Effect Of Specific Antibodies Research Articles

Immunogenicity studies of proteins forming the T4 phage head surface.

Advances in phage therapy and novel applications of phages in biotechnology encourage interest in phage impact on human and animal immunity. Here we present comparative studies of immunogenic properties of T4 phage head surface proteins gp23*, gp24*, Hoc, and Soc, both as elements of the phage capsid and as isolated agents. Studies comprise evaluation of specific antibodies in the human population, analysis of the proteins' impact on the primary and secondary responses in mice, and the effect of specific antibodies on phage antibacterial activity in vitro and in vivo in mice. In humans, natural antibodies specific to T4-like phages were abundant (81% of investigated sera). Among those, significantly elevated levels of IgG antibodies only against major head protein (gp23*) were found, which probably reflected cross-reactions of T4 with antibodies induced by other T4-like phages. Both IgM and IgG antibodies were induced mostly by gp23* and Hoc, while weak (gp24*) and very weak (Soc) reactivities of other head proteins were noticed. Thus, T4 head proteins that markedly contribute to immunological memory to the phage are highly antigenic outer capsid protein (Hoc) and major capsid protein (gp23*). Specific anti-gp23* and anti-Hoc antibodies substantially decreased T4 phage activity in vitro and to some extent in vivo. Cooperating with antibodies, the immune complement system also contributed to annihilating phages. Current descriptions of phage immunogenicity and its biological consequences are still vague and incomplete; thus, the central problem of this work is timely and may have strong practical implications. Here is presented the very first description of the contribution of bacteriophage proteins to immunological memory of the phage. Understanding of interactions between phages and mammalian immunology may help in biotechnological adaptations of phages for therapeutic requirements as well as for better appreciation of phage ecology and their role in the biosphere.

Effects of Specific Antibodies and Immunocompetent Cells on Tumor Growth in Passive Transfer Experiment

Experiments with passive transfer of immunocompetent cell and serum demonstrated suppression of tumor growth after transfer of splenocytes from animals immunized with Trypanosoma cruzi. The nonspecific constituent of antitumor effect of immunocompetent cells was detected. The previously reported oncoprotective effect of mucins 2 and 3 was not confirmed.

THE USE OF MTT [3-(4, 5-DIMETHYL-2-THIAZOLYL) -2, 5-DIPHENYL - 2H- TETRAZOLIUM BROMIDE]-REDUCTION AS AN INDICATOR OF THE EFFECTS OF STRAIN-SPECIFIC, POLYCLONAL RABBIT ANTISERA ON CANDIDA ALBICANS AND C. KRUSEI

There is only scanty data on the effects of specific antibody, with or without complement, on Candida albicans or Candida krusei in cell-free systems in vitro, although previously published work has shown that specific antibody mediates anti-Candida immunity in vivo by inhibition of adherence to host cells or surfaces and by the promotion of phagocytosis and intra-phagocytic killing.The MTT (3-[4, 5-dimethyl-2-thiazolyl] -2, 5-diphenyl -2H- tetrazolium bromide)-reduction method as a test of the viability of fungi was used to investigate the effect of complement, normal serum and immune serum on these two species of Candida that are of increasing importance as opportunistic pathogens. We report that normal rabbit serum or strain-specific, polyclonal anti-Candida rabbit antibody, with or without guinea pig complement, did not cause the reduction of total cell-mass or of the viability of either C. albicans or C. krusei, in vitro as determined by the MTT-reduction test. Complement alone without specific antibody, also, had no such effect on these two Candida species.

The use of mtt [3-(4, 5-dimethyl-2-thiazolyl) -2, 5-diphenyl -2h- tetrazolium bromide]-reduction as an indicator of the effects of strain-specific, polyclonal rabbit antisera on <i> Candida albicans</i> and <i> C. krusei</i>

There is only scanty data on the effects of specific antibody, with or without complement, on Candida albicans or Candida krusei in cell-free systems in vitro, although previously published work has shown that specific antibody mediates anti- Candida immunity in vivo by inhibition of adherence to host cells or surfaces and by the promotion of phagocytosis and intra-phagocytic killing. The MTT (3-[4, 5-dimethyl-2-thiazolyl] -2, 5-diphenyl -2H- tetrazolium bromide)-reduction method as a test of the viability of fungi was used to investigate the effect of complement, normal serum and immune serum on these two species of Candida that are of increasing importance as opportunistic pathogens. We report that normal rabbit serum or strain-specific, polyclonal anti- Candida rabbit antibody, with or without guinea pig complement, did not cause the reduction of total cell-mass or of the viability of either C. albicans or C. krusei, in vitro as determined by the MTT-reduction test. Complement alone without specific antibody, also, had no such effect on these two Candida species.

Biological effect of vaccination can be assessed directly from diluted whole blood of rainbow trout using homologous blood phagocytes as immunosensors

A rapid and simple method is presented for determining antibody activity following vaccination, directly from diluted fish blood. The proposed method evaluates the effects of specific antibodies on ingestion by blood phagocytes, and may be used for measuring antibody levels following vaccination. The enhancing effect of trout IgM on ingestion was measured by luminol-amplified chemiluminescence (CL) emission of blood phagocytes. Respiratory burst (RB) activity of blood phagocytes was induced with the strain MT004 of bacterial fish pathogen Aeromonas salmonicida. To determine the boosting level of specific IgM on ingestion, various volumes of purified trout IgM containing specific antibodies against A. salmonicida were added to blood samples collected from non-vaccinated fish, and the RB activity of blood phagocytes was measured. The presence of antibodies in plasma of artificially prepared immune blood (AIB) was confirmed using enzyme-linked immunosorbent assay (ELISA). At a final blood dilution of 1:250, the mean RB activity of blood samples boosted with IgM was more than seven times higher, compared to other tested blood dilutions boosted with equal amount of IgM. Accordingly, a dilution of 1:250 was employed in the field study of vaccinated and non-vaccinated fish. The levels of A. salmonicida-specific antibodies in plasma samples of vaccinated and non-vaccinated fish were additionally confirmed with the ELISA assay. Based on these results, it is proposed that the biological activity of elicited antibodies can be assessed directly from diluted fish blood, using homologous blood neutrophils as immune sensors.

Zur systemischen verfügbarkeit von bovinemimmunglobulin g und hühner‐immunglobulin y aus gefüttertem kolostrum bzw. volleipulver bei neugeborenen kälbern

Bei 26 neugeborenen männlichen Kälbern aus 23 verschiedenen Betrieben wurden im Rahmen eines Versuchs zur Prophylaxe von infektiösen Durchfallerkrankungen mit spezifischen Dotterantikörpern auch Untersuchungen zur systemischen Verfügbarkeit von kolostralem bovinen Immunglobulin G (blgG) und von Hühner‐Immunglobulin Y (IgY) aus zugefüttertem Volleipulver durchgeführt. Den Kälbern wurde dazu in den ersten 14 Lebenstagen täglich zum gleichen Zeitpunkt eine Blutprobe entnommen. In Verbindung mit der Kolostrumgabe war die blgG‐Konzentration am Tag 1 post natum am höchsten und lag im Mittel bei einem Wert von 9,3 mg/ml Serum. Der gemittelte blgG‐Spiegel nahm anschließend kontinuierlich ab und erreichte am Tag 12 post natum einen signifikant niedrigeren Wert von 4,9 mg/ml Serum. Bis zum Ende der Beobachtungsperiode (Tag 14 post natum) blieb die mittlere blgG‐Konzentration weitgehend stabil (5,2 mg/ml). Die Gesamtproteinkonzentrationen im Serum blieben hingegen im Beobachtungszeitraum relativ konstant (im Mittel 56,8 mg/ml; SD 11,2). Die Anzahl der Kolostrumgaben je Tier hatte keinen signifikanten Einfluß auf die Höhe der bIgG‐Konzentrationen. Die Streubreite der individuellen Konzentrationen war an den einzelnen Tagen der ersten beiden Lebenswochen enorm. Der mittlere Variationskoeffizient lag bei 52,1 % (SD 5,7). Bei der Berechnung der individuellen bIgG‐Kurvenverläufe mittels einer Regressionsgleichung ergaben sich zwei Gruppen mit signifikant verschiedenem Eliminationsverhalten. So zeigte eine Gruppe (n= 10) mit Eliminationskonstanten von k < —0,02 eine mittlere Halbwertszeit für blgG von 24,3 Tagen (SD 4,6). Bei den übrigen Kälbern (n = 16) mit einer Eliminationskonstante für blgG von k >—0,02 lag die berechnete Halbwertszeit möglicherweise aufgrund der frühzeitiger erfolgten blgG‐Eigensynthese bei einem theoretischen Wert von 68,5 Tagen (SD 36,7). An 18 Kälbern wurde im selben Versuchszeitraum täglich 20 g Volleipulver mit einem IgY‐Gehalt von 15 mg/g verabreicht. Wurde das Eipulver bereits erstmals in den ersten 12 Lebensstunden zugefüttert, so erreichten die Kälber maximale IgY‐Konzentrationen von im Mittel 1,9 ug/ml Serum. Ein späterer Beginn der Eipulverzulage hatte signifikant niedrigere IgY‐Spiegel zur Folge. Wurde sie beispielsweise zwischen der 25igsten und 48igsten Lebensstunde begonnen, so zeigte sich eine mittlere IgY‐Konzentra‐tion von nur 0,035 μg/ml Serum. Aus der Berechnung der individuellen Eliminationskonstanten mittels einer Regressionsgleichung (r2 = 0,84) ergab sich eine mittlere Halbwerfszeit für IgY von 5,0 Tagen (SD 2,5). Um die Resorption und damit auch die mögliche systemische Wirksamkeit von speziesfremden Antikörpern weitgehend zu verhindern, sollte Eipulver zur Prophylaxe von infektiösen Durchfallerkrankungen beim neugeborenen Kalb demzufolge erst 24 bzw. besser 48 Stunden post natum zugefüttert werden. Entscheidend für eine wirksame Prophylaxe gegen infektiöse Durchfallerkrankungen ist allein die hohe intestinale und nicht die systemische Verfügbarkeit von spezifischen Antikörpern.

Effects of specific antibodies on the ultrastructure of mouse oocytes

The effects of antiovarian antiserum and monoclonal antibodies to the oolemma antigens on the ultrastructure of mouse oocytes and their microenvironment are studied. The antioolemma monoclonal antibodies cause more pronounced degenerative changes in the oocyte that in its microenvironment. Antiovarian antiserum induces greater changes in the microenvironment than in the oocyte. Changes induced in the oocyte by the antiserum are secondary relative to changes occurring in the microenvironment, while changes observed in the oocyte treated with monoclonal antibodies are primary.

YY1 and NF1 both activate the human p53 promoter by alternatively binding to a composite element, and YY1 and E1A cooperate to amplify p53 promoter activity.

A novel transcription factor binding element in the human p53 gene promoter has been characterized. It lies about 100 bp upstream of the major reported start site for human p53 gene transcription. On the basis of DNase I footprinting studies, electromobility shift assay patterns, sequence specificity of binding, the binding pattern of purified transcription factors, effects of specific antibodies, and methylation interference analysis we have identified the site as a composite element which can bind both YY1 and NF1 in an independent and mutually exclusive manner. The site is conserved in the human, rat, and mouse p53 promoters. The occupancy of the site varies in a tissue-specific manner. It binds principally YY1 in nuclear extracts of rat testis and spleen and NF1 in extracts of liver and prostate. This may facilitate tissue-specific control of p53 gene expression. When HeLa cells were transiently transfected with human p53 promoter-chloramphenicol acetyltransferase reporter constructs, a mutation in this composite element which disabled YY1 and NF1 binding caused a mean 64% reduction in basal p53 promoter activity. From mutations which selectively impaired YY1 or NF1 binding and the overexpression of YY1 or NF1 in HeLa cells we concluded that both YY1 and NF1 function as activators when bound to this site. In transient cotransfections E1A could induce the activity of the p53 promoter to a high level; 12S E1A was threefold as efficient as 13S E1A in this activity, and YY1 bound to the composite element was shown to mediate 55% of this induction. Overexpressed YY1 was shown to be able to synergistically activate the p53 promoter with E1A when not specifically bound to DNA. Deletion of an N-terminal domain of E1A, known to be required for direct E1A-YY1 interaction and E1A effects mediated through transcriptional activator p300, blocked the E1A induction of p53 promoter activity.

Effect of specific antibodies on the cell-associated spread of pseudorabies virus in monolayers of different cell types.

The effect of specific pseudorabies virus (PRV) antibodies on the enlargement of plaques produced by PRV were studied in monolayers of different cell types. The plaque size was used as parameter for the efficacy of the cell-associated spread (CAS) of PRV. First, the effect of anti-PRV hyperimmune serum on the plaque growth was examined in monolayers of the continuous cell lines ST, SK-6 and MDCK and monolayers of the primary cultures of porcine fibroblasts, endothelial cells and endometrial cells. A tenfold increase in the serum concentration did reduce the plaque size with 50% in both SK-cells and fibroblasts and with 40, 28 and 16% in MDCK, endothelial and endometrial cells, respectively. In ST cells, no change in size was observed with increasing antibody concentrations. Secondly, the effects of monoclonal antibodies (mAbs) directed against PRV glycoproteins gB, gC, gD and gE and polyclonal antibodies against gC were evaluated in SK-6 cells. MAbs against gB, gD and gE were able to reduce the CAS with a cumulative effect between mAbs against gD and either mAbs against gB or mAbs against gE. Monoclonal and polyclonal antibodies against gC did not change the plaque size.

Antiproliferative effect of multiple autocrine loop blockade in human malignant glioma cell lines.

The effects of specific antibodies against growth factors and receptors on deoxyribonucleic acid (DNA) synthesis in two established human glioma cell lines, A172 and TM-1, were examined. Anti-platelet-derived growth factor (PDGF), anti-basic fibroblast growth factor (bFGF), and anti-epidermal growth factor receptor (EGF-R) antibodies inhibited thymidine incorporation by both cell lines in serum-free medium. Antibody specific to transforming growth factor-alpha only slightly suppressed DNA synthesis by both cell lines. Although the antiproliferative effects of anti-PDGF and anti-bFGF antibodies decreased in serum-supplemented medium, the effect of anti-EGF-R antibody was little changed. The combination of anti-PDGF, anti-bFGF, and anti-EGF-R antibodies significantly inhibited thymidine incorporation by the two cell lines even in serum-supplemented medium. This preliminary study suggests that simultaneous blockade of multiple autocrine loops may provide a new approach to the treatment of human malignant gliomas.

Characterization of a 58- and a 78-kD monocytic membrane protein with affinity to the acetylcholine receptor in myasthenia gravis patients.

The autoimmune disease myasthenia gravis (MG), caused by the effect of specific antibodies, directed towards the nicotinic acetylcholine receptor, is triggered by autoantigen-specific T cells. In order to investigate cellular parts of the immune response in MG, the authors investigated the binding of the nicotinic acetylcholine receptor (AChR) to peripheral blood mononuclear cells (PBMC) from MG patients. AChR binding cells were identified by rosetting experiments using AChR-coated fluorescein beads. Applying this technique, a significant percentage of PBMC (21.2 +/- 7.65%) from MG patients formed rosettes with AChR-coated beads. Membrane preparations of nycodenz- or percoll-separated monocytes from MG patients or T-cell depleted monocytic subpopulations were applied to SDS-PAGE under reducing conditions. Ligand-blotting studies with biotinylated AChRs revealed two cell-membrane proteins with molecular weights of 58- and 78-kD. In parallel the same results were obtained by affinity chromatography of monocytic membrane proteins using AChR-sepharose. A possible interference of anti-AChR IgG was excluded. The 58- and the 78-kD proteins are detectable under reducing conditions by ligand blotting with AChR-biotin, while under non-reducing conditions only the 58-kD protein can be detected. Furthermore, in experiments using Endoglycosidase-H, the 58-kD protein appears to be non-glycosylated, while the 78-kD protein bears carbohydrates. These findings suggest that monocytes which bind the AChR via specific membrane proteins on their surface might act as antigen-presenting cells and may lead to an induction of the T-cell response, in the early phase of the disease.

Trichinella spiralis: The Effect of Specific Antibody on Muscle Larvae in the Small Intestines of Weaned Rats

Weaned rats were passively immunized with rat IgG 2c monoclonal antibodies previously shown to protect infant rats against challenge with Trichinella spiralis. Although the antibodies did not protect rats against infection, the course of larval establishment in the intestine was altered in a way that has not been described previously. Specifically, larvae that invaded the epithelium were inhibited from migrating from intestinal tissue into saline during the standard recovery procedure. The inhibition was reversed at a time coincident with the first moult. Whole serum from infected rats had a similar effect. These results show that specific antibodies influence T. spiralis larvae in the intestinal epithelium, yet fail to effect their expulsion from adult rats.

Effect of specific antibody on adherence of Staphylococcus aureus to bovine mammary epithelial cells

Staphylococcus aureus is a major pathogen in the bovine mammary gland. The ability of S. aureus to adhere to epithelial cells in the ductules and alveoli of the bovine mammary gland is believed to add greatly to its virulence and may be necessary for colonization. Two in vitro methods were developed for the purposes of quantifying adherence and of determining the effect which specific antibody may have in inhibiting the adherence of this organism. Both methods utilize bovine mammary epithelial primary cells as targets for labeled bacteria. In one assay, the bacteria are labeled with [methyl-3H]thymidine and incubated on the primary epithelial monolayers. The second assay involves labeling the bacteria with biotin. An enzyme-linked immunosorbent assay is then performed with streptavidin conjugated to horseradish peroxidase. Both methods have proven to be reliable and allow for the testing of many criteria in one assay. Cows were immunized with a whole-cell vaccine, and immune serum and milk were collected. The bacteria were then incubated in the presence of serum or milk as a test for antiadherent capability. By using the methods described, distinct antiadherent activity in both serum and milk was demonstrated.

Cytochrome P-450-mediated activation of pro-carcinogens and promutagens to DNA-damaging products by measuring expression of umu gene in Salmonella typhimurium TA1535/pSK1002

A simple and sensitive procedure for the determination of cytochrome P-450 (P-450)-mediated activation of chemical procarcinogens and promutagens to DNA-damaging products has been developed using a method measuring the expression of the umu gene in Salmonella typhimurium TA1535/pSK1002, which is based upon the initial procedures as described by Oda et al. [ Mutation Res. 147, 219 (1985)]. The chemicals examined were a variety of potent carcinogenic and mutagenic compounds including heterocyclic aromatic amines, aromatic amines, polycyclic aromatic hydrocarbons and aflatoxin B 1. These chemicals were incubated with rat liver microsomes or a reconstituted monooxygenase system containing three forms of purified P-450 in the presence of a bacterial tester strain, and the induced- umu gene expression was determined by measuring the β-galactosidase activity produced by fusion gene in the cells. The activity was increased linearly for at least 2 hr with an initial lag time of 30 min and was dependent on the concentrations of P-450 in the reaction mixture. Thus, the metabolic activation of these compounds by P-450 could be compared on a basis of the specific β-galactosidase activity/min/ nmol P-450. Among three forms of P-450, two isozymes induced by 3-methylcholanthrene were found to be more active in catalyzing the metabolic activation of most of the chemicals examined than a form of P-450 which is induced by phenobarbital. Data also showed that a high spin form of P-450 isolated from 3-methylcholanthrene-treated rats had a profound role in the activation of procarcinogens and promutagens. This conclusion was based on the results of catalytic activities by three forms of P-450 in a reconstituted monooxygenase system, and on the effects of specific antibodies against these P-450s on the reactions catalyzed by liver microsomes.

Effects of specific antibodies, hormones, and lipoproteins on bacterial lipopolysaccharides injected into the rat.

When gram-negative lipopolysaccharides (LPS) are injected intravenously into experimental animals, approximately one-third of the LPS bind to high-density lipoproteins (HDL) in the plasma and are slowly taken up into tissues by HDL-mediated mechanisms. Molecules of LPS in the plasma that do not bind to HDL are taken up more rapidly by tissues that are rich in phagocytic cells (e.g., liver, spleen). In these experiments we evaluated the effects of several potential host factors on the binding of LPS to HDL and on the tissue uptake of LPS injected intravenously into rats. Antibodies to LPS inhibited LPS binding to HDL and increased the uptake of the injected LPS (as well as the LPS in preformed LPS-HDL complexes) by the liver and spleen. High levels of circulating HDL decreased the uptake of injected LPS and LPS-HDL complexes by the adrenal gland, presumably by occupying tissue receptors for HDL. Pretreating rats with dexamethasone unexpectedly decreased the uptake of injected LPS-HDL complexes by the adrenal gland and increased uptake of LPS by the gland, a result suggesting that this drug has opposing effects on the uptake of HDL-bound and -unbound LPS by the adrenal gland. The host factors studied appear to influence the fate of injected LPS by acting at different sites: IgG antibody to LPS blocks the binding of LPS to HDL in the plasma, whereas all of the factors studied have effects that modulate the uptake of LPS or LPS-HDL complexes or both by the cells of specific tissues.

Effect of specific antibodies on acetylcholine receptor turnover: increased degradation controls low density of cell surface receptor.

BC3H-1 cells express surface nicotinic receptors. We treated these cells with pooled serum from myasthenic patients. After 5 hours, the number of surface receptors decreased to one-half of baseline and remained at this low level for at least 72 hours. The rate of receptor degradation was increased by myasthenic serum, but the synthesis of new receptors was unaffected. The regulation of the number of surface nicotinic receptors is thus mediated by an accelerated internalization of the receptor.

The effect of specific antibodies on oxygen uptake and H + pumping by cytochrome c oxidase vesicles

Antibodies to solubilized cytochrome c oxidse and to subunit III were incubated with liposomal oxidase. In oxygen uptake experiments, the inhibiting effects on RCI of anti-oxidase (primarily anti- subunits II and IV) and anti-III were by different mechanisms: the former, by inhibiting the uncoupled rate; the latter, by stimulating the coupled rate. In experiments with H + translocation, anti-oxidase was without effect, while anti-III was a potent inhibitor of proton pumping. These results are conclusive evidence for redox-linked proton extrusion from the vesicles by the oxidase (and its subunit III).

Activation of peritoneal macrophages by concanavalin A or Mycobacterium bovis BCG for fungicidal activity against Blastomyces dermatitidis and effect of specific antibody and complement.

With a new short-term assay, where the reduction of CFUs in the inoculum could be measured, we investigated the killing of the dimorphic fungal pathogen Blastomyces dermatitidis in its yeast phase by murine peritoneal macrophages. Peritoneal macrophages from concanavalin A- or Mycobacterium bovis BCG-treated mice, but not resident or thioglycolate-elicited macrophages, significantly reduced the CFUs of B. dermatitidis in the inoculum. The activation of peritoneal macrophages for fungicidal activity by concanavalin A treatment was shown to be dose dependent and transient, i.e., absent after 72 h. These results indicate that it is possible for murine peritoneal macrophages to kill B. dermatitidis in vitro. The addition of specific antibody or complement or both did not enhance the killing of B. dermatitidis by these nonspecifically activated macrophages.

The effect of specific antibody on antibody-independent interactions between E. coli J5 and human complement.

We previously reported that Escherichia coli J5, the galactose epimerase-deficient mutant of E. coli O111:B4, can bind and activate purified human C1. The effects of hyperimmune rabbit anti-J5 IgG or IgM on E. coli J5 interactions with human C have been examined. Specific IgG or IgM increased the binding of 125I-C1 by J5. However, the rate of C1 activation, as determined by SDS-PAGE of eluted 125I-C1s, was decreased if bacteria were preincubated with immune IgG. Complexes formed between J5 preincubated with immune Ig and C1, under conditions in which all of the C1 was allowed to activate, consumed more C4 than J5 alone plus C1. However, the amount of C4 consumed per C1 molecule was identical for all bacteria preparations. Concentrations of specific IgG or IgM that significantly increased C1 binding did not appear to enhance C3b deposition upon incubation of E. coli J5 in NHS. Thus, although specific antibody may enhance C1 binding by E. coli J5, the ability of these additional C1 molecules to alter later events in the C cascade may depend on the control of C1 activation and its subsequent activity when bound to different membrane components.

Effects of specific antibodies on the interaction between the fungus Candida albicans and human oral mucosa

Host-parasite interactions were studied in four groups: non-infected controls; infected carriers of Candida albicans without evidence of candidiasis; subjects with acute candidiasis; and subjects with chronic candidiasis. Specific anti-candida antibodies were demonstrated in saliva from subjects of all four groups; the titres reflected the degree of antigenic stimulation, being significantly higher in candidiasis than in controls or infected carriers. The adherence of C. albicans to buccal epithelial cells was not significantly different in a given saliva, regardless of whether the assay was carried out with autologous C. albicans and epithelial cells or with a stock strain in a standardized assay. Therefore, the standard assay was used to study the effects of specific salivary antibodies on adherence. A significant inverse correlation was found between salivary IgA anti-candida antibodies and the adherence of C. albicans to buccal epithelial cells, suggesting that IgA antibodies can inhibit adherence of Candida to the oral mucosa. In some instances, removal of antibodies led to a significant increase in adherence; however, often this was not the case, indicating that some but not all of the antibodies present were capable of inhibiting the adherence of C. albicans to epithelial cells.