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Recent double-blind placebo-controlled trials for perennial allergic rhinitis have all clearly shown the efficacy of immunotherapy. Although several mechanisms for the clinical efficacy of immunotherapy have been proposed, the exact mechanisms related to the clinical effect still remain unclear. Since immunotherapy is a form of systemic treatment and its clinical benefit is likely to be, at least in part, a consequence of its systemic effects on different phases of immunological events, our study focused exclusively on several immunological parameters in serum. A total of 47 patients with perennial allergic rhinitis due to Dermatophagoides farinae enrolled in this prospective study. Venous blood was collected for determination of specific immunoglobulin (Ig)E, specific IgG4, soluble interleukin-2 receptor (IL-2R), interleukin-4 (IL-4), soluble intercellular adhesion molecule-1 (ICAM-1) and soluble vascular cell adhesion molecule-1 (VCAM-1), six times from 20 untreated patients and 27 patients on immunotherapy, at enrolment, and 1, 2, 3, 5, and 10 years after enrollment. No specific IgE, IgG4, soluble IL-2R, IL-4 and soluble ICAM-1 levels changed significantly for a span of 10 years in the untreated patients. By contrast, immunotherapy affected serum levels of specific IgE, specific IgG4, soluble IL-2R, IL-4 and soluble ICAM-1, but not of soluble VCAM-1. The rates of increase in specific IgG4 and the rates of decrease in soluble IL-2R were correlated with the rates of decrease in symptom scores during the first 3 years, but not 5 and 10 years after the course of immunotherapy. On the other hand, the rates of decrease in specific IgE, IL-4 and soluble ICAM-1 were significantly correlated with the rates of decrease in symptom scores at 5 and 10 years, but not during the first 3 years. Each immunological modulation by immunotherapy was likely to be involved in the working mechanism related to clinical efficacy at different phases of immunotherapy.
OBJECTIVE: To evaluate longitudinal change in arterial blood plasma levels of soluble adhesion molecules in infants of <30 weeks' gestation with respiratory distress syndrome (RDS) and to look for differences in these levels in neonates who subsequently developed bronchopulmonary dysplasia (BPD) compared with those neonates who did not, and also to investigate the effect of dexamethasone treatment on levels of soluble adhesion molecules in plasma. METHODS: We measured plasma concentrations of soluble L-selectin (sL-selectin), soluble E-selectin (sE-selectin), and soluble intercellular adhesion molecule-1 on days 1, 3, 7, 14, 21, and 28 of life and before and 2 to 3 days after initiating a 6-day course of dexamethasone treatment. Infants with RDS were followed until discharge and were classified as non-BPD and either 1) BPD day 28 reflecting oxygen requirement on day 28 but not at 36 corrected weeks or 2) BPD 36 weeks reflecting oxygen requirement at 36 (corrected) weeks' gestation. The classification of presence or absence of BPD by oxygen requirement was supported by and was consistent with radiologic findings of BPD for all infants. The difference between BPD day 28 and BPD 36 weeks was supported by more extensive radiologic effects in the latter. RESULTS: The arterial plasma level of sL-selectin in infants who had RDS and did not develop BPD was significantly decreased compared with term healthy infants, as was the level of sE-selectin. Compared with infants who had RDS and did not develop BPD, sL-selectin levels were even further decreased in infants who had RDS and did develop BPD both at birth and throughout the first 4 weeks of life (day 1 through day 28). Infants with BPD also showed increasing levels of sE-selectin during this period of time, whereas infants without BPD did not. Levels of soluble intercellular adhesion molecule-1 in infants without BPD were not different from infants with BPD initially but increased in infants with BPD compared with infants without BPD, significant on day 28 in both groups. Dexamethasone treatment increased concentration of sL-selectin and decreased concentration of sE-selectin. CONCLUSIONS: Low sL-selectin may be an early indicator of enhanced risk for BPD. Low levels of sL-selectin and increasing levels of sE-selectin may be risk factors for BPD. The effects of dexamethasone treatment include significant modulation of adhesion molecules.
Circulating HIV P24 antigen, beta 2-microglobulin, neopterin, soluble CD4, soluble CD8, and soluble interleukin-2 receptor were measured in 13 zidovudine-intolerant patients (8 with ARC and 5 with AIDS) treated with dideoxyinosine (ddI). Measurements were made at baseline and at several intervals during therapy. Mean levels of HIV P24 antigen decreased early and significantly (P less than 0.01) after 2 weeks of ddI administration and remained low at weeks 8 and 12. In addition, mean SCD8 levels decreased late and significantly (P less than 0.02) after 16 weeks of ddI treatment and remained low at 24 weeks. In contrast, ddI administration had no substantial effect on mean levels of beta 2-microglobulin, neopterin, soluble CD4, and soluble interleukin-2 receptor. ddI administration appears to have been associated with early reduction of HIV P24 antigen levels and later reduction of SCD8 mean levels in these patients.
Soluble L-selectin, E-selectin and P-selectin were measured in a small case control study of 42 patients with peripheral arterial disease and 42 age and sex matched controls. Levels of soluble L-selectin were 1204 +/- 221 ng/ml (mean +/- S.D.) in the patients compared to 1256 +/- 271 ng/ml in the controls (P = 0.37). There was also no difference in levels of soluble E-selectin (57 +/- 17 ng/ml versus 51 +/- 20 ng/ml, P = 0.15) but levels of soluble P-selectin were increased (249 +/- 101 ng/ml versus 198 +/- 98 ng/ml, P = 0.011). There were no significant correlations between any of the selectins and the risk factors for atherosclerosis or with any leucocyte index. The data point to different mechanisms of release of the soluble selectins in peripheral atherosclerosis and may have important implications for leukocyte/endothelial cell interactions.
Active SLE is characterized by immune deposits and subsequent vascular inflammation in many organs. Expression and up-regulation of adhesion molecules is basic to migration of inflammatory cells into the tissues. Recently, soluble isoforms of these molecules have been described which might be an expression of their up-regulation in the tissues and, as such, of disease activity. The purpose of this study was to evaluate whether changes in levels of soluble adhesion molecules reflect disease activity. We analysed serial sera in a 6-month period preceding 22 consecutive exacerbations of SLE for levels of soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1), and sE-selectin. Levels were related to clinical disease activity (SLEDAI), and levels of anti-dsDNA and complement. At the time of maximal disease activity, levels of sVCAM-1 in patients with SLE were higher than those in controls (P < 0.0001), levels in patients with renal involvement being higher than in those without (P < 0.02). Levels of sVCAM-1 correlated with SLEDAI scores (P < 0.05) and, inversely, with levels of C3 (P = 0.01). In addition, in the presence of anti-dsDNA, levels of sVCAM-1 tended to correlate with levels of these autoantibodies (P < 0.1). Levels of sICAM-1 were normal and sE-selectin levels even decreased compared with controls. Levels of sVCAM-1 were higher at the moment of relapse (P = 0.001) than at 6 months before this time point. This rise correlated with the rise in SLEDAI score (P < 0.02). Levels of sICAM-1 and sE-selectin did not rise, and remained in the normal range in all exacerbations studied. In conclusion, in contrast to sICAM-1 and sE-selectin, levels of sVCAM-1 are increased, rise parallel to disease activity during exacerbations in SLE, and are associated with decreasing levels of complement factors. This favours the hypothesis of immune deposit formation, activation of the complement cascade and activation of endothelial cells. Concurrent up-regulation of vascular adhesion molecules may thus result in transmigration of activated inflammatory cells inducing tissue damage.
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Two proteins which specifically bind tumor necrosis factor (TNF) have recently been isolated from human urine in our laboratory. The two proteins cross-react immunologically with two species of cell surface TNF receptors (TNF-R). Antibodies against one of the two TNF binding proteins (TBPI) were found to have effects characteristic of TNF, including stimulating phosphorylation of specific cellular proteins. Oligonucleotide probes designed on the basis of the NH2-terminal amino acid sequence of TBPI were used to clone the cDNA for the structurally related cell surface type 1 TNF-R. It is notable that although this receptor can signal the phosphorylation of cellular proteins, it appears from its amino acid sequence to be devoid of intrinsic protein kinase activity. The extracellular domain of the receptor is composed of four internal cysteine-rich repeats, homologous to structures repeated four times in the extracellular domains of the nerve growth factor receptor and the B lymphocytes surface antigen CDw40. The amino acid composition and size of the extracellular domain of the type I TNF-R closely resemble those of TBPI. The COOH-terminal amino acid sequence of the four cysteine rich repeats within the extracellular domain of the type I TNF-R matches the COOH-terminal sequence of TBPI. Amino acid sequences in the extracellular domain also fully match other sequences found in TBPI. On the other hand, amino acid sequences in the soluble form of the type II TNF-R (TBPII), while indicating a marked homology of structure, did not suggest any identity between this protein and the extracellular domain of the type I TNF-R. CHO cells transfected with type I TNF-R cDNA produced both cell surface and soluble forms of the receptor. The receptor produced by CHO cells was recognized by several monoclonal antibodies against TBPI, reacting with several distinct epitopes in this molecule. These data suggest that the soluble forms of the TNF-Rs are structurally identical to the extracellular cytokine binding domains of these receptors and are consistent with the notion that the soluble forms are, at least partly, derived from the same transcripts that encode the cell surface receptors.
The reactions of the water-soluble chelating phosphines 1,2-bis(bis(hydroxyalkyl)phosphino)ethane (alkyl = n-propyl, DHPrPE; n-butyl, DHBuPE; n-pentyl, DHPePE) with FeCl(2).4H(2)O and FeSO(4).7H(2)O were studied as routes to water-soluble complexes that will bind small molecules, dinitrogen in particular. The products that form and their stereochemistry depend on the solvent, the counteranion, and the alkyl chain length on the phosphine. In alcoholic solvents, the reaction of FeCl(2).4H(2)O with 2 equiv of DHBuPE or DHPePE gave trans-Fe(L(2))(2)Cl(2). The analogous reactions in water with DHBuPE and DHPePE gave only cis products, and the reaction of FeSO(4).7H(2)O with any of the phosphines gave only cis-Fe(L(2))(2)SO(4). These results are interpreted as follows. The trans stereochemistry of the products from the reactions of FeCl(2).4H(2)O in alcohols is suggested to be the consequence of the trans geometry of the Fe(H(2)O)(4)Cl(2) complex, i.e., substitution of the water molecules by the phosphines retains the geometry of the starting material. The formation of cis-Fe(DHPrPE)(2)Cl(2) is an exception to this result because the coordination of two -OH groups forms two six-membered rings, as shown in the X-ray structure of the molecule. DHBuPE and DHPePE reacted with FeSO(4).7H(2)O in water to initially yield cis-Fe(P(2))(2)SO(4) compounds, but subsequent substitution reactions occurred over several hours to give sequentially trans-Fe(DHBuPE)(2)(H(2)O)(SO(4)) and then trans-[Fe(DHBuPE)(2)(H(2)O)(2)]SO(4). The rate constants and activation reactions for these aquation reactions were determined and are consistent with dissociatively activated mechanisms. The cis- and trans-Fe(L(2))(2)X (X = (Cl)(2) or SO(4)) complexes react with N(2), CO, and CH(3)CN to yield trans complexes with bound N(2), CO, or CH(3)CN. The crystal structures of the cis-Fe(DHPrPE)(2)SO(4), trans-Fe(DHPrPE)(2)(CO)SO(4), trans-Fe(DHBuPE)(2)Cl(2), trans-[Fe(DHBuPE)(2)(CO)(Cl)][B(C(6)H(5))(4)], trans-Fe(DMeOPrPE)(2)Cl(2), trans-Fe(DMeOPrPE)(2)Br(2), and trans-[Fe(DHBuPE)(2)Cl(2)]Cl complexes are reported. As expected from using water-soluble phosphines, the complexes reported herein are water soluble (generally greater than 0.5 M at 23 degrees C).
OBJECTIVE: To measure the concentration of the cytokines interleukin-1beta (IL-1beta), interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-10 (IL-10), and tumour necrosis factor-alpha (TNF-alpha) and the modulators of their function interleukin-1 receptor antagonist (IL-1Ra), interleukin-2 soluble receptor alpha (IL-2 sRalpha), interleukin-6 soluble receptor (IL-6sR) and soluble tumour necrosis factor receptor I (sTNFR-I) in systemic and drained blood for the first six hours after a major orthopaedic operation. DESIGN: Prospective study. SETTING: University hospital, Oslo. PATIENTS: 8 patients operated on for thoracic scoliosis. MAIN OUTCOME MEASURE: Concentrations of IL-1beta, IL-2, IL-6, IL-10, TNF-alpha, IL-1Ra, IL-2 sRalpha , IL-6sR, and sTNFR-I were measured together with haemoglobin (Hb) concentration, white cell count (WCC), and differential count in arterial and drained blood at wound closure and 1, 2, 4, and 6 hours postoperatively. RESULTS: IL-1beta and IL-6 concentrations increased significantly in drained blood, whereas that of TNF-alpha increased only in arterial blood. The modulating factors IL-1Ra, sTNFR-I, and IL-10 were increased both in arterial and drained blood. IL-6sR had decreased slightly at 6 hours in drained blood. No IL-2 was found and IL-2 sRalpha decreased simultaneously with the haemodilution. In arterial blood there was a granulocytosis and in drained blood a relative lymphocytosis. CONCLUSION: Cytokine responses to surgical trauma include modulating factors such as soluble receptors and receptor antagonists that have different responses systemically and locally.
The aim of this prospective, randomized study was to investigate the serum levels of tumor necrosis factor-alpha (TNF-alpha), soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), and soluble interleukin-1 receptor antagonist (sIL-1RA) in patients with thyroid eye disease (TED) before and 1 and 3 months after treatment with somatostatin analogues (SM-a). Thirty patients, all with signs and symptoms of TED, were studied. Twenty-two patients (13 females) had active eye disease with a clinical activity score (CAS) > or = 4 (patients with active disease [PA]) and 8 patients (5 females) had inactive TED with CAS < or = 3 (patients with inactive disease [PI]). All PA patients had a positive orbital octreoscan, whereas PI patients had a negative one. Fifteen patients from the PA group were selected randomly and received SM-a (PA-S subgroup), while the remaining 7 patients were used as control subgroup (PA-C), received neither therapy, nor placebo. From the 15 patients who received SM-a (PA-S), 6 received octreotide (OCT) and 9 lanreotide (LRT). TED was reevaluated using the CAS 1 and 3 months after the initiation of SM-a treatment. Ten healthy individuals (6 females) were used as controls (group C). We found an increase in the basal levels of TNF-alpha (14.2 +/- 7.1 pg/mL), sICAM-1 (809.1 +/- 167.0 ng/mL), and sIL-1RA (542.1 +/- 259.0 pg/mL) in PA patients as a total group compared with the PI (1.6 +/- 1.9, 676.8 +/- 73.4, 267.6 +/- 152.8, respectively) group and C (1.9 +/- 1.4, 598.0 +/- 126.2, 258.6 +/- 155.1, respectively). The basal levels of TNF-alpha (13.3 +/- 8.3 pg/mL) and sIL-1RA (533.7 +/- 308.9 pg/mL) in PA-S as well as in PA-C (16.0 +/- 2.9, 560.2 +/- 107.3, respectively) subgroups were also increased compared with PI patients and C (1.9 +/- 1.4 and 258.6 +/- 155.1, respectively). The same was true for sICAM-1 when baseline levels compared with C (817.1 +/- 187.3 and 791.9 +/- 123.5, respectively vs. 598.0 +/- 126.2 ng/mL). After SM-a, serum levels of sICAM-1 and sVCAM-1 were decreased significantly 1 (781.2 +/- 205.9, 1,193.5 +/- 511.8 ng/mL) and 3 months (786.8 +/- 199.6, 1,122.1 +/- 225.3 ng/mL) after the initiation of treatment. In conclusion, serum levels of TNF-a, sICAM-1, and sIL-1RA were elevated in patients with active TED compared to controls. Furthermore, sICAM-1 and sVICAM-1 levels declined during the treatment with SM-a in patients with active TED.
We have shown that a soluble receptor for vascular endothelial growth factor (sVEGFR), which adsorbs VEGF and may function as a dominant-negative receptor, suppresses tumor angiogenesis and enhances apoptosis of cancer cells, thereby inhibiting tumor growth [Cancer Res 60 (2000) 2169-2177]. In the present study, using as many as 11 cancer cell lines, we tested two hypotheses: (a) that a soluble fibroblast growth factor receptor-1 (sFGFR1) might inhibit tumor angiogenesis and growth in sVEGFR-resistant cancers, and (b) that combining sFGFR1 with sVEGFR might produce an enhanced inhibitory effect. In two cell lines derived from human lung cancer, H460 and A549, both of which produce a considerable amount of FGF-2, sVEGFR and a soluble receptor for angiopoietin-1 were both ineffective; however, sFGFR1 inhibited tumor angiogenesis and growth, demonstrating the critical role that FGFs play in some cancers. In three cell lines (QG56 from lung cancer, T3M4 and Panc1 from pancreatic cancer), which produced both VEGF and FGF-2 at detectable levels, combined sVEGFR and sFGFR1 produced an enhanced inhibitory effect compared to their individual effects. The combined usage of sVEGFR plus sFGFR1 suppressed tumor growth in all cancer cell lines tested, suggesting possible effectiveness of this strategy against a wide range of cancers.
It has been reported that the severe complication of dengue virus infection, dengue hemorrhagic fever (DHF) is much more commonly observed during secondary dengue virus infections than primary infections. In order to elucidate the role of T lymphocytes in the pathogenesis of DHF, we attempted to determine whether T lymphocytes are activated in vivo during dengue virus infections, by examining the levels of soluble IL-2 receptor (sIL-2R), soluble CD4 (sCD4), soluble CD8 (sCD8), interleukin-2 (IL-2) and interferon-gamma (IFN gamma) in the sera of 59 patients with DHF and 41 patients with dengue fever (DF). The levels of sIL-2R, sCD4, sCD8, IL-2, and IFN gamma were significantly higher in the acute sera of patients with DHF than in the sera of healthy children (P less than 0.001 for all markers). The acute sera of patients with DF contained higher levels of sIL-2R, sCD4, IL-2, and IFN gamma than the sera of healthy children (P less than 0.001 for sIL-2R, IL-2, and IFN gamma; P less than 0.05 for sCD4), but did not have elevated levels of sCD8. The levels of sIL-2R (P less than 0.05), sCD4 (P less than 0.001), and sCD8 (P less than 0.001) were higher in DHF than in DF on days 3-4 after the onset of fever. The levels of IL-2 and IFN gamma in patients with DHF were highest 1 d before defervescence. There were no significant differences in the levels of sIL-2R, sCD4, sCD8, IL-2, and IFN gamma among grades 1, 2, and 3 of DHF. These results indicate (a) T lymphocytes are activated and produce IL-2 and IFN gamma in vivo during DHF and DF, (b) CD4+ T lymphocytes are activated in DHF and DF, and the level of activation is higher in DHF than in DF, and (c) activation of CD8+ T lymphocytes is evident in DHF, but not in DF.
Plasma levels of soluble interleukin-2 receptor (sIL-2R), soluble CD8 (sCD8) and soluble intercellular adhesion molecule 1 (sICAM-1) were determined by ELISA assays in about 100 patients with hairy cell leukemia (HCL), acute myelomonocytic leukemia (AMMoL), acute myelocytic leukemia (AML), chronic lymphocytic leukemia (CLL), prolymphocytic leukemia (PLL), acute lymphoblastic leukemia (ALL), adult T-cell leukemia (ATL), and mycosis fungoides (MF). Additionally, cultured AML, ALL, and CLL cells grown with and without 12-0-tetra-decanoyl-phorbol-13-acetate (TPA) were tested for IL-2R (CD25) expression by indirect immunofluorescence. Supernatants of these cultures were also tested for sIL-2R by ELISA. Elevated sIL-2R levels were found in HCL patients at initial diagnosis and relapse, in AMMoL, in AML, in the accelerated and non-accelerated phases of B-CLL, in PLL, in non-T/non-B ALL, in B-ALL in mixed lineage ALL, in T-CLL, in T-ALL, and in active MF. Reduced levels of sIL-2R were encountered in HCL patients in remission, in pre-T-ALL, and in MF patients in remission. Also, in non-accelerated CLL sIL-2R levels were less elevated than in later stages of the disease. In T-CLL, sIL-2R was only slightly elevated. Thus, we believe sIL-2R could prove to be a useful marker of disease stage, subtype, and prognosis in several hematologic malignancies. The cultures with and without TPA suggested that the undetermined source of sIL-2R in HCL, ALL and AML could indeed be the malignant cells but perhaps not so in the case of B-CLL. Plasma sCD8 was found to be below normal control levels in HCL, and lowest in relapsing cases. In addition, sCD8 levels were below normal in pre-T-ALL, and in MF. Levels in the non-accelerated phase of B-CLL approximated those of controls. Elevated levels of sCD8 were observed in AML, AMMoL, accelerated stage B-CLL, PLL, non-T/non-B ALL, B-ALL, mixed lineage ALL, T-ALL, T-CLL, and ATL. Thus, in a few instances, sCD8 may also correlate with disease subtype, as well as stage. Although sICAM-1 levels were elevated in all leukemias, its levels in CLL did not appear to be related to disease activity. Whether this is true or not for other leukemias would require additional work on sICAM-1 levels and its relationship to disease activity and prognosis.
OBJECTIVE: To evaluate the relationship between serum levels of soluble Fas(sFas), soluble Fas li gand(sFasL), soluble IL-2 receptor(sIL-2R) and coronary heart disease (CHD). METHODS: With enzyme-linked immunosorbent assay (ELISA) tests, sFas, sFasL and sIL-2R were measured in the sera from 30 patients with CHD and 26 subjects without CHD as controls. RESTULTS: Mean level of sFas was significantly higher in patients with CHD than in controls [(1 583.41+/-174.46)ng/L compared with (1 374.55+/-142.42)ng/L, P<0.01]. Compared with the controls, the mean level of sIL-2R was significantly higher in patients with CHD [(944.50+/-395.59)ng/L compared with (652.45+/-163.36)ng/L P<0.01]. Moreover, in patients with CHD sFas and sIL-2R were positively correlated (r=0.418 P<0.05). Whereas no such difference was found between both groups in sFasL (P<0.05). CONCLUSION: High levels of serum sFas and sIL-2R were associated with CHD, and elevation of sFas may inhibit apoptosis in activated T cells, leading to coronary events.
We investigated soluble interleukin-2 receptor (sIL-2R), soluble CD8 (sCD8) and soluble intercellular adhesion molecule-1 (sICAM-1) levels in the sera of patients with non-malignant diseases believed to have an autoimmune or immunosuppressive component, Crohn's disease, celiac disease, and systemic lupus erythematosus (SLE). Sera of healthy blood donors served as controls. All samples were analyzed by commercial ELISA kits for sIL-2R, sCD8, and sICAM-1. Our control level of sIL-2R (x +/- S.D) was 395 +/- 84 units/ml, sCD8 (x +/- S.D.) 263 +/- 90 units/ml and sICAM-1 405 +/- 118 ng/ml. The 8 Crohn's disease patients had an average sIL-2R level of 920 +/- 329 units/ml, and an average sCD8 level of 355 +/- 91 units/ml, and sICAM-1 952 +/- 329 ng/ml. The four celiac disease patients had an average sIL-2R concentration of 1740 +/- 1071 units/ml, a sCD8 level of 460 +/- 320 units/ml and sICAM-1 1221 +/- 720 ng/ml. The three systemic lupus erythematosus patients had an average sIL-2R of 1023 +/- 123 units/ml, and an average sCD8 of 395 +/- 69 units/ml, and sICAM-1 1153 +/- 219 ng/ml. Thus, sIL-2R and sICAM-1 were significantly elevated over control levels in all 3 patient groups, and sCD8 was mildly elevated. These results indicate enhanced immune activation which may be a common feature in the onset and/or progression of these idiopathic illnesses.
IL-6 mediates its pleiotropic functions through two membrane proteins, a ligand-binding molecule (IL-6 receptor, IL-6R) and a non-ligand-binding signal transducer (gp130). Starting with a previously isolated cDNA clone encoding human gp130, recombinant soluble gp130 (sgp130) lacking the transmembrane and cytoplasmic regions was expressed in COS7 cells or CHO cells. sgp130 could associate with a complex of IL-6 and soluble IL-6R (sIL-6R), also lacking transmembrane and cytoplasmic regions. This indicated that extracellular region of gp130 was responsible for the association with IL-6R which was occupied by IL-6. An enzyme-linked immunosorbent assay (ELISA) for the quantitation of sgp130 was established, which was based on the interaction of sgp130 with the complex of IL-6 and sIL-6R and could detect sgp130 as low as 1 ng/ml.
The serum levels of soluble interleukin-2 (sIL-2), sIL-2 receptors (sIL-2R), beta 2-microglobulin (beta 2M) and soluble intercellular adhesion molecule-1 (sICAM-1) were measured by the ELISA technique in 129 breast cancer patients and 40 controls. The median serum levels of sIL2-R, beta 2M and sICAM-1 were significantly higher and sIL-2 significantly lower than controls. sIL-2R, sICAM-1 and beta 2M levels were significantly higher in patients with metastatic disease compared to patients on long-term follow-up with no active disease. Initial study measurements of these markers could not identify patients at high risk for relapse. These findings suggest that the sIL-2R level is indicative of metastatic disease and together with other parameters of immune activation may be of help in monitoring disease activity in breast cancer patients.