A soluble form of the adhesion receptor CD58 (LFA-3) is present in human body fluids

The human adhesion receptor CD58 (LFA-3) is expressed on most human cell types. Here we report on a soluble form of CD58 (sCD58) in human serum, human urine, and culture supernatants of several cell lines. sCD58 partially purified from human serum, from supernatant of the Hodgkin cell line L428, and purified sCD58 from human urine were found to have a molecular mass of 40-70 kDa under denaturating conditions (sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blotting). However, gel filtration of sCD58 purified from human urine gave a molecular mass of 118-166 kDa, suggesting a noncovalent homotrimer conformation or its association with other molecules. Using an enzyme-linked immunosorbent assay specific for CD58 we found that sera from patients suffering from different forms of hepatitis contained elevated sCD58 levels (n = 108). Accordingly, there was a fivefold increase of supernatant sCD58 when the hepatocellular carcinoma cell line Hep G2 was incubated with 25 ng/ml recombinant tumor necrosis factor-α in vitro. In contrast, sCD58 serum levels of 337 additional patients suffering from various other immunological disorders were not found to be raised. At high concentrations sCD58 binds to CD2-positive cells and inhibits rosette formation of human T cells to human erythrocytes. Thus, local release of large quantities of naturally occurring sCD58 may interfere with intercellular adhesion in vivo.     

Soluble CD8 in patients with rheumatic diseases.

An ELISA was used to measure soluble CD8 (sCD8) in the sera and synovial fluids (SF) of patients with rheumatic diseases. Patients with rheumatoid arthritis (RA) had raised levels of sCD8 both in their sera and in their SF compared with patients with osteoarthritis and age-matched healthy controls. In individual RA patients, serial serum sCD8 levels initially fell and then rose preceding clinical improvement. In four patients where serum sCD8 levels rose and clinical improvement occurred, subsequent spontaneous decreases of serum sCD8 level preceded increased clinical disease activity by up to 2 weeks. In general, RA SF mononuclear cells (SFMNC) spontaneously produced high levels of sCD8. In contrast, autologous peripheral blood MNC only produced comparable levels after mitogenic stimulation. Incubation of SFMNC with increasing concentrations of human recombinant tumour necrosis factor alpha resulted in a dose-dependent potentiation of sCD8 release into the supernatant. There was an inverse relationship between the ability of SFMNC to release sCD8 and soluble interleukin-2 receptor, indicating that the CD8+ T cell population may play an important immunoregulatory role in RA.     

Levels of the soluble forms of CD80, CD86, and CD83 are elevated in the synovial fluid of rheumatoid arthritis patients

The release of soluble forms of CD80 (sCD80), CD86 (sCD86), and CD83 (sCD83) provide a potentially powerful immunoregulatory mechanism. We therefore investigated the potential presence and relative levels of these molecules in the synovial fluid (SF) and serum of patients with rheumatoid arthritis (RA) and osteoarthritis (OA). Serum and SF levels were measured by enzyme-linked immunosorbent assay. Serum levels of sCD80, sCD86, and sCD83 in RA and OA patients were similar to those present in normal donor serum (NDS) and the SF of OA patients. In contrast, when compared with NDS and OA SF levels, almost all RA SF samples had elevated sCD83 levels (32/35, >0.63 ng/ml) and a substantial proportion had elevated sCD80 (13/29, >0.22 ng/ml) or sCD86 (16/33, >2.31 ng/ml) levels. Analysis of matched pairs of serum and SF from RA patients demonstrated that the SF/serum ratio for sCD80 (95% CI = 1.7-3), sCD86 (95% CI = 1.5-3.1), and sCD83 (95% CI = 3.6-7.8) levels was >1 in almost all patients. In conclusion, this study shows that the SF from almost all RA patients contain elevated levels of sCD83 and the majority of these samples also contain elevated levels of sCD80 and/or sCD86. These molecules may play a role in modulating immune responses within the rheumatoid joint.     

Soluble CD4 in patients with rheumatoid arthritis and osteoarthritis

An ELISA was used to measure the soluble form of the leukocyte surface antigen CD4 (sCD4) in the sera and synovial fluids (SF) of patients with rheumatic diseases. Patients with rheumatoid arthritis (RA) had raised levels of sCD4 in both their sera and synovial fluid compared to age-matched healthy controls. In patients with osteoarthritis levels of sCD4 in SF and sera were lower than in RA but higher than in sera of healthy individuals. Mononuclear cells from the synovial fluid of RA patients were found to produce spontaneously high levels of sCD4, but autologous blood cells only produced comparable levels after in vitro stimulation with mitogenic lectin. In individual RA patients with active disease, serial sCD4 levels fell preceding clinical improvement. In three patients where serum sCD4 levels fell and clinical improvement occurred, subsequent small increases in serum sCD4 preceded increased clinical disease activity by up to 5 days. Synovial fluid levels of sCD4 correlated positively with soluble interleukin 2 receptor levels but no correlation was found with sCD8 levels. We conclude that the release of sCD4 reflects the involvement of T helper cells and macrophages in the pathogenesis of joint inflammation, especially in RA.     

Increased synovial fluid levels of soluble CD23 are associated with an erosive status in rheumatoid arthritis (RA)

Synovial fluid (SF) levels of soluble CD23 (sCD23) were determined in 96 patients presenting with an inflammatory knee effusion (73 with RA and 23 with reactive arthritis (ReA) serving as a control inflammatory non-erosive group) and were correlated with the degree of joint destruction, with local immune parameters (IL-1beta, IL-3, IL-4, IL-6, IL-8, IL-10, IL-12 and sCD25) and with serum markers of inflammation, C-reactive protein and erythrocyte sedimentation rate. RA patients, classified as erosive or not according to Larsen's grade, were separated as follows: (i) 13 patients with non-erosive RA; (ii) 16 RA patients with erosions in hands but not in knees, matched for disease duration with the first group; (iii) 44 RA patients with hand and knee erosions, matched with the second group for rheumatoid factor positivity but of longer disease duration. SF sCD23 levels were significantly increased in both erosive RA groups compared with non-erosive diseases, whether RA or ReA (P < 0.05), whose SF levels were not different. SF IL-10 showed a similar profile to that of SF sCD23 and was the only other parameter characteristic of erosive RA, but no direct correlation was found between the two. SF sCD23 was significantly correlated with IL-12 (r = 0.65, P = 0.0001) and sCD25 (r = 0.39, P = 0.0019) exclusively in the two erosive RA populations. In conclusion, these data showing that increased levels of sCD23 are not only found in the SF of erosive joints but also in knee SF of patients with erosive RA but without knee x-ray-diagnosed erosions suggest that this parameter might be of predictive value for joint destruction. Longitudinal studies are however needed to confirm its potential clinical interest.     

Changes in Soluble CD4 and CD8 Proteins in Healthy Pregnant and Postpartum Women

PROBLEM: We examined physiological changes in serum levels of soluble CD4 (sCD4) and soluble CD8 (sCD8) during pregnancy and 1–12 months postpartum to study changes in the maternal immune system during and after pregnancy. METHOD: The serum concentrations of sCD4 and sCD8 were measured by enzyme immunoassay in the sera separated from blood samples withdrawn from healthy women in the 1st, 2nd, and 3rd trimesters of pregnancy and 1,4,7, and 10–12 months postpartum (n=182) and healthy non-pregnant women (n=25), and in 90 of the women, the changes in sCD4 and sCD8 were compared with changes in the number of peripheral CD4⁺ and CD8⁺ cells measured by flow cytometry. RESULTS: The serum concentration of sCD4 decreased throughout pregnancy, from the first trimester, and recovered gradually after delivery. The serum concentration of sCD8 did not change significantly during or after pregnancy compared to the concentration in the nonpregnant controls, but the concentration 1 month postpartum was significantly higher than that in the 3rd trimester. The numbers of CD4⁺ and CD8⁺ cells decreased during pregnancy but did not change significantly after delivery. Interestingly, the ratio of the serum sCD4 level to the number of CD4⁺ cells decreased and the ratio of the sCD8 level to the number of CD8⁺ cells increased in the first and second trimesters of pregnancy, but these ratios were within the normal range from the third trimester of pregnancy to 10–12 months postpartum. CONCLUSIONS: Decreases in serum sCD4 concentration and in the ratio sCD4/CD4⁺ cells, and an increase in the ratio sCD8/CD8⁺ cells may be important factors in the immunological changes that occur during pregnancy.     

高盐高脂摄入致大鼠主动脉重构及辛伐他汀的阻断作用

目的: 探讨高钠盐与高脂肪喂养后大鼠血压、血脂变化、主动脉构型改变和辛伐他汀的干预作用及机制。方法: 60只成年雄性SD大鼠,随机分为5组(n=12):对照组(N组)、高盐组(S组)、高脂组(F组)、高盐高脂组(SF组)和高盐高脂加辛伐他汀组(T组)。喂养16周后,测量大鼠动脉压、血清甘油三酯(TG)、总胆固醇(TC)及可溶性CD40L(sCD40L)浓度;免疫组化法检测升主动脉根部血管壁组织CD40/CD40L表达;HE染色测量升主动脉起始段中膜层厚度和动脉内腔面积与血管腔横断面积比值。结果: (1) S组、F组和SF组收缩压与N组相比均明显增高(P<0.01),而T组与N组比增高但程度较SF组明显降低(P<0.05) ;(2)F组和SF组血清TG和TC明显升高,与N组和T组比较明显升高(P<0.001),而S组、N组和T组之间无明显差异;(3)S组、F组和SF组血清sCD40L浓度均高于N组和T组(P<0.05),SF组高于S组和F组(P<0.05),S组与F组、N组与T组间无明显差异;(4)S组、F组和SF组动脉组织CD40/CD40L表达强度高于N组和T组(P<0.05),且SF组高于S组和F组(P<0.05),S组与F组、N组、T组间无明显差异;(5)S组、F组与SF组动脉中膜厚度与N组比较明显增厚(P<0.01);T组与N组比无显著差异;S组、F组和SF组血管内腔面积/血管横断面积比(LA/TVA)与N组比较明显变小(P<0.05);T组与N组比较无显著差别。结论: 高盐高脂喂养可导致大鼠血压升高和诱发动脉粥样硬化,以及血清sCD40L浓度升高、动脉组织CD40/CD40L表达强度增高;复合刺激改变明显强于单一因素作用。他汀类药物可通过抑制血清sCD40L及动脉组织CD40/CD40L表达途径保护血管。     

The NH2-terminal domain of rat CD2 binds rat CD48 with a low affinity and binding does not require glycosylation of CD2

CD2, CD48 and CD58 are structurally similar cell adhesion-molecules forming a subset of the immunoglobulin superfamily (IgSF). In humans CD58 is a ligand for CD2 while in mice CD2 binds CD48. We constructed a soluble chimeric molecule comprising the extracellular portion of rat CD48 and domains 3 and 4 of rat CD4 (sCD48-CD4) and used it to examine whether CD2 is a ligand for CD48 in rats. sCD48-CD4-coated polystyrene Dynabeads? formed rosettes on rat CD2-transfected COS-7 cells, and this rosetting was blocked by anti-CD2 (OX34) and anti-CD48 (OX45) monoclonal antibodies. We used sucrose-gradient ultracentri-fugation to show that sCD48-CD4 binds, in solution, to soluble forms of rat CD2 including the single NH₂-terminal IgSF domain of rat CD2 expressed in bacteria. The upper limit of the affinity of the rat CD48-CD2 interaction is 4 × 10⁵ M^?1, lower than the published affinity of human CD2 for CD58. These results show that rat CD48 binds CD2 on its NH₂-terminal IgSF domain with a low affinity and that binding is independent of glycosylation.     

Association of CD28 IVS3 +17T/C polymorphism with soluble CD28 in rheumatoid arthritis

Objective: Rheumatoid arthritis (RA) is an autoimmune disease of unknown etiology in which inflammatory pathology involves T cell activation and the CD28 costimulatory molecule involved in T cell presentation. The gene includes the CD28 IVS3 +17T/C polymorphism that could be associated with susceptibility to RA whereas the soluble concentrations of CD28 (sCD28) could be related to clinical activity. Methods: We investigated the CD28 IVS3 +17T/C polymorphism in 200 RA patients and 200 healthy subjects (HS). Furthermore, we quantified the sCD28 concentrations in 77 samples of each group. We applied indexes focused to determine the activity and disability (DAS28 and Spanish HAQ-DI, respectively) in RA patients. Methods: We investigated the CD28 IVS3 +17T/C polymorphism in 200 RA patients and 200 healthy subjects (HS). Furthermore, we quantified the sCD28 concentrations in 77 samples of each group. We applied indexes focused to determine the activity and disability (DAS28 and Spanish HAQ-DI, respectively) in RA patients. Results: RA patients had significantly higher frequencies of the CD28 T allele compared to HS (p = 0.032 OR = 1.59, C.I. 1.02–2.49). In addition, the IVS3 +17 T/T genotype frequency was also increased in RA vs. HS (p = 0.026). The RA patients showed higher sCD28 serum levels than HS (p = 0.001). Carriers of the T/T genotype in RA patients showed higher sCD28 levels than C/C carriers (p = 0.047). In addition, a correlation between sCD28 and Spanish HAQ-DI (correlation, 0.272; p = 0.016), was found. Conclusion: The T allele in CD28 IVS3 +17T/C polymorphism is associated with a susceptibility to RA in Western Mexico. In addition, increased sCD28 levels are related to T/T genotype in RA patients.     

Urinary excretion of CD23 antigen in normal individuals and patients with chronic lymphocytic leukaemia (CLL)

A soluble form of CD23 (sCD23) was found in the urine from 12 normal individuals but was not present in 20 normal sera, suggesting that sCD23 produced by cells in tissues is eliminated in the urine. The sCD23 from urine differed in physicochemical properties from the sCD23 found in supernates from B-lymphoblastoid cell lines (B-LCL) and in the sera of patients with B type chronic lymphocytic leukaemia (B-CLL). On SDS-PAGE analysis under reducing conditions urinary sCD23 showed two bands corresponding to molecular weights of 45-60 kD and 28-35 kD indicating that sCD23 may be excreted in combination with another molecule. When subjected to gel filtration in its native state, sCD23 from urine showed a major peak at approximately 150 kD and a minor peak (probably a breakdown product) at 21 kD. Urinary sCD23 was more strongly held by DEAE-cellulose and required 0.5 M buffer pH 8.0 for elution, suggesting that it is more anionic than sCD23 from culture supernates. Five MoAbs recognizing different epitopes on sCD23 from B-LCL supernates were tested on urinary sCD23. Four of the MoAbs were reactive but one (EBVCS-1) was not. Urinary sCD23 did not bind to IgE. The level of sCD23 found in normal urine (approximately 0.02-0.05 micrograms/ml) was exceeded in 17 of 24 cases of B-CLL. In one case with a high cell count and a serum concentration of 10 micrograms/ml, the urine contained 80 micrograms/ml sCD23. In another case a high serum sCD23 was not matched by a high urinary level. In this case the gel filtration pattern was closer to that found with urine sCD23 rather than the B-LCL pattern found with sera of other B-CLL patients.     

Elevated serum levels of soluble CD30 in patients with atopic dermatitis (AD)

The immunopathology of AD is still unclear, but evidence for an immune response polarized towards Th2 activity has been provided. The CD30 molecule belongs to the tumour necrosis factor (TNF) receptor family and is expressed on activated T cells with a sustained expression in Th2 cells. This molecule also exists in a soluble form (sCD30). Elevated serum levels of sCD30 have been found in patients with Hodgkin's disease, chronic hepatitis B infection and HIV infection. Studies were undertaken to compare the serum levels of sCD30 in patients with AD (n=49) and healthy non-atopic controls (n=94). The presence of sCD30 was analysed with ELISA. A significantly higher concentration of sCD30 was noted in AD patients, median sCD30 level 29 U/ml (range 1–708 U/ml), compared with healthy non-atopic controls (P< 0.001), where the median level was 11 U/ml with a range of 1–1042 U/ml. No correlation was found between sCD30 levels and total serum IgE, or between the AD patients' SCORAD values and concentration of sCD30. sCD30 levels were also analysed in 20 AD patients, which during ketoconazole treatment had improved their clinical scores and reduced their serum IgE and eosinophil cationic protein levels. However, no significant decrease in sCD30 levels was noted after treatment. The results show that patients with AD have elevated levels of sCD30, but without correlation to total serum IgE or disease activity.     

Increased Levels of Soluble CD14 in Sera of Periodontitis Patients

Soluble CD14 (sCD14) mediates the response to lipopolysaccharide (LPS) in cells lacking membrane-bound CD14. We determined sCD14 concentrations in the sera of 38 periodontitis patients and 25 healthy controls by enzyme-linked immunosorbent assay. The sCD14 levels in the sera of patients with periodontitis were significantly higher than those of healthy subjects and decreased after treatment. Enhanced levels of sCD14 in serum may contribute to the host response to LPS in periodontitis. Furthermore, we showed in vitro that addition of LPS enhanced the release of sCD14 by monoblastic U937 cells treated with 1α,25-dihydroxyvitamin D₃. Thus, increased sCD14 levels in periodontitis patients may be due to chronic exposure to LPS.     

Elevated levels of soluble CD14 in serum of patients with systemic lupus erythematosus.

A soluble form of CD14 (sCD14) was assessed with an ELISA assay in the serum of the following three clinical groups: 35 patients with an inactive phase of systemic lupus erythematosus (SLE), 17 patients with SLE relapses, and 65 normal healthy volunteers. Increased levels of sCD14 were observed in all patients suffering from SLE compared with normal controls. In addition, patients with active SLE revealed higher serum concentrations of sCD14 (median 6.9 mg/l) than patients under remission (4.1 mg/l; P < 0.0001). Serum values of sCD14 correlated neither with the number of peripheral blood monocytes bearing the CD14 membrane antigen, nor with serum concentrations of IL-1 beta. Serum sCD14 was compared with other clinical parameters used to monitor the clinical course of patients with SLE, among them complement C3, anti-dsDNA antibodies and soluble IL-2 receptor (sIL-2R). A good correlation emerged between sCD14 and C3 as well as sIL-2R concentrations, but sCD14 and anti-dsDNA titres disclosed no significant correlation in both groups of patients with SLE. Serial studies in patients with severe SLE showed that serum sCD14 closely parallels the clinical course as defined by an activity score. Our data suggest that serum sCD14 represents a promising parameter to monitor disease activity in patients with SLE.     

Association of CD14 promoter polymorphisms and soluble CD14 levels in mite allergen sensitization of children in Taiwan

CD14 is responsible for environmental lipopolysaccharide recognition and is a positional candidate gene for allergy. We hypothesized that genetic polymorphisms in the promoter region of the CD14 gene may be associated with Dermatophagoides pteronysinnus (Der p) allergen sensitization in children. Three single nucleotide polymorphisms (SNPs) of the CD14 promoter region, C(–159)T, A(–1,145)G, and G(–1,359)T were genotyped, and analyzed in 240 randomized case–control school-age children in Taiwan. Serum concentrations of IgE and soluble CD14 (sCD14) were also assayed. We found a significant inverse correlation of sCD14 and total serum IgE levels in our study population. Moreover, sCD14 binds Der p allergen in vitro in a dose-dependent manner. The distribution of three SNPs genotypes was similar in asthmatic children and the control group. However, there was a significant difference in the distribution of genotype CD14 G(–1,359)T, but not C(–159)T, between mite-sensitive and non-sensitive children. Haplotype analysis showed strong linkage disequilibrium among these three SNPs in the CD14 promoter region. Carriers of the CD14–159C/–1,145A/–1,359T haplotype had the highest IgE and lowest sCD14 levels as compared to other haplotypes. Our results support the hypothesis that CD14 gene variants may play an important role in influencing allergen sensitization of children in Taiwan.     

Expression of CD5 and CD72 on T and B cell subsets in rheumatoid arthritis and Sjögren's syndrome.

A minority of B cells express the CD5 marker, which is found on virtually all T cells, and CD72 has been defined as the CD5 ligand on the B cell membrane. The mean fluorescence intensity (MFI) of the CD5 molecules was shown to be higher on CD4+CD29+ than CD4+CD45RA+ in peripheral blood (PB) and synovial fluid (SF) of rheumatoid arthritis (RA) patients (P < 0.0001 and < 0.001), and PB of Sjögren's syndrome (SS) patients and normal controls (P < 0.02 and < 0.03). This MFI declined once the CD4 expressed HLA-DR in PB of SS patients (P < 0.004) and normal controls (P < 0.02) or CD25 in PB of RA (P < 0.004) and SS patients (P < 0.0004). There was a correlation between the CD5 MFI on CD4+CD45RA+ and CD4+CD29+ in RA (P < 0.001) as well as SS (P < 0.0007) PB. The CD72 MFI was impressively higher on CD5+ than CD5- B cells in PB and SF of RA patients (P < 0.0001 and P < 0.005) and PB of SS patients (P < 0.005) and normal controls (P < 0.005). Our data suggest that, in association with CD4CD29, CD5 is involved in CD5+B/CD5+ B cell interactions in non-organ-specific autoimmune diseases.     

Elevated levels of soluble CD40 ligand (sCD40L) in serum of patients with systemic autoimmune diseases

The CD40–CD40L costimulatory pathway is involved in the evolution of many autoimmune diseases including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and Sjögren's syndrome (SS). Increased levels of sCD40L in the serum have been associated with disease activity in SLE. The aim of this study was to investigate the role of sCD40L in the development of lupus nephritis and examine its possible association with cryoglobulinemia in Sjögren's syndrome. We used a 2-site sandwich ELISA to measure the levels of sCD40L in sera, from 64 patients with SLE, RA and SS and 17 healthy blood donors. Biological specimens from the affected tissues such as urine from patients with lupus nephritis and saliva from patients with SS were also tested. In this regard, paired sera and first morning urine samples from 6 SLE patients (3 with active lupus nephritis and 3 with inactive lupus nephritis) were tested with the sCD40L ELISA protocol as well as paired sera and salivary samples from 5 patients with SS and cryoglobulinemia, 5 patients with SS and anti-Ro or anti-La autoantibodies and 5 age-matched healthy control donors. We also examined possible correlations of sCD40L levels with several laboratory and clinical parameters in SS and SLE. We found that sera from SLE and SS patients had significantly higher levels of sCD40L compared to sera from healthy control donors. No sCD40L was detected, in urine samples of patients with either active or inactive nephritis and in salivary samples from SS patients or normal subjects. Soluble CD40L is elevated in sera of SS and SLE patients but further investigation is needed to determine its possible role in SLE nephritis and Sjögren's syndrome.     

Soluble CD14 Activates Monocytic Cells Independently of Lipopolysaccharide

The glycoprotein CD14 acts as a receptor for lipopolysaccharide (LPS), either when anchored in the myeloid cell membrane (mCD14) or as a soluble molecule (sCD14) in serum. sCD14-LPS complexes activate cells devoid of mCD14. However, the role of sCD14 independent of LPS is unknown. Therefore, the effect of sCD14 on monocyte functions was investigated in the monocytic cell lines THP1 and Mono Mac 6 and in fresh human monocytes. Under serum-free conditions, endotoxin-free human recombinant sCD14_1–348 (rsCD14_1–348) induced tumor necrosis factor alpha (TNF-α). The TNF-α effect was stronger in THP1 cells than in Mono Mac 6 cells or monocytes. It was dose dependent, with a maximum at 1 μg/ml, and time dependent, with a maximum after 2 h. sCD14 purified from urine had the same cytokine-activating capacity. In contrast, C-terminally truncated rsCD14_1–152 was inactive. The rsCD14 effect was not due to LPS contamination, since it was resistant to polymyxin and lipid IVa but sensitive to heat and trypsin. The rsCD14-induced cytokine induction was blocked by preincubation of rsCD14 with a monoclonal anti-CD14 antibody that did not recognize the LPS-binding site. Release of the TNF-α disappeared upon pretreatment of rsCD14 in 50% plasma or in complete, heat-inactivated or sCD14-depleted serum. Moreover, cytokine production was no longer observed when rsCD14 was pretreated with thrombocytes. The thrombocyte effect was dose and time dependent. In conclusion, sCD14 is able to activate myeloid cells, and the effect is prevented by the presence of plasma, serum, or thrombocytes.     

可溶型猪CD2的分离纯化及其生物化学性质的研究

本文报告可溶型猪E受体的分离纯化及其生物化学性质的研究结果。以羊抗猪CD2的抗体制备亲和层析柱,从猪血清中分离反向玫瑰花实验和免疫双扩散均为阳性的组分后,再经制备SDS—PAGE和电泳洗脱纯化,得到两个猪可溶型CD2(sCD2)分子。其分子量分别为60和29KDa。sCD2在SDS—PAGE和IEF—PAGE 中均呈现单一区带,其等电点分别为6.6和5.5,酶联免疫分析所呈阳性反应。比较研究发现sCD2与膜结合型CD2的生物化学性质不同,前者对一定剂量范围内的ConA 或PHA 诱导的猪外周血淋巴细胞增强具有抑制作用,这种抑制效应具有量效关系,而后者与T 细胞激活有关,文中对两型CD2生物学活性的差别以及sCD2的生物学意义进行了讨论。     

Elevation of soluble CD23 in sera from patients with infectious mononucleosis

CD23 is induced in B cells upon infection by Epstein-Barr virus (EBV) and a soluble form (soluble CD23: sCD23) is found in culture supernatants from EBV-transformed B cell lines. Based on these observations, we measured serum sCD23 levels in patients with infectious mononucleosis (IM) caused by EBV infection. Sera from patients with IM at the time of diagnosis contained more sCD23 than sera from normal control subjects. Changes in serum sCD23 levels during the course of disease showed that serum sCD23 levels were elevated at the time of diagnosis and they decreased to the normal levels during the convalescent phase defined by the improvement of symptoms of IM. These results indicate that the elevated levels of sCD23 were observed at the acute phase of IM and may be useful in diagnosing IM. J. Med. Virol. 53:384–387, 1997. © 1997 Wiley-Liss, Inc.     

Chronic inflammation during osteoarthritis is associated with an increased expression of CD161 during advanced stage

Increasing evidence suggests a role of inflammation during the pathogenesis of osteoarthritis (OA). The local and systemic inflammation was studied in 33 patients of different KL grades, grade2 (n = 11), grade3 (n = 6) and grade4 (n = 16). The levels of cytokines, adipokines and matrix metalloproteinases (MMPs) were measured in serum and synovial fluid (SF) by flow cytometry and ELISA, respectively. The frequency of T cells and CD161 expression was measured by flow cytometry. The levels of IL‐1β, IL‐6 and IL‐10 were significantly higher in sera and SF of patients with OA as compared to healthy control's serum. Higher levels of MMP9 and leptin and lower levels of adiponectin were observed in SF as compared to serum. The MMP9 in SF and MMP13 levels in serum and SF decreased in KL grade 4 cases. In these patients, higher levels of leptin and lower levels of adiponectin were observed in SF versus patients of lower grades. There was increased infiltration of CD8+ T cells in SF of OA cases with decreased frequency in grade 4 cases. The expression of CD161 on T cells was significantly higher in SF than peripheral blood with significant upregulation in grade 4 patients. The CD161 expression had significant positive correlation with IL‐17 in the serum of patients. The ROC curves of CD161 expression significantly distinguished grade 2 and grade 4 patients. Collectively, an elevated CD161 expression on T cells in circulation and synovial compartment clearly distinguished lower and higher grade patients warranting studies to assess its role as a contributing factor towards OA progression.