Human vascular endothelial cell adhesion receptors for Plasmodium falciparum-infected erythrocytes: roles for endothelial leukocyte adhesion molecule 1 and vascular cell adhesion molecule 1

The clinical complications associated with severe and cerebral malaria occur as a result of the intravascular mechanical obstruction of erythrocytes infected with the asexual stages of the parasite, Plasmodium falciparum. We now report that a primary P. falciparum-infected erythrocyte (parasitized red blood cell [PRBC]) isolate from a patient with severe complicated malaria binds to cytokine-induced human vascular endothelial cells, and that this adhesion is in part mediated by endothelial leukocyte adhesion molecule 1 (ELAM-1) and vascular cell adhesion molecule 1 (VCAM-1). PRBC binding to tumor necrosis factor alpha (TNF-alpha)-activated human vascular endothelial cells is partially inhibited by antibodies to ELAM-1 and ICAM-1 and the inhibitory effects of these antibodies is additive. PRBCs selected in vitro by sequential panning on purified adhesion molecules bind concurrently to recombinant soluble ELAM-1 and VCAM-1, and to two previously identified endothelial cell receptors for PRBCs, ICAM-1, and CD36. Post-mortem brain tissue from patients who died from cerebral malaria expressed multiple cell adhesion molecules including ELAM-1 and VCAM-1 on cerebral microvascular endothelium not expressed in brains of individuals who died from other causes. These results ascribe novel pathological functions for both ELAM-1 and VCAM-1 and may help delineate alternative adhesion pathways PRBCs use to modify malaria pathology.     

大鼠骨髓间充质干细胞血管细胞黏附分子1及细胞间黏附分子1的表达(英文)

背景:骨髓间充质干细胞系统性输注后,何种因素促使其迁移到正确部位尤为关键,目前认为黏附分子在介导骨髓间充质干细胞向缺血或损伤组织迁移过程中起重要作用.目的:观察血管细胞黏附分子1与细胞间黏附分子1在大鼠骨髓间充质干细胞中的表达.方法:采用直接贴壁法体外分离培养大鼠骨髓间充质干细胞,免疫细胞化学染色检测血管细胞黏附分子1及细胞间黏附分子1蛋白的表达,应用免疫荧光直标法在流式细胞仪上检测血管细胞黏附分子1及细胞间黏附分子1抗原的表达率,RT-PCR半定量分析血管细胞黏附分子1及细胞间黏附分子1 mRNA的表达.结果与结论:免疫细胞化学染色结果显示,骨髓间充质干细胞血管细胞黏附分子1呈弱阳性表达,细胞间黏附分子1呈强阳性表达.流式细胞仪检测结果显示,血管细胞黏附分子1表达率为6%,细胞间黏附分子1表达率为100%.RT-PCR检测结果显示,血管细胞黏附分子1 mRNA呈微弱表达,细胞间黏附分子1 mRNA呈高度表达.提示在生理状态下,体外培养的大鼠骨髓间充质干细胞低表达血管细胞黏附分子1,高表达细胞间黏附分子1.     

Modulation of soluble phases of endothelial/leukocyte adhesion molecule 1, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1 with interleukin-1beta after experimental endotoxic challenge

OBJECTIVE: To evaluate the effect of treatment with interleukin 1beta (IL-1beta) on the concentrations of soluble adhesion molecules after an endotoxic challenge. DESIGN: Randomized, controlled study. SETTING: Experimental Unit, Virgen de las Nieves University Hospital. SUBJECTS: Seventy-two female CBA/H mice of 20 to 21 g, supplied by the animal center of the Experimental Unit. INTERVENTION: The mice were randomized into three groups of 24. Group 1 (sham) received two intraperitoneal (ip) doses of 0.1 mL of phosphate-buffered saline; group 2 (lipopolysaccharide) was injected with 125 mg/kg lipopolysaccharide (Escherichia coli) (i.p.) 24 hrs after 0.1 mL of phosphate-buffered saline; group 3 was pretreated with 80 ng (i.p.) of IL-1beta per mouse 24 hrs before the endotoxic challenge. MEASUREMENTS AND MAIN RESULTS: At 1, 2, 4, and 24 hrs after the endotoxic challenge, the concentrations of soluble endothelial/leukocyte adhesion molecule 1 (ELAM-1), intercellular adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1) were measured in the three groups. There was a significant increase (p <.01) in these concentrations at these times in comparison with the sham group. The use of IL-1beta produced a significant decrease (p <.05) in the three molecules among the treated group versus the group submitted only to the challenge; concentrations of ELAM-1 significantly decreased to below those of the sham group, and those of VCAM-1 reduced to levels that did not significantly differ from those of the sham group. CONCLUSION: Endotoxin administration significantly increases the concentrations of soluble ELAM-1, ICAM-1, and VCAM-1 in mice. Treatment with IL-1beta significantly decreases these concentrations, probably attenuating cell injury and organ dysfunction.     

粘附分子和白介素8在早期急性呼吸窘迫综合征中的作用研究

目的 :探讨急性失血致低血容量性休克后低剂量内毒素动物模型中血浆白介素 8(IL 8)、细胞间粘附分子 1(ICAM 1)、血管内皮粘附分子 1(VCAM 1)水平的改变及其与血浆 IL 1β水平的关系。方法 :2 2只新西兰白兔随机分成 4组 :1低血容量性休克组 (休克组 ,6只 ) :急性失血持续 1小时 ,以心排血量低于基础值 40 %为准 ,休克恢复 6 0分钟后再观察 4小时 ;2内毒素 (L PS)组 (6只 ) :以 1.0 0～ 1.2 5μg/ kg L PS静注 ;3休克 L PS组 (6只 ) :低血容量性休克恢复 6 0分钟后再静注低剂量 L PS;4正常对照组 (4只 )。分别在休克前、休克 6 0分钟、休克恢复 6 0分钟、静注 L PS2和 4小时 5个点抽血测 IL 8、IL 1β、ICAM 1和 VCAM 1水平。结果 :休克 L PS组血浆 VCAM 1水平于注射 L PS4小时后显著高于正常对照组 (P<0 .0 5 ) ;血浆ICAM 1水平于注射内毒素第 2和 4小时后亦均高于正常对照组 (P均 <0 .0 5 ) ;休克组、休克 L PS组血浆IL 8浓度在注射 L PS后 2小时均显著高于正常对照组 (P均 <0 .0 5 ) ;休克组和休克 L PS组兔在休克期血浆 IL 1β浓度显著升高 ,而休克 L PS组于静注 1μg/ kg L PS后 2和 4小时 ,血浆 IL 1β浓度再次显著升高。结论 :低血容量性休克后再注射低剂量内毒素可导致血浆 ICAM 1和     

Adhesion of human B cells to follicular dendritic cells involves both the lymphocyte function-associated antigen 1/intercellular adhesion molecule 1 and very late antigen 4/vascular cell adhesion molecule 1 pathways

Presentation of antigen in the form of immune complexes to B lymphocytes by follicular dendritic cells (FDC) is considered to be a central step in the generation of memory B cells. During this process, which takes place in the microenvironment of the germinal center, B cells and FDC are in close physical contact. In the present study, we have explored the molecular basis of FDC-B cell interaction by using FDC and B cells derived from human tonsils. We found that FDC express high levels of the adhesion receptors intercellular adhesion molecule 1 (ICAM-1 [CD54]) and vascular cell adhesion molecule 1 (VCAM-1), while the B lymphocytes express lymphocyte function-associated antigen 1 (LFA-1 [CD11a/18]), very late antigen 4 (VLA-4 [CD49d], and CD44. Furthermore, we established that both the LFA-1/ICAM-1 and VLA-4/VCAM-1 adhesion pathways are involved in FDC-B lymphocyte binding, and therefore, these pathways might be essential in affinity selection of B cells and in the formation of B memory cells.     

Carcinoembryonic antigen-related cell adhesion molecule 1 modulates vascular remodeling in vitro and in vivo

Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1), a cellular adhesion molecule of the Ig superfamily, is associated with early stages of angiogenesis. In vitro, CEACAM1 regulates proliferation, migration, and differentiation of murine endothelial cells. To prove that CEACAM1 is functionally involved in the regulation of vascular remodeling in vivo, we analyzed 2 different genetic models: in Ceacam1-/- mice, the Ceacam1 gene was deleted systemically, and in CEACAM1(endo+) mice, CEACAM1 was overexpressed under the control of the endothelial cell-specific promoter of the Tie2 receptor tyrosine kinase. In Matrigel plug assays, Ceacam1-/- mice failed to establish new capillaries whereas in CEACAM1(endo+) mice the implants were vascularized extensively. After induction of hind limb ischemia by femoral artery ligation, Ceacam1-/- mice showed significantly reduced growth of arterioles and collateral blood flow compared with their WT littermates. In agreement with a causal role of CEACAM1 in vascular remodeling, CEACAM1(endo+) mice exhibited an increase in revascularization and collateral blood flow after arterial occlusion. Our findings indicate that CEACAM1 expression is important for the establishment of newly formed vessels in vivo. Hence CEACAM1 could be a future target for therapeutic manipulation of angiogenesis in disease.     

L-精氨酸对动脉粥样硬化兔可溶性血管细胞黏附分子1表达的影响

目的：观察L-精氨酸对动脉粥样硬化模型兔血中可溶性血管细胞黏附分子1的影响,并探讨血中可溶性血管细胞黏附分子1水平与血管局部血管细胞黏附分子1表达的关系.方法：①实验于2003-9/2004-04在上海市第一人民医院心内科研究室完成.选用健康雄性新西兰大白兔24只,随机分为3组,每组8只：模型组、L-精氨酸组、对照组.②模型组、L-精氨酸组予高脂饮食10 d后,球囊拉伤右髂外动脉.继续喂以高脂饮食30 d后处死动物,L-精氨酸组从术后第2天起经饮水给予L-精氨酸1g/d.对照组以普通饲料喂养.③以双抗体夹心酶联免疫吸附实验检测实验前、术前及术后30 d各组兔血清中可溶性血管细胞黏附分子1水平.组织冰冻切片以原位杂交检测血管细胞黏附分子1 mRNA的表达,抽提蛋白行免疫印迹检测血管细胞黏附分子1蛋白.④计量数据间差异性比较采用t检验.结果：兔24只均进入结果分析.①血管细胞黏附分子1 mRNA表达：血管损伤后30 d,模型组明显增多,L-精氨酸组较轻,对照组阴性.②血管细胞黏附分子1蛋白表达：血管损伤后30 d,模型组明显增多,L-精氨酸组少于模型组,对照组少量.③血清可溶性血管细胞黏附分子1水平：各组3个时间点无差异（P＞0.05）.术后30 d,模型组明显高于术前（P＜0.05）;模型组明显高于对照组及L-精氨酸组（P＜0.01,0.05）,而L-精氨酸组与对照组差异不明显（P＞0.05）.结论：口服L-精氨酸能够降低动脉粥样硬化兔血中可溶性血管细胞黏附分子1水平,血中可溶性血管细胞黏附分子1水平可以反映球囊损伤血管局部的血管细胞黏附分子1变化.     

L-精氨酸对动脉粥样硬化兔可溶性血管细胞黏附分子1表达的影响

目的:观察L-精氨酸对动脉粥样硬化模型兔血中可溶性血管细胞黏附分子1的影响,并探讨血中可溶性血管细胞黏附分子1水平与血管局部血管细胞黏附分子1表达的关系。方法:①实验于2003-9/2004-04在上海市第一人民医院心内科研究室完成。选用健康雄性新西兰大白兔24只,随机分为3组,每组8只:模型组、L-精氨酸组、对照组。②模型组、L-精氨酸组予高脂饮食10d后,球囊拉伤右髂外动脉。继续喂以高脂饮食30d后处死动物,L-精氨酸组从术后第2天起经饮水给予L-精氨酸1g/d。对照组以普通饲料喂养。③以双抗体夹心酶联免疫吸附实验检测实验前、术前及术后30d各组兔血清中可溶性血管细胞黏附分子1水平。组织冰冻切片以原位杂交检测血管细胞黏附分子1mRNA的表达,抽提蛋白行免疫印迹检测血管细胞黏附分子1蛋白。④计量数据间差异性比较采用t检验。结果:兔24只均进入结果分析。①血管细胞黏附分子1mRNA表达:血管损伤后30d,模型组明显增多,L-精氨酸组较轻,对照组阴性。②血管细胞黏附分子1蛋白表达:血管损伤后30d,模型组明显增多,L-精氨酸组少于模型组,对照组少量。③血清可溶性血管细胞黏附分子1水平:各组3个时间点无差异(P>0.05)。术后30d,模型组明显高于术前(P<0.05);模型组明显高于对照组及L-精氨酸组(P<0.01,0.05),而L-精氨酸组与对照组差异不明显(P>0.05)。结论:口服L-精氨酸能够降低动脉粥样硬化兔血中可溶性血管细胞黏附分子1水平,血中可溶性血管细胞黏附分子1水平可以反映球囊损伤血管局部的血管细胞黏附分子1变化。     

癌胚抗原相关黏附分子1与肿瘤

癌胚抗原相关黏附分子1(CEACAM1)又名CD66a或胆汁糖蛋白(BGP),属于免疫球蛋白超家族,广泛表达于内皮细胞、上皮细胞、粒细胞、淋巴细胞和肿瘤细胞。CEACAM1作用广泛,参与细胞间黏附、增殖、迁移、凋亡、血管生成等多种病理生理过程。在肿瘤的发生、发展中也发挥着重要作用,对肿瘤细胞生长、浸润转移、血管生成等均有调节作用。在临床上,CEACAM1有作为一种新的肿瘤标志物的良好潜能,在肿瘤的早期诊断和预后判断方面有着重要作用。本文就CEACAM1与肿瘤的关系特别是其临床应用价值作一综述。     

Role of vascular cell adhesion molecule 1/very late activation antigen 4 and intercellular adhesion molecule 1/lymphocyte function-associated antigen 1 interactions in antigen-induced eosinophil and T cell recruitment into the tissue

To determine the role of vascular cell adhesion molecule 1 (VCAM- 1)/very late activation antigen 4 (VLA-4) and intercellular adhesion molecule 1 (ICAM-1)/lymphocyte function-associated antigen 1 (LFA-1) interactions in causing antigen-induced eosinophil and T cell recruitment into the tissue, we studied the effect of the in vivo blocking of VCAM-1, ICAM-1, VLA-4, and LFA-1 by pretreatment with monoclonal antibodies (mAb) to these four adhesion molecules on the eosinophil and T cell infiltration of the trachea induced by antigen inhalation in mice. The in vivo blocking of VCAM-1 and VLA-4, but not of ICAM-1 and LFA-1, prevented antigen-induced eosinophil infiltration into the mouse trachea. On the contrary, the in vivo blocking of VCAM-1 and VLA-4, but not of ICAM-1 and LFA-1, increased blood eosinophil counts after antigen challenge, but did not affect blood eosinophil counts without antigen challenge in sensitized mice. Furthermore, the expression of VCAM-1 but not ICAM-1 was strongly induced on the endothelium of the trachea after antigen challenge. In addition, pretreatment with anti-IL-4 mAb decreased the antigen-induced VCAM-1 expression only by 27% and had no significant effect on antigen-induced eosinophil infiltration into the trachea. The in vivo blocking of VCAM- 1 and VLA-4 inhibited antigen-induced CD4+ and CD8+ T cell infiltration into the trachea more potently than that of ICAM-1 and LFA-1. In contrast, regardless of antigen challenge, the in vivo blocking of LFA- 1, but not of ICAM-1, increased blood lymphocyte counts more than that of VCAM-1 and VLA-4. These results indicate that VCAM-1/VLA-4 interaction plays a predominant role in controlling antigen-induced eosinophil and T cell recruitment into the tissue and that the induction of VCAM-1 expression on the endothelium at the site of allergic inflammation regulates this eosinophil and T cell recruitment.     

Conditional vascular cell adhesion molecule 1 deletion in mice: impaired lymphocyte migration to bone marrow

We generated vascular cell adhesion molecule (VCAM)-1 "knock-in" mice and Cre recombinase transgenic mice to delete the VCAM-1 gene (vcam-1) in whole mice, thereby overcoming the embryonic lethality seen with conventional vcam-1-deficient mice. vcam-1 knock-in mice expressed normal levels of VCAM-1 but showed loss of VCAM-1 on endothelial and hematopoietic cells when interbred with a "TIE2Cre" transgene. Analysis of peripheral blood from conditional vcam-1-deficient mice revealed mild leukocytosis, including elevated immature B cell numbers. Conversely, the bone marrow (BM) had reduced immature B cell numbers, but normal numbers of pro-B cells. vcam-1-deficient mice also had reduced mature IgD+ B and T cells in BM and a greatly reduced capacity to support short-term migration of transferred B cells, CD4+ T cells, CD8+ T cells, and preactivated CD4+ T cells to the BM. Thus, we report an until now unappreciated dominant role for VCAM-1 in lymphocyte homing to BM.     

Neonatally induced inactivation of the vascular cell adhesion molecule 1 gene impairs B cell localization and T cell-dependent humoral immune response

Vascular cellular adhesion molecule (VCAM)-1 is a membrane-bound cellular adhesion molecule that mediates adhesive interactions between hematopoietic progenitor cells and stromal cells in the bone marrow (BM) and between leukocytes and endothelial as well as dendritic cells. Since VCAM-1-deficient mice die embryonically, conditional VCAM-1 mutant mice were generated to analyze the in vivo function of this adhesion molecule. Here we show that interferon-induced Cre-loxP-mediated deletion of the VCAM-1 gene after birth efficiently ablates expression of VCAM-1 in most tissues like, for example, BM, lymphoid organs, and lung, but not in brain. Induced VCAM-1 deficiency leads to a reduction of immature B cells in the BM and to an increase of these cells in peripheral blood but not in lymphoid organs. Mature recirculating B cells are reduced in the BM. In a migration assay, the number of mature B cells that appears in the BM after intravenous injection is decreased. In addition, the humoral immune response to a T cell-dependent antigen is impaired. VCAM-1 serves an important role for B cell localization and the T cell-dependent humoral immune response.     

舒血宁注射液对脑梗死患者血清可溶性血管细胞黏附分子的影响

目的观察舒血宁注射液对脑梗死患者血清可溶性血管细胞黏附分子(sVCAM-1)的影响。方法将71例脑梗死患者随机分为治疗组39例和对照组32例。两组均予常规治疗,治疗组在此基础上加用舒血宁注射液20 ml/次,1次/d,连用14 d。检测治疗前后两组血清sVCAM-1浓度变化及疗效。结果治疗组显效率和总有效率均高于对照组,差异有统计学意义(P<0.01)。血清sVCAM-1的浓度明显低于对照组,差异有统计学意义(P<0.01)。结论早期对脑梗死患者应用银杏叶制剂可减轻缺血脑细胞的损害,有利于病情恢复,其保护机制可能是抑制sVCAM-1的产生,从而阻断白细胞向缺血区的浸润。     

急性髓系白血病细胞血管细胞黏附分子1、CD34和CD117的表达

背景:血管细胞黏附分子1与白血病浸润密切相关,白血病细胞本身是否表达血管细胞黏附分子1,以及与疾病难治是否相关尚无定论。目的:分析血管细胞黏附分子1、CD34、CD117在急性髓系白血病细胞表面的表达,3者之间的相互关系及与难治性急性髓系白血病的相关性。方法:采用流式细胞技术检测16例急性髓系白血病细胞中血管细胞黏附分子1、CD34、CD117的表达,其中难治组6例,非难治组10例;同时以正常骨髓单个核细胞标本作对照。结果与结论:急性髓系白血病细胞CD34、CD117表达高于对照组(P<0.05)。难治组急性髓系白血病细胞CD34表达明显高于非难治组(P<0.05)。难治组与非难治组CD117表达差异无显著性意义(P>0.05)。急性髓系白血病细胞血管细胞黏附分子1表达与对照组比较差异无显著性意义(P>0.05)。难治组与非难治组血管细胞黏附分子1表达差异无显著性意义(P>0.05)。表明急性髓系白血病细胞伴CD34表达,为不良预后指标之一,CD117、血管细胞黏附分子1表达与其是否难治无明显相关性。     

急性髓系白血病细胞血管细胞黏附分子1、CD34和CD117的表达

背景：血管细胞黏附分子1与白血病浸润密切相关,白血病细胞本身是否表达血管细胞黏附分子1,以及与疾病难治是否相关尚无定论。目的：分析血管细胞黏附分子1、CD34、CD117在急性髓系白血病细胞表面的表达,3者之间的相互关系及与难治性急性髓系白血病的相关性。方法：采用流式细胞技术检测16例急性髓系白血病细胞中血管细胞黏附分子1、CD34、CD117的表达,其中难治组6例,非难治组10例;同时以正常骨髓单个核细胞标本作对照。结果与结论：急性髓系白血病细胞CD34、CD117表达高于对照组（P〈0.05）。难治组急性髓系白血病细胞CD34表达明显高于非难治组（P〈0.05）。难治组与非难治组CD117表达差异无显著性意义（P〉0.05）。急性髓系白血病细胞血管细胞黏附分子1表达与对照组比较差异无显著性意义（P〉0.05）。难治组与非难治组血管细胞黏附分子1表达差异无显著性意义（P〉0.05）。表明急性髓系白血病细胞伴CD34表达,为不良预后指标之一,CD117、血管细胞黏附分子1表达与其是否难治无明显相关性。     

人脐静脉内皮细胞黏附分子1表达与活血中药对单核-血管内皮细胞黏附性能的干预

目的:观察活血注射液对氧化型低密度脂蛋白损伤人脐静脉内皮细胞后血管细胞黏附分子1的表达及与人单核细胞黏附的影响,探讨中药复方制剂防治动脉粥样硬化的作用机制。方法:实验于2004-03/12在北京中医药大学东直门医院中医内科学教育部重点实验室完成。①实验材料:活血注射液由丹参、川芎、红花、赤芍组成,比例为丹参2,其余药物为1,含生药2000g/L。新生儿脐带(由中日友好医院妇产科提供,产妇及其家属知情同意,实验符合赫尔辛基宣言中的伦理学标准)。②实验过程:以培养人脐静脉内皮细胞作为靶细胞,在内皮细胞培养基中加入氧化型低密度脂蛋白制备细胞损伤模型。③实验评估:采用蛋白定量法检测人脐静脉内皮细胞与单核细胞的黏附率[将人脐静脉内皮细胞,用M199培养液(对照组)和含不同浓度(10,20,40ml/L)的活血注射液、氧化型低密度脂蛋白等实验因子的培养液(实验组)温育12,24h,再加含单核细胞的M199培养液];反转录聚合酶链反应检测人脐静脉内皮细胞的血管细胞黏附分子1的mRNA表达;用流式细胞仪测定人脐静脉内皮细胞的血管细胞黏附分子1的蛋白表达[(将人脐静脉内皮细胞,分为对照组、氧化型低密度脂蛋白组与氧化型低密度脂蛋白 活血注射液(终浓度分别为10,20,40ml/L)组,分别作用12,24h)。结果:①人单核细胞与人脐静脉内皮细胞的黏附率在氧化型低密度脂蛋白作用12,24h后升高,均明显高于对照组(P<0.01),不同剂量活血注射液可明显抑制人单核细胞与人脐静脉内皮细胞的黏附率,与氧化型低密度脂蛋白组相比差异均有显着性(P<0.01),这种作用随着剂量的增加而增强。②氧化型低密度脂蛋白能明显上调人脐静脉内皮细胞的血管细胞黏附分子1的mRNA和蛋白表达水平,而不同剂量活血注射液能显著下调血管细胞黏附分子1的mRNA和蛋白的表达水平(P<0.05,P<0.01),与氧化型低密度脂蛋白组相比差异均有显着性(P<0.05,P<0.01),这种作用随着剂量的增加而增强。结论:氧化型低密度脂蛋白促进内皮细胞的血管细胞黏附分子1表达,活血注射液能通过下调血管细胞黏附分子1的表达抑制单核-血管内皮细胞黏附,保护人内皮细胞免受氧化型低密度脂蛋白所致毒性损伤,从而减少或抑制动脉粥样硬化的形成。     

Functional studies of truncated soluble intercellular adhesion molecule 1 expressed in Escherichia coli.

We have expressed in Escherichia coli the two N-terminal immunoglobulin (Ig)-like domains of the intercellular adhesion molecule 1 (ICAM-1). The first 188 residues of ICAM-1 were expressed with an N-terminal methionine (MP188) or as a maltose-binding fusion protein which was cleaved with factor Xa (XP188). After refolding, both MP188 and XP188 were active in binding to the leukocyte integrin lymphocyte function-associated antigen 1, which has previously been shown to bind to the N-terminal Ig domain of ICAM-1. The major group of rhinoviruses and malaria-infected erythrocytes bind to distinct sites within the first Ig-like domain of ICAM-1. Both MP188 and XP188 bound to malaria-infected erythrocytes; however, only XP188 inhibited human rhinovirus plaque formation. A product (MdQ1P188) with the initiation methionine fused to residue 2, i.e., with glutamine 1 deleted, inhibited plaque formation. MdQ1P188 was able to induce a conformational change of the virus capsid as shown by conversion of 149S particles to 85S particles, whereas MP188 had no effect. These results show that functionally active fragments of ICAM-1 can be produced in E. coli, that glycosylation is not required for ligand binding, and that the N-terminal residue of ICAM-1 is proximal to or part of the human rhinovirus-binding site.