bluuebunny/crossref_metadata_2025_split huggingface dataset:
Immunologic control of the ascites form of murine adenocarcinoma 755. III. Efficacy of serum therapy is controlled by a single genetic locus.
Authors: Roloson G J , Haagensen D E , Chambers C A , Bolognesi D P 
Published: December 2022

Abstract
We have previously described a passive serum therapy system in which potent protection against challenge of syngeneic mice with large doses (10(4) X LD100) of AD755a tumor cells can be accomplished by administration of as little as 2 to 5 microliters/mouse of hyperimmune anti-tumor cell serum. The present results demonstrate that the efficacy of the serum protection effect is strain-dependent and is under the control of a single genetic locus, denoted ADP-1. Through a series of crosses between highly protected C57BL/6J and nonprotected BALB/cJ mice, the ADP-locus has been mapped to chromosome 2 [linkage group V], approximately 23 centimorgans toward te centromere from the locus controlling agouti coat color. Thus, the protection locus is not linked to either the H-2 region or to previously described loci regulating the replication and disease induction of type-C viruses closely related to the virus associated with the AD775a tumor. The possible functions of the ADP-1 locus are discussed and further aspects of this experimental model are described in the accompanying papers.
Cross-reactions between mouse Ia and human HLA-D/DR antigens analyzed with monoclonal alloantibodies.
Authors: Pierres M , Rebouah J P , Kourilsky F M , Dosseto M , Mercier P , Mawas C , Malissen B 
Published: December 2022

Abstract
Two mouse monoclonal anti-I-E/Ck alloantibodies (H7-8.26 and H10-81.10) directed against 2 distinct determinants of the specificity Ia-7 and 1 anti-I-Ak alloantibody (H8-15.9) directed against a public determinant common to the I-A subregion products of the H-2k, H-2b, H-2d, H-2q, and H-2ja haplotypes identified cross-reactive determinants on lymphoid cells from various mammalian species, including rat, dog, pig, cow, hamster, and guinea pig. In man, these antibodies detected nonpolymorphic determinants of DR antigens on B cell-enriched peripheral blood lymphocytes from 50 unrelated individuals. These cross-reactive DR determinants were also detected on lymphoblastoid B cell lines, on PHA-activated peripheral T lymphocytes, and on allospecific cytolytic T cell clones, but not on various DR-negative human T leukemia cell lines. Two chains of 29,000 and 35,000 daltons m.w., corresponding to DR antigens, were precipitated by H7-8.26 and H8-15.9 antibodies from radiolabeled membrane extracts of Raji cells. Competitive binding experiments indicated that the 3 mouse anti-Iak antibodies identified 3 distinct cross-reactive determinants on human cells. The results indicate that: a) The cross-reactivity described between mouse I-E/C gene products (Ia-7) and human DR antigen(s) involves, in fact, several distinct and topologically distant determinants. b) At least 1 determinant cross-reacting with DR can be identified on I-Ak gene products. c) The intriguing genetic problem of mouse MHC allotypic determinant(s) being nonpolymorphic in man cannot be simply explained by the deletion of an I-E alpha chain in some strains of mice.
Activation of autologous reactive helper T lymphocytes for differentiation of human B lymphocytes.
Authors: Shin H S , Wang C Y , Choi Y S 
Published: December 2022

Abstract
We present experimental evidence that autologous reactive T cells are triggered to proliferate by HLA-D or Ia-like antigens on pokeweed mitogen-pulsed non-T cells and that a subpopulation of these proliferating cells in turn helps PWM-primed B cells to differentiate into immunoglobulin-secreting cells. These helper T cells displayed a proliferation kinetics different from that of other autologous reactive T cells in peaking on the second day of culture and were relatively resistant to irradiation or treatment with mitomycin C. Since heterologous anti-Ia antibody (F(ab')2 reagent) inhibits proliferation of helper T cells and the generation of plaque-forming cells, Ia antigen is an essential component in PWM-stimulated B cell differentiation. Anti-Ia reagent was shown to interfere with B cell differentiation in 2 ways. First, it abrogates the ability of PWM-primed non-T cells to activate helper T cells. Second, it directly affects a differentiation of B cells into Ig-secreting cells even in the presence of the activated helper T cells.
Experimental allergic encephalomyelitis in Lewis rats: inhibition by bacterial lipopolysaccharides and acquired resistance to reinduction by challenge with myelin basic protein.
Authors: Raziuddin S , Kibler R F , Morrison D C 
Published: December 2022

Abstract
In 2-mo-old Lewis rats immunized with bacterial lipopolysaccharides (LPS) precomplexed to guinea pig myelin basic protein (BP), the clinical and histologic manifestations of experimental allergic encephalomyelitis (EAE) were diminished compared with BP-treated controls. Similarly, in animals immunized with BP and challenged with BP-LPS at the same time or as long as 5 days after, the immunization with BP also inhibited the disease. That this capacity to reduce the incidence of BP-induced EAE is a unique property of LPS was suggested by the fact that other negatively charged molecules, such as DNA, RNA, and dextran sulphate, were not effective in inhibiting the clinical signs of EAE. After recovery from EAE induced by BP, some animals develop a recurrence of the disease if challenged with BP at appropriate intervals. However, after recovery from mild EAE induced by BP-LPS and after challenges with EAE-initiating BP antigens, secondary EAE was inhibited significantly.
Genetics of a non-H-2 antigen that stimulates "unrestricted" helper T cells and MLR.
Authors: Coutinho A , Augustin A A , Forni L , Fischer-Lindahl K 
Published: December 2022

Abstract
The inheritance of antigens expressed by C3H/Tif B cells that stimulate MHC-unrestricted helper T cells from C3H/HeJ was investigated. F1 hybrids between C3H/HeJ and C3H/Tif and 39 C3H/HeJ X F1 backcross mice were characterized as to the ability of their spleen cells to stimulate a proliferative C3H/HeJ T helper cell response and to respond to helper cell activity by the development of polyclonal plaque-forming cell responses. Backcross progeny wee also typed for the following markers segregating in this cross: 1) Responsiveness to the B cell mitogen lipopolysaccharide (LPS); 2) LyM-1 allotype; 3) antigen(s) stimulating a primary non-H-2 MLR between these strains, previously ascribed to Mls locus differences, 4) expression of target antigens for cytotoxic T cells raised in the same strain combination. The antigen(s) recognized by helper cells and those stimulating primary MLR are controlled by autosomal gene(s) and segregate as a single trait. These antigens, however, are not encoded in genes linked to either the Lps or the Mls loci, and are not recognized by cytotoxic T cells raised in the same strain combination.
Antigen-specific helper factor reacts with antibodies to human beta 2 microglobulin.
Authors: Lamb J R , Zanders E D , Sanderson A R , Ward P J , Feldmann M , Kontiainen S , Lehner T , Woody J N 
Published: December 2022

Abstract
Antigen-specific helper factor was induced in vitro from lymphoid cells of monkeys and mice by using an antigen derived from Streptococcus mutans. Helper activity was removed from supernatants of monkey cells by affinity chromatography on Sepharose 4B insolubilized antibodies specific for human beta 2-microglobulin (H beta 2M) prepared in chicken, rabbit and rat, and an insolubilized monoclonal mouse anti-H beta 2M antibody-bound monkey helper factor activity. However, guinea pig antibody to human beta 2M was inactive. In parallel studies, the pattern of absorption of mouse helper factor (HF) was different from that of the monkey in that insolubilized guinea pig anti-H beta 2M bound helper factor, whereas rabbit and monoclonal anti-H beta 2M failed to do so. Although these findings were not compatible with an intact beta 2M chain being present in helper factor, they may imply a cross-reactivity of beta 2M with a "constant region" of helper factor that may share common sequences with beta 2M. This may suggest that factor genes have evolved from the same ancestral genes as beta 2M.
Cellular interactions affecting the maturation of murine B lymphocyte precursors in vitro.
Authors: Kincade P W , Lee G , Paige C J , Scheid M P 
Published: December 2022

Abstract
Clonable B cells arose in liquid cultures of slg+ cell-depleted bone marrow suspensions, and a majority of these derived from rapidly sedimenting (presumably large) precursors. Such immature (pre-B) cells were not demonstrable in adult lymph nodes. The development of functional B cells in vitro depended on adherent cells present in adult bone marrow or peritoneal exudates and in the presence of optimal numbers of these accessory cells; not FCS or 2-ME or LPS were essential for B cell maturation. In contrast, the ability of fetal liver cell suspensions to generate B cells in culture was not affected by the removal of adherent cells or addition of macrophages, and LPS consistently reduced numbers of colony-forming B cells recovered. A type of nonadherent cell present in the bone marrow of adult CBA/N mice dramatically enhanced B cell maturation in normal CBA/H-T6T6 fetal liver cell cultures. These results indicate that 2 types of accessory cells may augment transition of pre-B cells to functional B cells in culture. One is adherent and can be replaced by macrophages, whereas the other is nonadherent and is present in limiting numbers in embryos. When fetal liver cultures were incubated with optimal numbers of adult accessory cells, the rate of emergence of B cells was dependent on the gestational age of the donor embryo. This suggests that B cell formation in utero may be limited by the availability of B cell precursors as well as nonadherent accessory cells. The possibility exists that fetal pre-B cells typify intermediates in the B lineage which are infrequent in adult marrow. Alternatively, B cells may be produced in adult life through processes that do not precisely recapitulate embryonic events.
Differential anti-inflammatory effects of LPS in susceptible and resistant mouse strains.
Authors: Verghese M W , Snyderman R 
Published: December 2022

Abstract
Most mouse strains are highly susceptible to endotoxin (LPS) lethality and are responsive to LPS stimulation in vitro (e.g., B cell mitogenesis, macrophage activation). They are, however, capable of mounting only a small inflammatory response to LPS when it is injected i.p. The present study demonstrates that LPS is in fact a potent, anti-inflammatory agent in all of the five normally LPS susceptible strains tested. LPS was also anti-inflammatory in F1 hybrid mice from susceptible (C3HeB/FeJ) x-resistant (C3H/HeJ) parents. Anti-inflammatory effects of LPS in susceptible strains were achieved by either i.v. or i.p. treatment and were observed toward a variety of phlogistic stimuli including mitogens, C-activating substances, and nonspecific irritants. The most dramatic inhibitory effect of LPS was directed toward the accumulation of inflammatory macrophages. Kinetic studies indicated that the anti-inflammatory effect of a single dose of LPS persisted for at least 72 hr but was maximal when LPS was given simultaneously with the inflammatory stimulus. In contrast to normal mice, two mutant, LPS resistant strains (C3H/HeJ and C57BL10/ScCR) responded to increasing doses of LPS i.p. with a progressively increasing influx of inflammatory cells. In addition, in resistant strains, LPS often enhanced and never depressed the inflammatory response to other phlogistic agents. These studies demonstrate that the genetic regulation of the inflammatory responses to LPS also controls the anti-inflammatory effects of LPS. These responses may be another relevant parameter in determining strain susceptibility to LPS lethality.
Analysis of Ir gene function using monoclonal antibodies: independent regulation of GAT and GLPhe T cell responses by I-A and I-E subregion products on a single accessory cell population.
Authors: Nepom J T , Benacerraf B , Germain R N 
Published: December 2022

Abstract
T cell proliferative responses to the synthetic polypeptides GAT and GLPhe are under Ir gene control. GAT responses are regulated by gene(s) in the I-A subregion, and GLPhe responses are controlled by a pair of complementing genes mapping to the I-A and I-E subregions. We demonstrate that monoclonal antibody to the I-A gene product inhibits GAT proliferation but not the GLPhe response, whereas a monoclonal antibody to the I-E associated Ia-7 determinant inhibits GLPhe but not GAT proliferation, which indicates independent involvement of each Ia determinant in antigen presentation for the T cell response to these antigens. Use of the same subregion-specific monoclonal antibodies in complement-dependent lysis demonstrates that the antigen-presenting cells for GAT and GLPhe express both I-A and I-E products. The possibility that an Ia subregion-specific "self-receptor" functions on the reactive T cells as a regulatory element is discussed.
Ultraviolet light induces tumors with both unique and host-associated antigenic specificities.
Authors: DeWitt C W 
Published: December 2022

Abstract
Murine tumors induced by ultraviolet light (UV) are immunogenic in syngeneic and semi-syngeneic hosts, evoking antibody of several different specificities. Cytotoxic antibody specific for the immunizing syngeneic tumor (tumor-specific antigen) comprises the early response and a minor portion of the later response of C3H and C3H.SW mice. It is the primary specificity to which C57BL/6 and C57BL/10 hosts respond. The major portion of the antibody produced by C3H and C3H.SW against syngeneic tumors cross-reacts strongly with other tumors, both UV and chemically induced, arising in C3H and C3H.SW but not in B6.H2k, C57BL/6, C57BL/10, or (C3H X B6)F1. Normal adult cells or embryonic fibroblasts do not cross-react with the antisera. These results are interpreted as evidence for the involvement of a host component (non-MHC) in this tumor-associated antigen (TAA). (C3H X B6)F1 and (C3H X BALB/c)F1 hosts respond to C3H tumors with antibody with cross-reactive specificities identical to those of the C3H and C3H.SW hosts. thus detecting the TAA(C3H) specificity. (C3H X B6)F1 hosts respond to syngeneic F1 tumors, however, with a totally cross-reactive antibody that is interpreted as evidence for the existence of a common antigen in addition to the evident immune response control. An undetected TAA (B6) specificity in the (C3H X B6)F1 tumors is speculatively proposed.
Strain variation in BCG-induced chronic pulmonary inflammation in mice: control by a cyclophosphamide-sensitive thymus-derived suppressor cell.
Authors: Moore V L , Mondloch V M , Pedersen G M , Schrier D J , Allen E M 
Published: December 2022

Abstract
We previously reported that only certain strains of inbred mice develop intense chronic granulomatous inflammation (CGI) in the lungs and spleen in response to an i.v. injection of killed BCG in an oil-in-saline emulsion (BCG-E). The capacity to respond did not appear to be controlled by genes within the H-2 complex; subsequent studies have shown that genes linked to the Igh allotype complex influence the development of CGI. In other systems, unresponsiveness to certain antigens has been shown to be because of cyclophosphamide- (Cy) sensitive suppressor cells. We therefore used Cy as a probe to study mechanisms of unresponsiveness in low-responder (LR) CBA mice. The results indicate that LR mice could be converted into high responders (HR) by treatment with 100 mg of Cy per kilogram of body weight 2 days before injection with BCG-E. In addition, the effects of Cy were inhibited by the provision of syngeneic whole or purified spleen T cells from mice injected 7 days previously with BCG-E. Cells responsible for abolition of the Cy effect were sensitive to anti-Thy-1 serum + C. Thus, the intensity of BCG-E-induced CGI in mouse lungs is controlled by a population of Cy-sensitive T lymphocytes.
Immunologic consequences of antibiotic-induced abridgement of bacterial infection: effect on generation and loss of protective T cells and level of immunologic memory.
Authors: North R J , Berche P A , Newborg M F 
Published: December 2022

Abstract
Ampicillin was employed in mice to determine the effect of rapidly abridging bacterial infection on the generation of T cell-mediated antibacterial immunity. It was found that antibiotic-induced abridgement of infection with Listeria monocytogenes had a pronounced effect on the generation of splenic T cells capable of adoptively immunizing normal recipients against a Listeria challenge infection. Ampicillin given at the time of maximum bacterial growth at 24 hr caused a striking reduction in the number of protective T cells produced at the time of peak response on day 6. Although the greatest effect was caused by giving ampicillin early in infection, a significant reduction in peak T cell production occurred even when Ampicillin was given as late as day 5. On the other hand, the effect of abridging infection at the onset of decay of the anti-Listeria response was to cause protective T cells to be lost from the spleen at a much faster rate. These results clearly show that regardless of any immunoregulatory mechanism involved, the duration of generation, and the onset and duration of decay of the anti-Listeria response are determined by the number of replicating Listeria in the tissues. Moreover, Ampicillin-induced abridgement of infection, either before or at the time of peak primary response, resulted in the expression of greatly reduced levels of immunologic memory at a later time. This indicates that memory cells are generated throughout the entire course of the primary anti-Listeria response, including the period of its decay.
Mechanism of action of macrophage-derived suppressor factor produced by soluble immune response suppressor-treated macrophages.
Authors: Aune T M , Pierce C W 
Published: December 2022

Abstract
After a 2-hr incubation with soluble immune response suppressor (SIRS), a product of concanavalin A-activated murine T cells, macrophages release a factor, M phi-derived suppressor factor (M phi-SF), which nonspecifically suppresses immune responses in vitro. The mechanism(s) of action of M phi-SF and range of cell types affected by M phi-SF have been investigated. M phi-SF suppressed antibody responses to background levels if added at culture initiation and by 80 to 90% if added as late as 2 hr before assay. Primary and secondary IgM and IgG antibody responses, proliferative responses to T cell and B cell mitogens, antibody and protein secretion, and the division of several tumor cell lines in culture were inhibited by M phi-SF. Division of synchronized tumor cells was inhibited when M phi-SF was added at any point prior to and during mitosis; this inhibition could be reversed with 2-mercaptoethanol. In the presence of M phi-SF, asynchronous tumor cells accumulated in the cell cycle just prior to cell division and could be released into mitosis by 2-mercaptoethanol. These data indicate that M phi-SF inhibits cell division by causing a block at or in mitosis and suggest that M phi-SF may be a general inhibitor of cellular proliferation and possibly of protein secretion.
Activation of murine macrophages. I. Different pattern of activation by poly I:C than by lymphokine or LPS.
Authors: Taramelli D , Varesio L 
Published: December 2022

Abstract
The ability of poly I:C to activate mouse macrophages (M phi) to become tumoricidal was evaluated and compared with the ability of 2 other agents, lipopolysaccharide (LPS) and M phi-activating factor (MAF), to induce a tumoricidal state. All these agents were able to stimulate proteose-peptone-elicited M phi to kill RL male 1 tumor cells in an 18-hr 51Cr release cytotoxicity assay. High levels of cytotoxicity were obtained with concentrations as low as 1 microgram/ml of LPS or poly I:C and with 1/81 dilution of MAF. However, in the presence of reagents shown to contain less than 0.01 ng/ml of LPS by the LAL assay (LPS free), we found that poly I:C induced strong reactivity, whereas MAF was ineffective. The addition of 10 ng/ml of LPS during the stimulation period did not enhance the cytotoxicity induced by poly I:C, but it did restore MAF-induced, M phi-mediated cytotoxicity. In addition, poly I:C induced strong tumoricidal activity in resident M phi and in peritoneal exudate cells from the genetically defective C3H/HeJ mice that normally do not respond to LPS and MAF treatment. Therefore, it seems that although LPS is required as a second signal for MAF-induced cytotoxicity, such a second signal is not required for poly I:C-induced cytotoxicity. From the above results, it appears that poly I:C is a more powerful activating agent than LPS and MAF and either activates M phi via a different pathway or is effective on subpopulations of M phi that are not activated by the other agents.
"Mature" thymocytes are not glucocorticoid-resistant in vitro.
Authors: Triglia D , Rothenberg E 
Published: December 2022

Abstract
Dexamethasone, administered in vitro either continuously or for a 30-min pulse period followed by a chase of 18 to 24 hr, is shown to decrease protein synthetic rates as well as cellular viabilities in a dose-dependent manner in murine thymocytes. Differential effects on cortical and medullary thymocyte subpopulations should be detectable by alterations in the rates of synthesis of specific molecules which are stable in vitro, relative to total protein synthesis, in the absence of steroids. However, terminal deoxynucleotidyl transferase (TdT), a marker for cortical cells, and Qa-1 and H-2, preferentially expressed in medullary cells, continue to be produced as constant fractions of total synthesis even after treatment with up to 10(-6) M dexamethasone. Furthermore, thymocytes obtained from normal and in vivo cortisone-treated mice show little, if any, difference in their intrinsic sensitivities to dexamethasone in vitro. The results reported here suggest that a corticoresistant thymocyte per se does not exist in vitro and that the thymus may produce factor(S) in vivo that protect the medullary subpopulation from in vivo glucocorticoid-induced lysis.
Suppressive effects of cyclosporin A on the induction of alloreactivity in vitro and in vivo.
Authors: Wang B S , Heacock E H , Collins K H , Hutchinson I F , Tilney N L , Mannick J A 
Published: December 2022

Abstract
The purpose of the present study was the investigation of the effect of cyclosporin A (CsA) on the induction of alloreactivity in vitro and in vivo. Addition of CsA to mouse mixed lymphocyte cultures (MLC) not only inhibited lymphocyte proliferation but also prevented the generation of alloreactive cytolytic lymphocytes (CL). It was necessary to add CsA within the first 3 days of a 5-day MLC in order to achieve a significant suppressive effect. Lymphocytes, after being cultured in MLC with CsA for 4 days or longer, were incapable of being activated upon re-exposure to the same alloantigens although their responses to unrelated antigens remained intact, indicating antigen specificity of the suppression induced by CsA and its long-lasting effect. Furthermore, lymphocytes from mice treated with CsA after allosensitization failed to manifest primary cytotoxicity and could not be reactivated in a secondary MLC. Finally, CsA had no effect on those CL already generated, suggesting that CsA acts upon the induction of CL rather than the effector phase.