bluuebunny/crossref_metadata_2025_split huggingface dataset:
Comparison of the T lymphocyte-dependent induction of angiotensin-converting enzyme and leucine aminopeptidase in cultured human monocytes
Authors: ROHRBACH M S , CONRAD A K 
Published: July 2010

SUMMARY
The T lymphocyte-mediated induction of angiotensin-converting enzyme (ACE) in cultured autologous peripheral blood monocytes has been proposed as a model system for the investigation of the in vivo induction of ACE in the monocyte-derived granuloma epithelioid cells of some granulomatous diseases such as sarcoidosis. The studies described here were designed to evaluate the specificity of the model system by comparing the parameters for induction of ACE with those for the induction of another monocyte metallo-ecto-peptidase, leucine aminopeptidase (LAP). The concentration of LAP in freshly isolated monocytes was 009 mU/106 monocytes (s.e.m. 0.04) and increased to a maximal value of 019 mU/106 monocytes (s.e.m. 0.32) after 3 days when monocytes were cultured alone. ACE was not detectable in freshly isolated monocytes. However, after 6 days of culture, monocytes contained 0.22 m U ACE/106 monocytes (s.e.m. 0.04). Comparison of the levels of ACE and LAP induced during culture of monocytes alone indicated that the induction of these two enzymes was correlated. The induction of both enzymes was further enhanced by the presence of T lymphocytes in a dose-dependent manner. At 4 × 106 T lymphocytes per culture, ACE levels increased to 1.81 mU/106 monocytes (s.e.m. 0.24) and LAP levels to 1.03 mU/106 monocytes (s.e.m. 0.35). The enhancement of ACE activity required autologous lymphocytes, while heterologous T lymphocytes were equally effective in inducing LAP. Comparison of the levels of ACE and LAP induced during co-culture of autologous T lymphocytes and monocytes from 21 independent donors, demonstrated no correlation between the induction of ACE and LAP. These data indicate that, although T lymphocytes also enhance the induction of LAP, the underlying mechanism must differ from that of ACE induction.
A role for prostaglandins in the suppression of cutaneous cellular immunity and tumour development in benzo(a)pyrene- but not dimethylbenz(a)anthracene-treated mice
Authors: ANDREWS F J , HALLIDAY G M , MULLER H K 
Published: July 2010

SUMMARYProstaglandins have been implicated in the immune suppression associated with the development of some tumours. Application of the prostaglandin synthetase inhibitor indomethacin, to murinc skin prior to treatment with the chemical carcinogens benzo(a)pyrene (BP) or7, 12 dimethylbenz(a)anthracene (DMBA), restored contact sensitivity responses to2,4-dinitrofluorobenzene in BP- but not DM BA-treated mice. However, indomethacin failed to restore antibody responses in either group of mice. Prolonged treatment with BP or DMBA led to cutaneous tumour formation. Indomethacin was found to delay the onset and reduce the size of tumours in BP- but not DM BA-treated mice. It is proposed that prostaglandin-induced suppression of cellular cutaneous immunity may play a role in BP- but not DMBA-induced cutaneous carcinogenesis.
Identification of autoantigens in canine autoimmune haemolytic anaemia
Authors: BARKERM R N , GRUFFYDD-JONES T J , STOKEST C R , ELSON C J 
Published: July 2010

SUMMARYAutoantigens in canine autoimmune haemolytic anaemia (AIH A) were identified by immunoprecipi-tation using autoantibody eluted from the erythrocytes of affected dogs. At least three patterns of precipitated antigen were identified in six cases of AIH A. The most commonly precipitated antigen pattern was a combination of 42-kD and 29-kD peptides. associated with up to three other membrane components. These autoantigens may be canine glycophorins, which are of similar molecular mass, or may possibly represent an equivalent of the human Rhesus complex. An autoantigen identical in molecular mass to band3, the erythrocyte anion channel protein, was precipitated in one case of AIHA, and unknown peptides of 37 kD and 100 kD were isolated by autoantibody from another dog. In one case, no antigens were precipitated by the eluted antibody, indicating that the autoantibody may have bound a non-protein membrane component such as phospholipid. Overall it is considered that the different patterns observed may reflect differences in the aetiology of the condition. In other studies, sera from dogs with AIHA failed to immunoprecipitate autoantigens, but were shown by immunoblotting to contain autoantibodies to proteins of the erythrocyte cytoskeleton. Such autoantibodies were also demonstrated in normal canine sera and it is suggested that they are unlikely to play a role in the pathogenesis of AIHA, but may be part of a normal clearance mechanism for damaged red blood cells.
Maintained pregnancy levels of oestrogen afford complete protection from post-partum exacerbation of collagen-induced arthritis
Authors: MATTSSON R , MATTSSON A , HOLMDAHL R , WHYTE A , ROOK G A W 
Published: July 2010

SUMMARY
Pregnancy is known to influence the course of rheumatoid arthritis (RA) in women, as well as type II collagen-induced arthritis (CIA) in DBA/1 mice. A characteristic feature is the remission during gestation and the exacerbation of the diseases during the post-partum period. In the case of CIA in DBA/1 mice, two hormonal changes have been assumed to be critical for the induction of the post-partum flare: (i) the fall in steroid hormone levels from those present during pregnancy; and (ii) surges of prolactin (PRL) release at and after delivery. Our results show that treatment with oestradiol during a short period immediately after parturition protects the mouse from a post-partum flare of the disease, and that treatment with bromocriptine, a drug known to inhibit the endogenous PRL release, has a significant though less marked effect. Studies of lactating (i.e. animals with physiological stimulation of endogenous PRL release) and non-lactating arthritic mice revealed no clear-cut differences, indicating that PRL is of minor importance for the induction of the post-partum flare. Some steroids other than oestradiol, which may be implicated in the exacerbation of arthritis, namely progesterone and hydrocortisone, had no clinical effect, Analyses of agalactosyl IgG levels in mice with CIA, and anti-collagen II antibodies in sera collected at the end of the experiments revealed no significant differences between the oestradiol and the control groups. The successful oestradiol treatment of the mice indicates that the drop in endogenous oestradiol levels prior to delivery ends the oestrogen-mediated protection against arthritis during pregnancy.
Induction of anti-mycobacterial and anti-listerial activity of human monocytes requires different activation signals
Authors: ZERLAUTH G , EIBL M M , MANNHALTER J W 
Published: July 2010

SUMMARYThe requirements Tor activation of anti-mycobacterial and anti-listerial activity of human monocytes were investigated, Human monocytes could be activated to display enhanced anti-mycobacterial activity by a 24-h treatment with Hpopolysaccharide, The mediator induced by this treatment was identified as being tumour necrosis factor-alpha (TNF-αAQl), Addition of recombinant TNF-α (rTNF-α) to the cultures of human monocytes for 24 h yielded comparable results (minimal dose required for induction of anti-mycobacterial activity, 10 U/ml) Addition of anti-TNF-α antibody completely abrogated the effect, A similar treatment protocol failed to activate enhanced anti-listerial activity, To trigger anti-listerial activity, sequential treatment of human monocytcs with rTNF-α and IL-2 was required, Treatment of monocytes with 10 U/ml rTNF-α for 24 h followed by incubation in the presence of 200 U/ml of IL-2 for an additional 24 h yielded a reduction of listcrial growth which was moderate but statistically significant (P &lt; 0.00l), The activation of monocylcs observed with rTNF-a/IL-2 treatment was (i) dependent on both cytokincs; (ii) sequence dependent (i,e, when IL-2 was added prior to rTNF-α, no effect was observed); and (iii) absent in cells treated with one cytokine only, Enhancement of anti-listerial activity by sequential use of cytokincs was not accompanied by an increase in oxidativc burst, which indicated that oxidative mechanisms were not the reason for the observed Listeria monocytogenes growth restriction, Further support for this hypothesis was obtained after intcrfcron-gamma treatment of human monocytcs which led to an augmented PMA-inducible release of active oxygen radicals, but was not paralleled by growth restriction of L, monocytogenes, Our results indicate that TNI-α plays a crucial role in the activation of monocylcs for growth restriction of intraccllular microbes, Activation of human monocytcs to restrict the growth of the facultative intracellular bacteria Mycohacterium avium intracellulare and L, monocytogenes, however, follows different patterns, the initial trigger in both cases being provided by TNF-α-indueed signals
Immunological tolerance induced by liver grafting in the rat: splenic macrophages and T cells mediate distinct phases of immunosuppressive activity
Authors: YOSHIMURA S , GOTOH S , KAMADA N 
Published: July 2010

SUMMARYIn the rat combination DA into PVG, liver grafts are not rejected but induce donor-specific transplantation tolerance. We have examined the immunosuppressive properties of spleen cells from PVG recipients of DA liver grafts at various times post-grafting. The results indicate the development of two phases of cell-mediated suppressor activity, which appear to be mediated by separate spleen cell populations. Mitomycin-C-treated spleen cells taken from animals between 5 and 28 days post-grafting were able to suppress rat mixed lymphocyte reactions (MLRs). These ‘early’ suppressor cells were glass adherent and absent from populations purified by passage through nylon wool or G10 Sephadex columns. Suppression of MLR by purified glass adherent cells was not specific for either stimulator or responder haplotypes and was blocked by indomethacin. Nylon wool purified T cells were not suppressive at this time. Spleen cell suppressor activity declined to background levels after 35 days post-grafting. However, spleen cells from long-term surviving liver graft recipients (20 weeks or more) were again able to suppress MLR; the ‘late’ suppressor cells were nylon wool non-adherent and suppression was specific for the donor (DA) MHC type. We conclude that liver grafting in this combination generates early and late phases of suppression among spleen cells, that the early phase is produced by macrophages and mediated by prostaglandins and that the late phase is dependent on allospecific suppressor T cells.
Selective and early increase of IL-1 inhibitors, IL-6 and cortisol after elective surgery
Authors: DI PADOVA F , POZZI C , TONDRE M J , TRITAPEPE R 
Published: July 2010

SUMMARYAfter trauma, inflammatory, immunological and hormonal changes are well documented. Surgical intervention is a form of programmed trauma. Through the study of surgical patients, changes in early endogenous mediators of inflammation, immune response and tissue repair can be investigated. Here we analysed changes in serum levels of IL-1 inhibitors, IL-1β, IL-6, tumour necrosis factor-alpha (TNF-α) and cortisol in patients undergoing elective surgery. C-reactive protein (CRP) was measured as a marker of the acute-phase response. Rises in serum levels of IL-1 inhibitors. IL-6 and cortisol were detected as early as 1 h after the intervention. Peak levels were reached between 2 and 5 h. Serum levels of IL-6 and cortisol remained elevated for several days implying a persistent production. Serum levels of IL-1 and TNF did not change after the intervention. CRP levels peaked on day 2. The communication system sustained by endogenous mediators is activated after surgery as shown by selective changes in IL-1 inhibitors, IL-6 and cortisol. These mediators have different kinetics in serum and IL-6 is not the only early mediator detected. Some IL-1 inhibitors might be involved in the immunological depression observed after major surgery, in the regulation of the inflammatory response or in tissue repair. IL-6 and cortisol seem to act synergistically to activate the acute-phase response. A systemic role for IL-l and TNF is not evident, even if the possibility that these lymphokines may act locally is not ruled out.
Human recombinant erythropoietin directly stimulates B cell immunoglobulin production and proliferation in serum-free medium
Authors: KIMATA H , YOSHIDA A , ISHIOKA C , MASUDA S , SASAKI R , MIKAWA H 
Published: July 2010

SUMMARYThe effect of human recombinant erythropoietin (Epo) on B cell responses was studied in a serum-free medium. Epo enhanced IgM production and thymidine uptake by a human IgM-producing lymphoblasloid cell line, CBL. This effect was specific to Epo since enhancement was blocked by anti-Epo antibody but not by control antibody. Among the various cytokines, interleukin-4 (IL-4) enhanced IgM production and thymidine uptake while IL-6 enhanced IgM production without affecting thymidine uptake. In contrast, other cytokines including IL-1β, IL-2, IL-5, interferon-alpha (IFN-α), interferon-gamma (IFN-γ), or granulocyte/macrophage colony-stimulating factor (GM-CSF) were without effect. However, the enhancing effect of Epo is different from that of IL-4 or IL-6, since Epo effect was not blocked by anti-IL-4 antibody or anti-IL-6 antibody. Moreover, specific binding of Epo was detected on CBL cells. Epo also enhanced immunoglobulin (IgG, IgM and IgA) production and thymidine uptake by purified tonsil small resting B cells stimulated by Staphylococcus aureus Cowan strain I (SAC) or by large activated B cells. In contrast, Epo had no effect on unstimulated smalt resting B cells. These results indicate that Epo could directly stimulate activated and differentiated B cells and could enhance B cell immunoglobulin production and proliferation.
Regulation of human B cell proliferation and differentiation by seminal plasma
Authors: LEE H-K , LEE H-H , PARK Y-M , LEE J-H , HA T-Y 
Published: July 2010

SUMMARYTo investigate the role of seminal plasma in human B cell functions, its effect on the proliferation and antibody secretion of tonsillar B cells and an Epstein -Barr virus (EBV) transformed human B cell line, A4, was examined. Seminal plasma inhibited both the proliferation and differentiation of normal B cells only when added to the cultures at the early period of culture. If addition of seminal plasma was delayed beyond 5 to 6 days, it failed to inhibit IgG secretion. Seminal plasma did not show any inhibitory effect on A4 cells, but rather enhanced both the proliferation and IgG secretion of this B cell line. When the low and high mol. wt fractions of seminal plasma were tested for their biological effects on normal and transformed B cells, the low mol. wt fraction (less than 1 kD) was associated with the inhibitory effect of seminal plasma on normal B cells, whereas high mol. wt fractions (both dialysed and 1500-kD fraction) was involved in the enhancing effect on A4 cells. We conclude that (i) seminal plasma inhibits the early proliferation of normal human B cells, but does not inhibit the antibody-secreting capacity of mature B cells; and (ii) different molecules of seminal plasma act on the different stages of B cell maturation.
Defects in proliferative responses of T cells from patients with common variable immunodeficiency on direct activation of protein kinase C
Authors: NORTH M E , WEBSTER A D B , FARRANT J 
Published: July 2010

SUMMARYDNA synthesis in response to mitogens has been studied in T cells from nine patients with common variable immunodeficiency (CVI) and seven normal individuals. Five out of the nine patients had cells with subnormal responses to the mitogen phytohaemagglutinin (PHA). As PHA-induced responses are largely mediated through activation of Ca2+-dependent protein kinase C, we studied whether the defective response was still present on direct activation of protein kinase C. This was done using combinations of concentrations of phorbol 12,13,-dibutyrate and the calcium ionophore ionomycin which induced proliferation in normal T cells. We found that in CVI patients with T cells which had normal responses to PHA, responses to phorbol ester and ionomycin were at the same level as in normal T cells. However, with this treatment, in which the linkage between the membrane receptor and protein kinase C is bypassed, the level of DNA synthesis was still depressed in the patient group whose T cells had subnormal responses to PHA. IL-2 failed to restore the DNA synthesis to normal levels when added with the phorbol ester and ionomycin to T cells from one patient in this group. These data suggest that in a group of CVI patients there are defects in T cell activation pathways at or down-stream of protein kinase C.
New Zealand black mice are immunologically resistant to high-dose, but not low-doseLeishmania mexicanainfection
Authors: DOREA R C C , ALEXANDER J , GALLAGHER G 
Published: July 2010

SUMMARYThe course of infection following s.c. inoculation of a wide dose range of L. mexicana stationary-phase promastigotes (SPP) was examined in sexually mature and immature NZB mice of both sexes. Infection with a high dose (&gt; 107 SPP) was able to induce a protective in vivo response, which could be adoptively transferred with parasite-immune T cells, into naive, syngeneic recipients. In contrast, s.c. infection with a low dose (&lt; 107 SPP) induced non-healing lesions; disease susceptibility could also be transferred into naive animals with T cells from non-immune donors. When the ability to mount a delayed-type hypersensitivity (DTH) reaction was tested in these two groups, the high-parasite dose group gave a significantly higher response. The in vivo protection and high DTH response were reflected in the ability of cells derived from the high-dose resistant (but not low-dose susceptible) mice to mount an antigen-specific T cell response in vitro. The possible immunological effector mechanisms underlying high-dose resistance and low-dose susceptibility are discussed.
Detection of DNA-bound immunoglobulins in patients with lupus nephritis, using monoclonal anti-DNA antibody
Authors: KOYAMA A , KOBAYASHI M , SUZUKI S , SUZUKI M , YAMAGUCHI N , NARITA M 
Published: July 2010

SUMMARYIn order to investigate the relationship between renal histopathology and the characteristics of circulating immune complexes (CICs) in patients with lupus nephritis (LN), we measured the sizes of CICs, DNA-bound immunoglobulins in patients with systemic lupus erythematosus (SLE) and different histopathological forms of nephritis. Sera were obtained from nine patients: four with diffuse proliferative LN (DPLN), four with membranous LN (MLN), and one with mesangial LN, who fulfilled the criteria of the American Rheumatism Association for SLE. The DNA-bound immunoglobulins were measured by ELISA, in which ELISA plates were coated with mouse monoclonal anti-DNA antibodies. The sizes of CICs were analysed by sucrose density gradient ultracentrifugation. Large (larger than 19S), intermediate (19-7S) and small (nearly 7S) sized DNA-bound immunoglobulins (high peaks of IgG and IgA, but low IgM peaks) were found in the patients with DPLN. By contrast, in patients with MLN, the sizes of ICs; DNA-bound IgG, IgA were in general slightly larger than 7S. In one patient with DPLN, at the onset, various sized DNA-bound IgG, IgA and IgM were found. After the methylprednisolone pulse therapy, CICs became smaller and gradually disappeared. We conclude that the characteristics of DNA-anti-DNA IgG, IgA complexes may determine the localization of ICs in the glomeruli and suggest that CICs play an important role in the pathogenesis of LN.
Serum levels of soluble IL-2 receptor, IL-4 and IgE-binding factors in childhood allergic diseases
Authors: MATSUMOTO T , MIIKE T , YAMAGUCHI K , MURAKAMI M , KAWABE T , YODOI J 
Published: July 2010

SUMMARYThe serum levels of soluble IL-2 receptor (sIL-2R), IL-4 and IgE-binding factors were examined in children with allergic diseases, and compared with those in non-allergic controls of the same age and sex. The results showed age-related decreases in the serum levels of sIL-2R and IgE-binding factors, but not in that of IL-4 in both allergic and non-allergic individuals. Significant elevation of sIL-2R was observed in sera from children with atopic eczema or history of an anaphylactic reaction to food, as compared with that in non-allergic controls. The serum concentration of IL-4 was elevated in all allergic groups, including cases of atopic eczema, bronchial asthma and anaphylaxis to food, compared with non-allergic controls, and was correlated significantly with the serum level of IgE (r= 0.59). The IgE-binding factor levels in sera from patients aged 6-10 years with bronchial asthma, or patients aged 1-5 years with a history of food anaphylaxis were elevated as compared with those in non-allergic controls of same age. There was no significant correlation between the serum levels of IgE-binding factors and IgE. Since sIL-2R is released by activated T cells, the present study is in favour of T cell activation causing allergic skin disorders. The serum levels of IL-4 as well as IgE did not differ among allergic patients of different clinical categories. The role of IgE in atopic eczema and other allergic diseases is not clearly established; however, it seems likely that IL-4 is deeply involved in the increased production of IgE seen in allergic individuals. The possible involvement of IgE-binding factors in the age-related changes of clinical manifestations in childhood allergic diseases was also discussed.
Serum CD14 levels in poly traumatized and severely burned patients
Authors: KRÜGER C , SCHÜTT C , OBERTACKE U , JOKA T , MÜLLER F E , KNÖLLER J , KÖLLER M , KÖNIG W , SCHÖNFELD W 
Published: July 2010

SUMMARYRecently it has been demonstrated that the CD14 molecule which is expressed on monocytes and macrophages serves as a receptor for lipopolysaccharide (LPS) bound to LPS-binding protein (LBP) and thus mediates LPS-induced tumour necrosis factor (TNF) production. Here we report that CD14 is found as a soluble (s) molecule in serum. In healthy volunteers sCD14 levels (mean ± s.e.m.) were 3.7±0.05 μg/ml (n= 30, 25–50 years of age) as determined by ELISA (detection limit 20 μg/ml serum) using two monoclonal antibodies in a sandwich technique. In polytraumatized patients (n= 16) significantly decreased levels (1.7 ± 0.3) were detected immediately after the trauma, which increased to 4.9±0.3 μg/ml within the first 6 days post trauma. sCD14 remained elevated during the first 14 days post trauma in patients with the most severe injuries (injury severity score &gt; 45 points), whereas a return to normal levels was observed in patients with an injury score of &lt; 45 points. In addition, the levels of the high-density lipoproteins that partially inactivate free endotoxin are significantly decreased post trauma. No correlation between parameters of inflammation (C3a and neopterin levels, leucocyte counts, amount of band cells), liver function and sCD14 levels was established. Comparable to polytraumatized patients, increased sCD14 serum levels were observed in five patients with burn trauma (burned area &gt; 35%) within the second week post trauma when clinical signs of septicaemia were evident.