C57BL/6, all other H-2b strains tested, including C57BL/10, C57L, and 129, were responders. In contrast, H-2k strains of both "high leukemic" (AKR) and "low leukemic" (AKR.Fv-1b and CBA) phenotype appeared to be low- or nonresponders with respect to their ability to generate H-2k-restricted anti-AKR/Gross virus CTL after appropriate stimulation. Furthermore, B6.H-2k congenic mice were also poorly responsive, suggesting that H-2b and H-2k were responder and nonresponder haplotypes, respectively. The finding that (responder X nonresponder)F1, i.e., (B6 X CBA)F1 mice mounted CTL responses to H-2b, but not H-2k, GCSA+ tumors, was consistent with this interpretation and suggested the presence of H-2-encoded dominant immune response genes. The tumors of AKR background that were efficient in the in vivo priming of C57BL/6 mice were relatively inefficient in priming (B6 X CBA)F1 mice for a subsequent in vitro H-2b-restricted anti-AKR/Gross virus CTL response. Because of the similarities in background minor H genes of the AKR and CBA strains, this latter observation was in keeping with the requirement for in vivo stimulation with tumor cell alloantigens in addition to the virus-associated target antigens.
Generalized systemic and mucosal immunity in mice after mucosal stimulation with cholera toxin.
Authors: Elson C O , Ealding W 
Published: December 2022

Abstract
Cholera toxin (CT) has been found to be an extremely potent immunogen for mucosal IgA responses when administered via the intestine. This study has examined both mucosal and systemic immune responses after feeding CT and compared these responses with those obtained after feeding keyhole limpet hemocyanin (KLH), another protein that is strongly immunogenic in mice. Feeding CT to mice resulted not only in IgA antibody in intestinal secretions but also resulted in substantial plasma IgG and IgA antibody levels. Feeding KLH in much larger quantity resulted in little or no antibody response in intestinal secretions or plasma. Lymphoid cells from various tissues of mice fed CT were cultured in vitro for 10 days and the supernatant was tested for antibody to CT. Spontaneous antibody synthesis (no antigen added to cultures) was present in cultures of each cell type, but IgG anti-CT was found mainly in cultures of spleen and mesenteric lymph node cells and IgA anti-CT mainly in cultures of Peyer's patch and lamina propria cells. Peyer's patch cells cultured with CT as antigen synthesized both IgG and IgA anti-CT, suggesting that the antibody response to both isotypes originated in this site. Helper T cell activity for both IgA and IgG anti-CT was detected in spleens, mesenteric lymph nodes, and Peyer's patches. Lastly, when KLH and CT were fed to mice at the same time, an intestinal IgA anti-KLH and plasma IgG anti-KLH response was stimulated, a response pattern similar to that occurring to CT after CT was fed alone. We conclude that mucosal stimulation by CT generates both a systemic IgG and mucosal IgA response to this antigen, and that CT can cause a similar pattern of response to an unrelated protein antigen when both are administered into the intestine at the same time. The data favor the idea that both the IgG and IgA responses originate in GALT and then disseminate to other tissues. We propose that CT accomplishes these effects by altering the regulatory environment within GALT.
Suppression of BCG cell wall-induced delayed-type hypersensitivity by pretreatment with killed BCG: induction of nonspecific suppressor T cells by the adjuvant portion (MDP) and of specific suppressor T cells by the antigen portion (TAP).
Authors: Kato K , Yamamoto K , Kimura T , Azuma I , Askenase P W 
Published: December 2022

Abstract
We showed previously that antigen-nonspecific suppressor T cells induced by i.v. injection of heat-killed bacillus Calmette-Guérin (BCG) were involved in suppression of delayed-type hypersensitivity (DTH). We suggested that the adjuvant portion of BCG might be involved in the induction of these cells. In this report, we show that BCG cell wall-induced DTH responses in mice pretreated with muramyl dipeptide (MDP), a minimum adjuvant constituent of BCG, were suppressed nonspecifically. In addition, we show that pretreatment with tuberculin active peptide (TAP), the antigenic peptide from Mycobacterium tuberculosis, induces antigen-specific suppression of DTH responses. In both instances, suppression was shown to be due to non-adherent cells that act to inhibit elicitation of DTH. Furthermore, using the macrophage migration inhibition assay, an in vitro correlate of DTH, we found that antigen-nonspecific and antigen-specific suppressor T cells were induced by the injection of MDP and TAP, respectively. Thus, suppressor T cells induced by the adjuvant and antigen portions of BCG may act by interfering with the lymphokine-dependent mechanisms by which DTH effector T cells elicit DTH.