Phospholipase A2 activating protein and idiopathic inflammatory bowel disease.

BACKGROUND: Crohn's disease and ulcerative colitis are idiopathic inflammatory bowel diseases (IBD) involving synthesis of eicosanoids from arachidonic acid (AA), which is released from membrane phospholipids by phospholipase A2 (PLA2). A potentially important regulator of the production of these mediators is a protein activator of PLA2, referred to as PLA2 activating protein (PLAP). AIMS: The purpose of this investigation was to discover if PLAP values might be increased in the inflamed intestinal tissue of patients with IBD and in intestinal tissue of mice with colitis. PATIENTS: Biopsy specimens were taken from patients with ulcerative colitis and Crohn's disease undergoing diagnostic colonoscopy, and normal colonic mucosa was obtained from patients without IBD after surgical resection. METHODS: Immunocytochemistry with affinity purified antibodies to PLAP synthetic peptides was used to locate PLAP antigen in sections of intestinal biopsy specimens from IBD patients compared with that of normal intestinal tissue. Northern blot analysis with a murine [32P] labelled plap cDNA probe was performed on RNA extracted from the colons of mice fed dextran sulphate sodium (DSS) and cultured HT-29 cells exposed to lipopolysaccharide (LPS). RESULTS: PLAP antigen was localised predominantly within monocytes and granulocytes in intestinal tissue sections from IBD patients, and additional deposition of extracellular PLAP antigen was associated with blood vessels and oedema fluid in the inflamed tissues. In contrast, tissue sections from normal human intestine were devoid of PLAP reactive antigen, except for some weak cytoplasmic reaction of luminal intestinal epithelial cells. Similarly, colonic tissue from DSS treated mice contained an increased amount of PLAP antigen compared with controls. The stroma of the lamina propria of the colonic mucosa from the DSS treated mice reacted intensely with antibodies to PLAP synthetic peptides, while no reaction was observed with control mouse colons. These data were supported by northern analysis which showed that PLAP mRNA was increased in the colons of DSS treated mice and cultured HT-29 cells exposed to LPS. CONCLUSIONS: As PLAP values were increased in the intestinal mucosa of IBD patients and mice with colitis, as well as in LPS treated cultured HT-29 cells, a role was postulated for PLAP in increasing PLA2 activity, which leads to the increased synthesis of eicosanoids in intestinal tissues of patients with these inflammatory diseases.     

Giardiasis in mice: analysis of humoral and cellular immune responses to Giardia muris

Summary Humoral and cellular immune responses have been evaluated in two inbred strains of mice which differ markedly in their susceptibility to infection with Giardia muris. Serum IgG and IgA antibody levels and IgA levels in intestinal washes were determined by a solid-phase radioimmunoassay using G. muris antigen prepared by sonication of trophozoites, while cell-mediated immunity was assessed by a radiometric ear-assay for delayed-type hypersensitivity. Following infection of BALB/c mice (resistant) and C3H/He mice (susceptible), the IgG and IgA antibody levels in serum progressively increased over the period of study with C3H/He mice having significantly higher titres of IgA antibodies than BALB/c late in the infection. Systemic immunization with G. muris trophozoites resulted in high titres of IgG antibodies in the serum. IgA antibodies were detected in intestinal washes 2 weeks after infection with a subsequent fall in levels in BALB/c mice but a progressive increase in levels in C3H/He mice. Prior immunization resulted in IgA antibodies being detected earlier in the intestinal washings after a challenge infection. Delayed-type hypersensitivity to G. muris antigens could not be detected during an infection but a positive response was elicited following antigen priming in mice pretreated with cyclophosphamide. The immune responses evaluated in this study were assessed using a whole G. muris trophozoite sonicate and variations in the quantitative aspects of the responses did not account for observed differences in the course of infection in the two strains of mice.     

Histological response and antigen transmission in the lymph nodes of athymic nu/nu mice inoculated with Crohn's disease tissue filtrates.

Lymph node histology and antigen transmission in the nu/nu mouse in response to animal inoculation with Crohn's disease tissue filtrates were re-evaluated. We found that a hyperplastic lymph node response in nu/nu mice occurred with Crohn's disease (CD), ulcerative colitis (UC), or other intestinal disease (OID) tissue inoculations. In addition, antigen transmission to lymph nodes as detected by indirect immunofluorescence using CD sera was observed in all inoculation groups. The immunofluorescent reaction also occurred independently of lymph node histology. Thus, we confirm that CD sera recognize an antigen(s) expressed in lymph nodes of athymic mice inoculated with CD tissue filtrates. The antibody (or antibodies) in CD sera was not specific for this 'CD antigen or antigens', however, as tested in the nu/nu mouse system, because the CD sera antibodies also recognised antigens in UC inoculated and OID inoculated animals.     

Broadly neutralizing DNA vaccine with specific mutation alters the antigenicity and sugar-binding activities of influenza hemagglutinin

The rapid genetic drift of influenza virus hemagglutinin is an obstacle to vaccine efficacy. Previously, we found that the consensus hemagglutinin DNA vaccine (pCHA5) can only elicit moderate neutralization activities toward the H5N1 clade 2.1 and clade 2.3 viruses. Two approaches were thus taken to improve the protection broadness of CHA5. The first one was to include certain surface amino acids that are characteristic of clade 2.3 viruses to improve the protection profiles. When we immunized mice with CHA5 harboring individual mutations, the antibodies elicited by CHA5 containing P157S elicited higher neutralizing activity against the clade 2.3 viruses. Likewise, the viruses pseudotyped with hemagglutinin containing 157S became more susceptible to neutralization. The second approach was to update the consensus sequence with more recent H5N1 strains, generating a second-generation DNA vaccine pCHA5II. We showed that pCHA5II was able to elicit higher cross-neutralization activities against all H5N1 viruses. Comparison of the neutralization profiles of CHA5 and CHA5II, and the animal challenge studies, revealed that CHA5II induced the broadest protection profile. We concluded that CHA5II combined with electroporation delivery is a promising strategy to induce antibodies with broad cross-reactivities against divergent H5N1 influenza viruses.     

Antibody cross-linking as a factor in immunity to cholera in infant mice.

Several antibody preparations were tested for their ability to reduce adsorption of Vibrio cholerae to isolated intestinal epithelial cells, and this ability was related to agglutination and protective activity in infant mice. The results demonstrate that (1) the reduction in adsorption of V. cholerae to epithelial cells correlates with the degree of agglutination for given antibody preparation; (2) intact tantibodies protect infant mice from cholera only at concentrations that agglutinate the bacteria; and (3) purified antibodies to flagellar antigens protect infant mice from cholera. These results indicate that cross-linking of bacteria by antibody causes a reduction in the number of organisms adsorbed to the intestinal wall. Thus antibody cross-linking plays an important role in immunity to cholera in infant mice.     

空肠弯曲菌galE变异株免疫原性及免疫保护性评价

目的评价galE变异株免疫原性及免疫保护效力。方法分别采用galE变异株低菌量及高菌量单次或重复免疫(口服)BALB/c小鼠,ELISA方法检测动物肠液及血清中特异性sIgA及IgG的滴度。免疫后26d,用大剂量CJ攻击被免疫动物,观察galE变异株的保护效应。结果①低菌量及高菌量galE变异株单次或重复免疫后,动物肠液及血液中sIgA及IgG滴度均明显增高,与阴性对照组比较差异非常显著(P<0.01);未显示低剂量与高剂量之间、单次免疫与重复免疫之间抗体水平有明显差异(P>0.05);与亲代株免疫组比较,抗体水平也无明显不同(P>0.05)。②galE变异株免疫可明显降低动物受CJ攻击后的疾病指数(P<0.01),变异株的临床保护效率为79.5%～83.1%;清除CJ肠定植的能力明显高于阴性对照组(P<0.05);低菌量与高菌量之间,单次及重复免疫清除肠道感染效力无明显差异(P>0.05)。结论①galE变异株保留与亲代株相似的免疫原性及免疫保护性,可刺激动物产生特异性抗体,有效保护细菌攻击,明显降低动物疾病指数,缩短细菌肠道定植时间。②galE变异株仅小剂量单次口服即可产生良好的免疫效果。     

日本血吸虫24—26kDa抗原和重组Sj26抗原的...

This paper reports on the comparison of the recombinant Sj26 (rSj26) antigen originated from the Philippine strain and 24-26 kDa antigen isolated and purified from Chinese mainland strain of S. japonicum for their antigenicity and immunogenicity. The results showed that there were obvious cross reactions between rSj26 and 24-26 kDa antigen when rSj26 antigen was tested against specific antibodies in sera from mice infected with the mainland strain of S. japonicum or 24-26 kDa antigen was tested against specific anti-rSj26 antibodies by ELISA, IFA and Western blotting etc. Both of 24-26 kDa and rSj26 antigen had weak cross reaction with SEA antigen. The worm reduction rate after challenging with mainland strain cercariae in mice immunized with rSj26 was 26-32%, similar to that in mice immunized with 24-26 kDa antigen. It is suggested that rSj26 antigen can induce certain level of specific protective immunity to protect the host against infection by Chinese strain of S. japonicum cercaciae.     

日本血吸虫24-26kDa抗原和重组Sj26抗原的抗原性和免疫原性比较研究

本文报告从日本血吸虫大陆株成虫抽提的24—26kDa抗原与源于日本血吸虫菲律宾株的重组Sj26抗原之间在抗原性和免疫原性上所进行的一系列比较研究。ELISA、IFA和Westernblotting等方法观察结果均表明,24—26kDa和rSj26抗原免疫后所诱导的特异性抗体与其对应的抗原之间具有明显的抗原交叉反应,而与其它血吸虫抗原如可溶性虫卵抗原也有交叉反应。若以两种抗原加福氏佐剂分别免疫小鼠,以日本血吸虫大陆株尾蚴攻击感染,减虫率相似(26～32％),表明两种抗原存在一定程度的交叉免疫保护性。这些研究结果为开发rSj26抗原,或是根据已知Sj26 cDNA核苷酸序列制备DNA探针,从已构建的日本血吸虫(大陆株)cDNA库筛选相关目的基因,加速血吸虫疫苗的研制起着重要作用。     

Seropositivity in Dutch Crohn's disease patients against primed nude mouse lymph nodes, and the difference with lymphocytotoxic antibodies.

Sera from patients with Crohn's disease have been reported to show positive immunofluorescence with lymph nodes of nude mice primed with a filtrate of intestinal tissue affected with Crohn's disease. An indirect immunofluorescence assay was used to test sera of 63 unrelated patients with Crohn's disease, 21 with ulcerative colitis and 36 control subjects against lymph nodes of athymic nude (nu/nu) mice which had been injected with Crohn's disease and ulcerative colitis intestinal tissue filtrates. Forty nine per cent of Crohn's disease patients, 10% of ulcerative colitis patients and 3% of control sera reacted against lymph nodes of mice injected injected with ulcerative colitis intestinal tissue filtrates, 18% of Crohn's disease sera were with intestinal tissue homogenate from Dutch Crohn's patients. With the lymph nodes of mice injected with ulcerative colitis intestinal tissue filtrates, 18% of Crohn's disease sera were positive, whereas all ulcerative colitis and control sera were negative. Lymph nodes from 18 of the 19 mice injected with Crohn's disease tissue filtrates reacted with Crohn's disease sera, whereas only three of these 19 mice reacted with ulcerative colitis sera. A comparative study, carried out in parallel with Crohn's disease filtrate induced hyperplastic lymph nodes from the Bilthoven colony (W2) and from the New York colony (E671) using sera from 54 Crohn's disease patients from Leiden, showed immunoreactivity with 44 and 57% of the Crohn's disease sera against the two hyperplastic lymph nodes. Thirty six of the 54 Crohn's disease sera (67%) reacted with either or both lymph nodes. Only 11% of the Crohn's disease sera which were examined for immunofluorescence and lymphocytotoxic antibodies had lymphocytotoxic antibodies, whereas 40% and 46% of the same sera showed positive immunofluorescence against E671 and W2, respectively. Absorption studies indicated that lymphocytotoxic antibodies activity and the immunofluorescence against the primed nude mouse lymph node are mediated by different serum antibodies in Crohn's disease. The reproducibility of the nude mouse immunofluorescence test system for a preferential immunoreactivity of Crohn's disease sera against Crohn's disease tissue primed murine lymph nodes has been confirmed by the present study. Further studies are necessary to find out whether crossreactive antigen(s) as recognised by some of the Crohn's disease sera in mice injected with ulcerative colitis tissue filtrate is similar to the antigen(s) detected by Crohn's disease sera in mice injected with Crohn's disease tissue filtrates.     

抗大肠杆菌O157∶H7鸡卵黄抗体的制备及其被动保护作用的研究

目的　制备鸡蛋卵黄免疫球蛋白IgG抗体 (YolkImmunoglobulin ,IgY) ,研究其对肠出血性大肠杆菌 (EHEL)O15 7∶H7的被动保护作用。方法　采用EHECO15 7∶H7933菌株制备抗原 ,免疫SPF莱杭鸡 ,用脱脂和盐析的方法 ,从其所产鸡蛋中提取IgY抗体 ,用所得抗体对乳鼠进行动物毒性试验及动物被动保护实验。结果　用酶联免疫吸附试验 (ELISA)检测提取IgY抗体滴度达到 1∶2 0 0 0 0 0以上 ,SDS -聚丙烯酰胺凝胶电泳 (SDS -PAGE)检测所提取抗体纯度及回收率较高。未发现IgY抗体对动物的毒性作用 ,被动保护实验结果表明 ,IgY抗体对乳鼠感染模型具有明显的保护作用。 结论　 (1)通过常规免疫技术 ,可使SPF鸡产生高效价的IgY抗体。 (2 )脱脂和盐析是一种简便有效的IgY抗体制备方法。 (3)建立了EHECO15 7∶H7的乳鼠肠道感染模型。 (4)IgY抗体是治疗肠道感染的一种有潜力的口服药物     

Antibody responses to heat-killed, phenol preserved parenteral typhoid vaccine

The heat-killed, phenolized parenteral typhoid vaccine was tested in informed volunteers. Assessment for its immunogenicity was performed using Widal test and enzyme-linked immunosorbent assay (ELISA). The anti-H antibody, which is a marker of the vaccine antigenicity peaked at one month after the vaccination and appeared throughout the one year course of the study. The anti-O antibody peaked at 7th day after vaccination and lasted only for 6 months. Classes of specific antibodies were determined by ELISA using single extracted lipopolysaccharide from Salmonella typhi 0901 as antigen. The possible protective role of serum derived intestinal IgG and IgA were discussed. Based on the agglutinating antibodies, the results indicate that the heat-killed, phenolized typhoid vaccine conferred at least 6 months protective period.     

Nutrition, immunity and helminth infection: effect of dietary protein on the dynamics of the primary antibody response to Trichuris muris (Nematoda) in CBA/Ca mice

The effect of dietary protein on the specific antibody responses (total immunoglobulins, IgG1 and IgA) to the intestinal nematode Trichuris muris was studied in CBA/Ca mice fed isocaloric diets containing 16% or 4% protein. Mice fed the 16% diet and given a high infection dose of 650 eggs expelled almost their entire primary infection by day 21 post infection. In similarly infected animals fed the 4% protein diet, there was prolonged survival of adult worms. At a low infection dose of 10 eggs, there was no evidence of an expulsion response in either dietary group. The primary antibody response to parasite excretory/secretory (E/S) antigen was time-dependent, regardless of dietary protein or infection dose, and was predominantly an IgG1 response. Within each dietary group, antibody production and antigen recognition occurred earlier and the antibody responses were more intense in mice given the higher infection dose. The principal finding was that the specific antibody response was more vigorous, both quantitatively (serum titres) and qualitatively (antigen recognition by IgG1), in mice on a low protein diet, even though worm expulsion did not occur in these hosts. This result suggests that serum antibody level or antigen recognition is not related simply to protective immunity against T. muris in CBA/Ca mice.     

弓形虫GJS株表面抗原1基因的原核细胞表达及其抗原性分析

目的构建弓形虫GJS株表面抗原1（SAG1）重组表达质粒,研究SAG1蛋白疫苗诱导的保护性免疫作用。方法根据RH株弓形虫SAG1基因序列设计1对引物,利用PCR方法获得SAG1基因,克隆入pMD18-T载体,测序后进行序列分析;重新设计引物将其亚克隆至原核表达载体pET-30a中,在大肠杆菌中经IPTG诱导表达;重组抗原经纯化和复性后免疫小鼠,ELISA法测定其抗体滴度的变化,并用弓形虫速殖子攻击检测免疫保护力。结果与已知的SAG1基因核苷酸序列（$76248）及其编码氯基酸序列的同源性分别为99％、97％;表达的SAG1蛋白以包涵体形式存在,该重组抗原能被羊抗弓形虫阳性血清所识别;经间接ELISA检测,小鼠免疫后产生了较高的抗体;动物保护性实验表明,虽然与对照组相比免疫组小鼠存活时间有一定的延长,但差异无显著性。结论成功构建了弓形虫SAG1重组表达质粒,SAG1蛋白疫苗诱导小鼠的免疫保护力不强。     

The influence of salicyl-azo-sulfapyridine on the immune response to antigenic tumour cells inoculated into the coecal lumen of C3H mice.

Pretreatment of C3H mice with salicyl-azo-sulfapyridine (SASP) was found to increase the susceptibility of the intestine to malignant ascites cells inoculated into the coecal lumen. The response to intestinal immunization was radically changed by prior treatment of mice with SASP. In non-treated animals protection against a subsequent graft followed the intracoecal inoculation of ascites tumour cells. By prior treatment of the mice with SASP the protective immune response was suppressed and some of the treated animals showed enhanced tumour growth of the challenging graft. The immunological enhancement induced in SASP-treated animals was transferable by spleen cells to untreated mice. In sera from SASP-treated and intestinally immunized animals were found factors which in a competitive manner interfered with the binding of antibodies to antigenic sites on the tumour cell membrane. It is proposed that treatment with SASP modifies the intestinal immunity by suppressing antibody production and increasing production of antigen-specific factors lacking some of the immunoglobulin determinants.     

旋毛虫排泄分泌抗原对小鼠的保护性免疫

目的比较旋毛虫成虫排泄分泌抗原(ES抗原)、肌幼虫ES抗原、成虫和肌幼虫ES混合抗原对小鼠的免疫保护作用。方法用生理盐水培养法从培养液中提取成虫ES抗原、肌幼虫ES抗原,分别用成虫ES抗原、肌幼虫ES抗原、成虫和肌幼虫ES混合抗原免疫小鼠,同时设佐剂组和对照组,间隔7d共免疫3次。末次免疫后7天,每只小鼠用200条旋毛虫感染期幼虫经口进行攻击感染。感染后7天和30天检查各组小鼠肠道成虫数和肌幼虫数。结果旋毛虫成虫ES抗原组、肌幼虫ES抗原组、成虫和肌幼虫ES混合抗原组的成虫减虫率分别为87.95%、69.48%、84.34%,肌幼虫减虫率分别为74.79%、87.97%、86.87%。成虫ES抗原组、成虫与肌幼虫ES抗原混合组的成虫减虫率均高于肌幼虫ES抗原组(P均<0.05)。肌幼虫ES抗原组、成虫与肌幼虫ES抗原混合组的肌幼虫减虫率均高于成虫ES抗原组(P均<0.01)。结论旋毛虫成虫和肌幼虫ES混合抗原均能诱导小鼠产生抗成虫及肌幼虫较强的免疫力。     

Monoclonal antibodies specific for the outer surface protein A (OspA) of Borrelia burgdorferi prevent Lyme borreliosis in severe combined immunodeficiency (scid) mice.

We have recently shown that viable Borrelia burgdorferi organisms induce a chronic infection associated with arthritis and carditis in severe combined immunodeficiency (scid) mice but not in immunocompetent mice. The disease is similar to that found in patients suffering from Lyme disease. We now show that B. burgdorferi-specific immune mouse sera as well as a monoclonal antibody to the spirochetal outer surface antigen A (31 kDa) but not monoclonal antibodies specific for the 41-kDa antigenic component of the periplasmic flagella are able to prevent (or mitigate) the development of the disease in scid mice when passively transferred at the time of the bacterial inoculation. The identification of a B. burgdorferi-associated protective antigen suggests that the corresponding spirochetal protein should be tested as a vaccine against Lyme disease.     

A Schistosoma mansoni epitope recognized by a protective monoclonal antibody is identical to the stage-specific embryonic antigen 1.

In infections with the parasitic trematode Schistosoma mansoni, a component of the host defense is directed against the invading larval form, and carbohydrates on the surface of these larvae are targets for the immune attack during the early stages of infection. To identify such carbohydrate epitopes, which may be suitable for immunization against schistosomiasis, we have previously generated monoclonal antibodies to surface antigens; some of these confer protection to naive mice when passively administered. Here we show that one of the protective antibodies recognizes a determinant present in both the parasite and its mammalian hosts. The immunohistochemical distribution of this determinant in the head of embryonic mice was found to be identical to the stage-specific embryonic antigen 1 (SSEA-1), an epitope abundant in pre-implantation embryos, several adult tissues, and malignant tumors. Oligosaccharides containing the SSEA-1 trisaccharide Gal beta 1-4(Fuc alpha 1-3)GlcNAc inhibit antibody binding to parasite antigen. SSEA-1 antibodies generated from mice immunized with rodent neural antigens bind to the surface of the schistosome larvae and mediate antibody-dependent cellular cytotoxicity. SSEA-1 antibodies are also elicited during human schistosomiasis infection, and this autoantibody response may be involved in the development of the natural immunity against the parasite.     

Characterization of a 35-kDa carbohydrate larval antigen (CarLA) from Trichostrongylus colubriformis; a potential target for host immunity

In an accompanying paper we show that antibodies in intestinal mucus that recognize a 35-kDa antigen from the surface of the L3 stage of the sheep intestinal nematode parasite, Trichostrongylus colubriformis, are strongly associated with immune rejection of L3 in a truncated infection model of immunity in sheep. Monoclonal antibody PAB-1 was used to immunopurify this antigen from T. colubriformis L3. The antigen is resistant to digestion with a range of proteases including proteinase K and does not stain on gels or blots treated with protein-detecting reagents but does stain with carbohydrate-detecting reagents. The antigen is also resistant to degradation by the action of lipases and is not soluble in organic solvents, suggesting that lipid components are not present or not accessible. Treatment with glycosidases does not affect the antigen, indicating either that sialic acid and N-linked or O-linked sugars are not present or that they are not accessible to enzyme attack. The antigen is not destroyed by harsh alkaline degradation with up to 8 m NaOH with or without borohydride reducing agent, or by extensive hydrazinolysis. Strong acid hydrolysis with trifluoroacetic acid or boiling in hydrochloric acid for 20 min does destroy the antigen. The antigen migrates as a poorly defined high molecular weight complex on native electrophoresis gels, but is detected as a major band at 35 kDa on SDS PAGE either by carbohydrate staining or by immunoblotting with antibody from immune sheep intestinal mucus and with mAb PAB-1. Proteinase K digestion and alkaline degradation of extracts from L3 of 10 other parasitic nematode species revealed that L3 of each species contained a carbohydrate staining molecule which can be detected by mAb PAB-1 and by mucus antibody from immune sheep. Because antibodies in intestinal mucus are directed against these antigens and may be responsible for protective immunity, carbohydrate larval antigens (CarLA) could represent a new family of molecules with potential as targets for stimulating host immunity.     

Monoclonal IgG can ameliorate immune thrombocytopenia in a murine model of ITP: an alternative to IVIG

Intravenous immunoglobulin (IVIG) is used to treat immune thrombocytopenia resulting from a variety of autoimmune and nonautoimmune diseases such as idiopathic thrombocytopenic purpura (ITP), heparin-induced thrombocytopenia, and posttransfusion purpura. IVIG is a limited resource and although considered safe, may nevertheless carry some risk of transferring disease. Its high cost makes monoclonal antibodies, capable of mimicking the clinical effects of IVIG, highly desirable. We show here, using a murine model of ITP, that selected monoclonal antibodies can protect against thrombocytopenia. SCID mice were pretreated with 1 of 21 monoclonal antibodies before induction of thrombocytopenia by antiplatelet antibody. Four antibodies reacted with the CD24 antigen on erythrocytes. Two antibodies were of the IgM class, and although one IgM antibody caused a minimal degree of anemia (P <.05), neither antibody ameliorated immune thrombocytopenia. One of 2 anti-CD24 antibodies of the IgG class ameliorated immune thrombocytopenia and blocked reticuloendothelial system function at the same doses that protected against thrombocytopenia. Some antibodies reactive with other circulating cell types also protected against immune-mediated thrombocytopenia while no antibody without a distinct target antigen in the mice was protective. Protective monoclonal antibodies significantly prevented thrombocytopenia at down to a 1000-fold lower dose (200 microg/kg) as compared with standard IVIG treatment (2 g/kg). It is concluded that monoclonal IgG with specificity for a circulating cellular target antigen may provide an alternative therapeutic approach to treating immune thrombocytopenia.     

Protection against infection with Vibrio cholerae by passive transfer of monoclonal antibodies to outer membrane antigens

Ten monoclonal antibodies (MAbs), produced by hybridomas obtained through the cell fusion of mouse myeloma cells and spleen cells from mice immunized with outer membrane antigens of Vibrio cholerae, were mixed with suspensions of V. cholerae and administered orally to infant rabbits. Six of these MAbs, each one recognizing a different outer membrane antigen, did not confer protection from fatal V. cholerae infection. Four MAbs that reacted with the 18-kDa antigen, also called the cholera protective antigen, were highly protective against infection with V. cholerae.