Immune response to vaccination in the elderly.

The immune system develops from childhood until the late age. Each of these periods has its own specialities. Aging is typical for immunity, depending on the conversion of hematogenous bone marrow to adipose, involution of the thymus and persistent viral infections (e.g. CMV). In the elderly, whose numbers have been increasing in recent decades, there is a need to understand the changes in the immune system also called as immunosenescence. The substantial remodeling of the immune system during aging leads to a decline in its functional activity in both innate (complement, cytokines, granulocytes, NK cells, macrophages) and adaptive immunity (B lymphocytes and antibody production, T lymphocytes, cytokine production and cytotoxic response, NKT cells, regulatory T lymphocytes with suppressor activity) with advancing age, resulting in increased risk of chronic diseases, infections, autoimmunity and vaccination failure.

Th1, Th2 and Th17 lymphocytes in autoimmune thyreopathies.

Among the most common organ-specific autoimmune diseases are autoimmune thyreopathies. We have focused on the importance of Th1, Th2 and Th17 lymphocytes in autoimmune thyroiditis (AT). The cohort consisted of 136 treated patients in the full clinical course of AT (24 men, mean age 41.0±16.8 years and 112 women, mean age 44.6±17.6 years). The control group consisted of 17 healthy men (mean age 44.0±5.0 years). Box-Cox transformation of the data, t-tests and Pearson correlation analysis were used for statistical calculations. Lymphocyte subpopulations were determined by flow cytometry. We found statistically significant correlations between Th and Tc lymphocytes (r = -0.5605, p = 0.0000), total T and B lymphocytes (r = -0.4877, p = 0.0000), Th1 and Th17 lymphocytes (r = 0.4346, p = 0.0000), Tc and Th1 lymphocytes (r = 0.4124, p = 0.0000), IRI and Th1 lymphocytes (r = -0.4076, p = 0.0000), total T lymphocytes and NK cells (r = -0.8175, p = 0.0000), memory Th and Th1 lymphocytes (r = 0.7982, p = 0.0000), naive Th and Th1 lymphocytes (r = -0.7995, p = 0.0000), Tc lymphocytes and NK cells (r = -0.4014, p = 0.0000), Tc and total T lymphocytes (r = 0.4551, p = 0.0000), Th and total T lymphocytes (r = 0.4135, p = 0.0000). The determination of lymphocyte subpopulations is an aid in the diagnosis and treatment of autoimmune diseases, helps to clarify the clinical manifestations of the disease and can complement the interpretation of commonly determined autoantibodies. It can help determine whether the phase is destructive (Th1, Th17, Tc lymphocytes) or protective (Th2 lymphocytes, antibodies).

Glucocorticoids Reduce Aberrant O-Glycosylation of IgA1 in IgA Nephropathy Patients.

BACKGROUND/AIMS: IgA nephropathy is associated with aberrant O-glycosylation of IgA1, which is recognized by autoantibodies leading to the formation of circulating immune complexes. Some of them, after deposition into kidney mesangium, trigger glomerular injury. In patients with active disease nonresponding to angiotensin-converting enzyme inhibitors or angiotensin II blockers, corticosteroids are recommended. METHODS: The relationship between the corticosteroid therapy and serum levels of IgA, aberrantly O-glycosylated IgA1, IgA-containing immune complexes and their mesangioproliferative activity was analyzed in IgA nephropathy patients and disease and healthy controls. RESULTS: Prednisone therapy significantly reduced proteinuria and levels of serum IgA, galactose-deficient IgA1, and IgA-IgG immune complexes in IgA nephropathy patients and thus reduced differences in all of the above parameters between IgAN patients and control groups. A moderate but not significant reduction of mesangioproliferative potential of IgA-IgG immune complexes and IgA sialylation was detected. CONCLUSION: The prednisone therapy reduces overall aberrancy in IgA1 O-glycosylation in IgA nephropathy patients, but the measurement of IgA1 parameters does not allow us to predict the prednisone therapy outcome in individual patients.

[Psycho-immuno-endocrinology of the thyroid gland]. / Psycho-imuno-endokrinologie stítné zlázy.

Historically endocrinologists and psychiatrists are aware that disturbances in thyroid disease in beginning or even in clinically intensified states of thyrotoxicosis or hypothyroidism exhibit pathological mental manifestations, masking or potentiating the underlying disease. Immune system disorders cause thyroid organ-specific autoimmune process. This autoimmune thyroid disease binds with a number of disorders in both endocrine or non-endocrine organs. This appears in vascular, neurological, skin, connective tissue, gastrointestinal tract and mental pathology. These disorders are part of autoimmune polyglandular syndromes (APS) type I -III, especially the APS type III. Originally it was assumed that these mental disorders are caused by direct exposure to excess or deficiency of thyroid hormones. Recently, however, it appears that these psycho-immune-endocrine disorders have common etiologic mechanisms of formation and on cellular and molecular level they involve similar, if not in some cases, common mechanisms.Key words: antithyroid peroxidase antibody - autoimmune polyglandular syndrome type I., II., III. - autoimmune thyroid disease - bipolar disorder - depression - Hashimotos encephalopathy - postpartum psychosis - psycho-immuno-endocrinology - schizophrenia.

[IgA Nephropathy. Facts, uncertainties, and potential causal therapy approaches]. / IgA nefropatie--jistoty, pochybnosti a výhledy kauzální lécby.

IgA nephropathy is currently the most frequently investigated glomerulonephritis. The disease is defined by the presence of dominant or co-dominant deposits of IgA1 in the glomerular mesangium. Circulating immune complexes are most likely the source of the deposited IgA1. However, it is also possible that the aggregates of structurally altered IgA1 or enhanced binding to IgA receptors expressed on mesangial cells lead to deposition. The cause of the formation of immune complexes responsible for IgA nephropathy lies in the incomplete O-linked oligosaccharide side chains, which, due to the deficiency of corresponding glycosyltransferases, lack terminal galactose residues leading to the exposure of N-acetylgalactosamine. Naturally occurring antibodies of the IgG or IgA1 isotype bind to this sugar antigen. In the clinical course, we differentiate between the early stage usually characterized by hematuria, and a variable late stage characterized either by a clinical remission, by persistence of hematuria, or by increasing proteinuria and blood pressure and decreasing renal function in one third of the patients. In the early stage, it is difficult to predict the prognosis of IgA nephropathy, either on the basis of clinical presentation and morphological findings, or according to the level of galactose-deficient IgA1 in the circulation. The reliable criteria of serious prognosis emerge only in the later stages of the disease and include proteinuria, hypertension, and histologically apparent tubular atrophy and interstitial sclerosis. The dominant trend in the treatment of IgA nephropathy is the emphasis on administration of ACE inhibitors/sartans, which are introduced into the treatment at the time of microalbuminuria. If proteinuria does not decrease below 1 g/24 h, treatment with prednisone is justifiable. New findings concerning the molecular/cellular mechanism involved in the pathogenesis of IgA nephropathy suggest the possible therapeutical interference with the generation of nephritogenic immune complexes by a selective blocking of the IgA1 molecules with altered glycan structures using monovalent reagents.

Prevalence of Helicobacter pylori in adenotonsillar hypertrophy in children.

CONCLUSION: Our results encourage the notion that the pharynx could be an extragastric reservoir of Helicobacter pylori (HP). The study confirmed the presence of HP in adenotonsillar tissue in children. It could have importance in the pathophysiology of upper respiratory diseases. However, its precise role in these processes remains unclear and requires further studies. OBJECTIVE: A prospective study was carried out to evaluate the presence of HP in tonsillar and adenoid tissue in children. The study focused on real-time PCR analyzing CagA and VacA genotypes of HP strains. METHODS: A total of 37 consecutive pediatric patients with adenotonsillar hypertrophy indicated for surgery were observed in a prospective study. Adenoidectomy and/or tonsillectomy was performed in each patient; 49 specimens were taken, 32 from adenoids and 17 from tonsils. The presence of HP and its genotype were tested in all samples by real-time PCR analysis. RESULTS: Of 49 samples analyzed, 48 were positive for the presence of HP (98%), so only 1 sample was negative. While the genotype VacAs1bm2 was definitely dominant in adenoid tissue, wider distribution was observed in tonsillar tissue. Cag(+) strains represented one-fifth of all samples (21%).

Detection of Helicobacter pylori in oropharyngeal lymphatic tissue with real-time PCR and assessment of its carcinogenic potential.

Helicobacter pylori (HP) is considered a major gastric pathogen with oncogenic potential. The aim of this study was to determine whether HP is present in oropharyngeal lymphoid tissue and whether oropharyngeal HP strains carry virulence factor genes known to be involved in gastric carcinogenesis. The study included 104 subjects (41 patients with tonsillar carcinoma, 38 with chronic tonsillitis and 25 with obstructive sleep apnoea syndrome--OSAS). Detection of specific serum anti-HP antibodies was performed with an ELISA. The presence of HP in tissue was determined by culture and real-time PCR. Detection of virulence factors genes was also performed. Specific antibodies were found in 78.05% of tumour cases, 34.21% of chronic tonsillitis cases, and 72.0% of OSAS cases. The presence of HP in the tissue was detected in 73.91% of tonsillar tumours, 70.0% of tonsillitis cases, and 69.23% of OSAS specimens. The results of the virulence factor gene analysis showed the majority of the s1b (52.4%) and m2 (59.5%) alleles of vacA gene and limited abundance of cagA gene (12.5%). Results confirm that HP may colonise oropharyngeal lymphoid tissue. Oropharyngeal HP colonisation was frequently found in the oropharyngeal cancer group and in patients with benign oropharyngeal diseases. A virulence factor gene analysis showed differences from the predominant strains most commonly found in the stomach. The strains obtained from the oropharynx differed primarily by the lower abundance of the cagA gene and carried the less virulent vacA gene allele combination.

Presence of different genotypes of Helicobacter pylori in patients with chronic tonsillitis and sleep apnoea syndrome.

Helicobacter pylori, a well-known gastric pathogen, has been detected in the oral cavity and oropharynx in tonsillar tissue. In our study, the presence of H. pylori in the tonsillar tissue of patients with chronic tonsillitis and sleep apnoea syndrome (SAS) was investigated. The aim was to detect and genotype H. pylori for a collection of data supporting the possible role of H. pylori in the aetiology of chronic tonsillitis and SAS. Helicobacter pylori was detected by real-time polymerase chain reaction (rt-PCR). 89 patients, 60 with a diagnosis of chronic tonsillitis and 29 with SAS, were tested. In the chronic tonsillitis group, Helicobacter was detected in 48 (80 %) specimens, cagA gene was detected in 12 samples (25 %) and 12 samples were negative. In SAS group, Helicobacter was found in 24 samples (82.76 %), cagA gene was detected in 5 (20.83 %) and 5 samples (17.24 %) were negative. Helicobacter pylori-specific immunoglobulins were tested by ELISA in the serum of 57 patients only with 41 (71.93 %) showing positive. Our results on H. pylori DNA detection and H. pylori seropositivity show 26.32 % discrepancy, slightly in favour of rt-PCR (15.79 % compared to 10.53 %). The H. pylori presence in tonsillar tissue does not depend on the type of oropharyngeal disease (p = 0.756). This study shows that oropharynx constitutes an extragastric reservoir of H. pylori infection which could serve as an aetiopathogenetic factor for chronic tonsillitis and tonsillar hyperplasia by SAS. No conclusion has yet been drawn about the mechanism of the process.

[D vitamin and immunity]. / D vitamin a imunita.

Active vitamin D3 is a key factor in many pathological states. In this review its influence on the immune system will be discussed, especially in the scope of innate and adaptive immunity. D3 has a crucial importance in defense against infections and in development of immunopathological reactions, especially in autoimmunity.

Adjuvant effect of Bacillus firmus on the expression of cytokines and toll-like receptors in mouse nasopharynx-associated lymphoid tissue (NALT) after intranasal immunization with inactivated influenza virus type A.

Due to the persisting threat of development of new highly pathogenic influenza A subtypes, a mucosal vaccination which would induce a potent and cross-protective reaction is desirable. We succeeded in mucosal immunization of mice with an inactivated influenza A virus by using delipidated Bacillus firmus (DBF) as adjuvant. The mechanism of adjuvant effect was followed in NALT by comparing the response after intranasal immunization by inactivated influenza virus type A (H1N1) alone, adjuvant alone (DBF), or by a mixture of virus+DBF. Expression of selected gene groups was tested via qPCR at 7 different time-points: cytokines (IL-2, IFN-γ, IL-4, IL-6, and IL-10), type I interferons (IFN-α4, IFN-α11, IFN-α12, and IFN-ß), toll-like receptors (TLR2, TLR3, TLR7, and TLR9), iNOS and CCR7. Intranasally administered DBF and the mixture of virus+DBF induced an elevated expression of IFN-γ, IL-6 and IL-10 cytokines, type I interferons, iNOS, and pDC markers in NALT. Multimarker qPCR data was analyzed by relative quantification and by principal component analysis. DBF has been shown to be a very efficient adjuvant for the stimulation of innate immunity after IN immunization. DBF accelerated, increased, and prolonged the antiviral response.

The role of environmental factors in autoimmune thyroiditis.

Environmental factors can play an important role in the development of autoimmune thyroiditis (AT) and other autoimmune diseases. This article reviews the role of heavy metals and infectious agents in AT. Currently, the genes responsible for a metal-induced pathology are known in experimental animals but similar knowledge is lacking in man. Metals such as nickel or mercury induce delayed type T cell hypersensitivity (allergy) which is relatively common, especially in women. T-cell allergy can be studied with the lymphocyte transformation test, LTT-MELISA. It has been found that patients with AT and other autoimmune diseases, such as multiple sclerosis, psoriasis, systemic lupus erythematosus and atopic eczema, show increased lymphocyte reactivity in vitro to inorganic mercury, nickel and other metals compared to healthy controls. The important source of mercury is dental amalgam. Replacement of amalgam in mercury-allergic subjects resulted in improvement of health in about 70% of patients. Several laboratory parameters such as mercury-specific lymphocyte responses in vitro and anti-thyroid autoantibodies were normalized as well. In contrast, no changes in health and laboratory results were observed in mercury-allergic patients who did not have their amalgams replaced. The same was true for non-allergic patients who underwent amalgam replacement. Infectious agents such as Helicobacter pylori (Hp) may cause chronic inflammation and autoimmune reactivity in susceptible subjects. The results of in vitro experiments performed with lymphocytes from Hp infected patients indicate that Hp can cause immunosuppression which might be eliminated by successful eradication therapy. In conclusion, heavy metals and Hp infection may play an important role in AT. Laboratory tests, such as LTT-MELISA, can help to determine the specific etiological agents causing inflammation in individual patients. The treatment of AT and other autoimmune diseases might be improved if such agents are eliminated and any future exposure restricted.

Changes of immunological profiles in patients with chronic myeloid leukemia in the course of treatment.

In the previous paper of ours we compared, prior to start any treatment, a number of immunological parameters in 24 chronic myeloid leukemia patients with the same number of healthy subjects matched by age and sex. We found significant differences in the levels of immunoglobulins, the C4 component of complement, the C-reactive protein, interleukin 6, the composition of lymphocyte population and the production of some cytokines by stimulated CD3+ cells. Eleven of these patients were followed longitudinally. After treatment with hydroxyurea, interferon alpha, imatinib mesylate and dasatinib, or various combinations thereof, hematological remission was achieved in all patients and complete cytogenetic remission in nine of them. There was a nearly general tendency towards normalization of the abnormalities observed in the patients at their enrollment.

Protective and cross-protective mucosal immunization of mice by influenza virus type A with bacterial adjuvant.

Mucosal immunization by inactivated viruses often fails to evoke a sufficient immune response. Intensive efforts have been made to enhance the response by suitable adjuvants. We used the G+ nonpathogenic delipidated bacterium Bacillus firmus with pronounced immunostimulatory properties as an adjuvant for immunizing mice with inactivated influenza virus type A. BALB/c mice were immunized intratracheally with inactivated influenza A H1N1 and H3N2 viruses. The production of antibodies in sera and secretions was determined by the ELISA. The local situation in the lungs was assessed histologically and by testing the cytokine expression. The protective and cross-protective effect against infection was tested in in vivo experiments after infection with influenza virus A H1N1. B. firmus as adjuvant increased both systemic and mucosal antibody responses, improved protection against homologous virus and induced cross-protection against virus H1N1 after immunization with virus H3N2.

Natalizumab in the treatment of patients with multiple sclerosis: first experience.

Multiple sclerosis (MS) usually develops in young adults with a complex predisposing genetic background. Polymorphisms in the gene for chemokine receptor CCR5 have been proposed to confer susceptibility to or protection from MS. Study of molecules participating in the inflammatory process contributed to the development of a new humanized monoclonal antibody, natalizumab, aimed at the adhesive molecule VLA-4. Natalizumab (Biogen Idec/Elan) went through successful clinical studies and its clinical testing was also carried out in the Czech Republic. Twenty-one patients with MS were included in the AFFIRM study (2-year, placebo-controlled study and consecutive 7-month unblinded natalizumab treatment); immunophenotyping of the cerebrospinal fluid (CSF)- CD4+CCR5+CXCR3+ lymphocytes, using flow cytometer FACSCalibur and monoclonal antibodies (BD Biosciences), was done at the end of natalizumab treatment and 1 year after the therapy withdrawal. Compared to MS patients receiving other therapy, the patients treated with natalizumab had statistically significantly (P < 0.0001) higher levels of CCR5+ and lower levels of CD4+ T lymphocytes in CSF, whereas the levels of CXCR3+ lymphocytes were almost the same as in other patients. CCR5-positive CSF lymphocytes decreased 1 year after treatment withdrawal. Natalizumab treatment alters the percentage of CCR5+ and CD4+ cells in CSF. In view of the excellent temporary clinical results of the therapy, which are yet to be assessed in the course of a longer time period, our results show a possible explanation for the therapeutic success of this drug as well as for the development of progressive multifocal leukoencephalopathy.

Effect of breast milk of healthy and allergic mothers on in vitro stimulation of cord blood lymphocytes.

Maternal milk has beneficial effects on the development and function of the newborn's immune system. Whether the milk of allergic mother has the same effects as the milk of healthy mothers is not yet quite clear. To contribute to the characterization of its immunomodulatory action, we tested the effect of milk of healthy and allergic mothers on the proliferation and immunoglobulin formation in cultures of cord blood mononuclear leucocytes (CBML) of newborns of healthy and allergic mothers. CBML proliferation was tested by (3)H-thymidine incorporation, IgM, IgG and IgA production by reverse ELISPOT. CBML response was examined in unstimulated cultures and after stimulation with polyclonal activators in the presence or absence of colostrum or milk. The cells of children of allergic mothers have a significantly higher proliferative activity than those of children of healthy mothers. Maternal colostrum/milk in high doses markedly suppresses cell proliferation after stimulation with polyclonal activators, whereas lower milk doses in the cultures have no such effect and exert a rather stimulatory action. Immunoglobulin production by cord blood lymphocytes is also different in the two groups of children. Low basal immunoglobulin formation is increased after stimulation with a strong polyclonal activator of B cells--Bacillus firmus, CBML of children of allergic mothers produce more IgA than those of children of healthy mothers. The stimulated production of all immunoglobulin classes in cells of children of healthy mothers is still enhanced by colostrum/milk. Children of allergic mothers show a markedly increased production of only IgM and IgA. The effect of healthy and allergic colostrum and milk on cell proliferation and immunoglobulin production is similar. The lymphocytes of children of allergic mothers differ from the lymphocytes of children of healthy mothers in their proliferative activity and the ability to form immunoglobulin already at birth.

The influence of metals on the expression of surface antigens on human lymphocytes in vitro.

OBJECTIVES: Metals have different effects on the immune functions. Through the experimental in vitro model, we studied the changes in the activation and co-stimulatory surface markers in human lymphocytes cultivated with selected metal salts. METHODS: Whole human blood was cultivated with cadmium (Cd) or zinc (Zn) sulfate for 18 hours. The number of lymphocytes positive for activation and co-stimulatory markers was evaluated by flow cytometry. RESULTS: Elevation of the CD69 and CD23 markers as well as higher expression of CD28 was found in cultures of lymphocytes incubated with Cd. In cultures incubated with Zn, minor elevation of the HLA-DR antigen expression was observed in comparison to Cd-treated cell cultures. Decrease of CD3 expression was observed after cultivation with both Cd and Zn salts. CONCLUSION: Cd and Zn exhibit different effects on the expression of human surface activation antigens and co-stimulatory molecules. Cd in non-toxic concentrations stimulated expression of early activation molecules and therefore could change the early phase of immune response. This was not the case for Zn, where the results were similar to untreated cell cultures.

Removal of dental amalgam decreases anti-TPO and anti-Tg autoantibodies in patients with autoimmune thyroiditis.

OBJECTIVES: The impact of dental amalgam removal on the levels of anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin (anti-Tg) antibodies was studied in patients with autoimmune thyroiditis (AT) with and without mercury allergy. METHODS: Thirty-nine patients with AT were tested by an optimized lymphocyte proliferation test MELISA for allergy (hypersensitivity) to inorganic mercury. Patients were divided into two groups: Group I (n = 12) with no hypersensitivity to mercury and Group II (n = 27) with hypersensitivity to mercury. Amalgam fillings were removed from the oral cavities of 15 patients with hypersensitivity to mercury (Group IIA) and left in place in the remaining 12 patients (Group IIB). The laboratory markers of AT, anti-TPO and anti-Tg autoantibodies, were determined in all groups at the beginning of the study and six months later. RESULTS: Compared to levels at the beginning of the study, only patients with mercury hypersensitivity who underwent amalgam replacement (Group IIA) showed a significant decrease in the levels of both anti-Tg (p=0.001) and anti-TPO (p=0.0007) autoantibodies. The levels of autoantibodies in patients with or without mercury hypersensitivity (Group I and Group IIB) who did not replace amalgam did not change. CONCLUSION: Removal of mercury-containing dental amalgam in patients with mercury hypersensitivity may contribute to successful treatment of autoimmune thyroiditis.

Metal alloys in the oral cavity as a cause of oral discomfort in sensitive patients.

OBJECTIVE OF THE STUDY: The occurrence of galvanism with its heterogeneous symptomatology is often the source of considerable problems. Abrasion and corrosion not only damage dental alloys but also burden the organism by release of metallic particles. The objective of this study is to evaluate the hypothesis that measurement of galvanic currents could be a useful diagnostic method. PATIENT GROUPS AND METHODOLOGY: Three hundred fifty-seven persons with dental metal restorations were divided into groups according to abnormal values of galvanic currents and by oral discomfort. In all persons a detailed examination of the oral cavity was performed, and galvanic currents were measured. In one hundred fifty-nine patients abnormal galvanic currents were found. Measurement of metallic elements in saliva was performed in these patients and in a group of 21 healthy volunteers without any metals in the oral cavity. Thirty-three patients agreed to treatment which involved removal of the causative alloys and their replacement by non-metallic restorations. RESULTS: No correlation was found between the values of measured currents and the number of teeth treated by metal restorations. However, patients with metal restorations had significantly higher contents not only of mercury, but also of tin, silver, copper, and gold in the saliva than patients without metallic restorations. After removal of the electro-active restorations, both the contents of metals in saliva and galvanic currents decreased in comparison with the levels before the treatment. CONCLUSIONS: Galvanic effects as well as metal particles may induce a series of local or systemic pathological phenomena in sensitive individuals. The occurrence of pathologically acting galvanic effects is influenced not only by the composition and combination of different dental alloys, but to a significant degree also by the quality of used materials and processing.

Autoimmune thyroiditis and Helicobacter pylori--is there a connection?

OBJECTIVES: In this study we examined the anti-Helicobacter pylori (anti-H. pylori) antibodies in patients with autoimmune thyroiditis, with and without different polyglandular involvement, and in healthy controls. MATERIAL & METHODS: Patients with autoimmune thyroiditis (AT) were divided into three groups: Group A: 23 patients with isolated AT, Group B: 30 patients with AT as a part of polyglandular activation of autoimmunity, and Group C: 7 patients with AT as a part of autoimmune polyglandular syndrome type II. Thirty healthy individuals served as controls (Group D). Anti-H. pylori antibodies were determined first by ELISA for classes IgG, IgA, and IgM, and subsequently by immunoblot for classes IgG and IgA. RESULTS: ELISA: The number of patients with IgA antibodies in Group A (39%) and Group B (30%) differed significantly from controls (7%, p<0.05). Immunoblot: Anti-CagA antibodies were found in 13% of patients in Group A, 7% of Group B, 0% of Group C, and 20% of Group D. A higher seroprevalence, as compared to controls, was found for IgG to the VacA (p=0.01), 30 kDa (p=0.001), and 17 kDa (p=0.008) antigens in Group A and for IgG to the 30 kDa antigen in Group C (p=0.037). A significantly higher seroprevalence, as compared to controls, was likewise found for IgA to the 17 kDa antigen in Group A (p=0.015). CONCLUSIONS: A different distribution of antibodies to H. pylori antigens was found in patients with isolated AT compared to patients with AT coupled with a polyglandular syndrome.

Cytokine levels in healthy and allergic mothers and their children during the first year of life.

To assess the regulatory changes of immune system in children genetically pre-disposed to allergic diseases and in their mothers, we tested cytokines IL-4, IL-5, IL-6, IL-10, IL-13, IFN-gamma and TGF-beta in 21 healthy and 21 allergic mothers (serum at the time of delivery, colostrum and milk throughout the suckling period) and their children (cord blood, venous blood and stool filtrates) up to 1 yr of age. Samples were taken at the time of delivery, 4 days post-partum and then after 3, 6 and 12 months. Significant differences between the healthy and the allergic group were found in the levels of IL-4, IL-10, IL-13 and IFN-gamma. The levels of IL-4 in the allergic group were generally higher; the levels in the sera of children of allergic mothers during the post-natal life decreased, reaching levels typical for the healthy group at 1 yr of age. Allergic mothers exhibited markedly higher IL-10 levels in the serum at the time of delivery and in milk 3 months after delivery than healthy mothers while after 6 months the IL-10 levels in all samples from the allergic group were very low. Children from allergic group had lower intestinal content of IL-13 in comparison with the healthy counterparts. At 1 yr of age, the levels of IFN-gamma in sera and stool of children from the allergic group sharply increased. TGF-beta levels in the sera of both groups were high, while in the milk they were relatively low and substantially lower that in the children's stool. TGF-beta of mammary secretions is therefore unlikely to exert a decisive regulatory influence on the children's immunity. Long-term clinical monitoring of the children will be performed to evaluate the potential prognostic significance of these changes for the future development of allergies.