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P Bauscher

Publications and source records attributed to P Bauscher.

4 recordsLinked to original sources

Defective CD2 T cell pathway activation in common variable immunodeficiency (CVID).

Clonal T cell expansion requires simultaneous activation of the TCR and secondary signals, e.g. CD2, CD4, CD28. Interference of CD2/CD58 interaction with MoAbs abrogates the primary immune response and antibody production. Given this functional importance of CD2/CD58 interaction for the generation of specific immune responses, we demonstrate for the first time a defective CD2 pathway activation in patients with CVID (seven children and four adults). The costimulatory effect of monocytes upon CD2-triggered proliferation was significantly impaired in CVID patients: 4.080 ct/min versus 20.769 ct/min in controls (P < 0.05). Second, IL-1, which is a strong comitogenic factor for activation via CD2 in normal T cells, showed a defective amplifier function of the CD2 pathway in most patients (median 1.714 ct/min in patients versus 17.521 ct/min in controls; P < 0.05). In addition, by using a mitogenic combination of CD2 plus CD45 MoAb, median proliferation of T cells was severely depressed in patients: 10.577 ct/min versus 34.685 ct/min in controls (P = 0.005). In conclusion, the marked dysfunction seen in responsiveness to phytohaemagglutinin (PHA) (median 24.594 ct/min in patients versus 52.229 ct/min in controls; P < 0.001) and after CD2 triggering, together with the unaffected response to TCR-CD3, suggest that the T cell deficiency in CVID is in part due to deficiencies in the CD2 pathway. Since direct activation of protein kinase C(PKC) by phorbol ester restores defective T cell responses to normal, our results suggest that an early signal-transducing defect might exist at a step proximal to PKC activation in patients with CVID.

Adolescent↗

[Effectiveness of Haemophilus influenzae B-diphtheria conjugate vaccination in German children].

BACKGROUND: In 1990 the Haemophilus influenzae b-Diphtheria conjugate vaccine (Hib-D) was introduced in Germany. In addition, most children under 18 months of age failed to develop protective levels of Hib antibodies in response to systemic infections. METHODS: To evaluate the protective efficacy of the Hib-D vaccine in Germany a post marketing case-control study was performed during 1.5. 1990-30.4. 1992. Surveillance for invasive Hib-infections was maintained by pediatricians of 8 hospitals in the Rhein-Main area. The antibody responses to Hib were evaluated by ELISA at the onset (days 0-3) and during remission of disease. RESULTS: During the first year of the study 23 cases per 100,000 children of invasive Hib-infections were recorded. Of these children, 15 suffered from meningitis, 6 from epiglottitis and one from cellulitis and pericarditis respectively. None of these patients had been vaccinated except for one, who received two injections of Hib-D. Due to increased acceptance of the Hib-D vaccine we found a significant reduction of invasive Hib-infections (6 cases per 100,000 children) in the second year of the study. Again, of these children only one child was vaccinated. As expected, in all patients investigated the initial Hib antibody level was below 1 microgram/ml. The development of Hib specific immunity to invasive disease was clearly age dependent: 10 of 11 children below 18 months failed to produce any Hib antibodies (> 0.15 microgram/ml) in response to their infection. In contrast 8 of 10 children older than 18 months developed protective antibody levels to Hib. CONCLUSIONS: The incidence of serious Hib-disease has significantly decreased in Germany since the introduction of the Hib-D vaccine. Because no other Hib vaccine was licensed in Germany our data confirm efficacy and safety of Hib-D reported previously. In addition, children, who contracted disease before 18 months of age, remain susceptible to Hib and require active immunization for protection.

Antibodies, Bacterial↗

[IgG subclass level in healthy children].

In 159 healthy German children aged 3 months to 16 years IgG subclass concentrations were measured by radial immunodiffusion using polyclonal antisera. IgG-4 levels were also determined by a monoclonal ELISA kit (Binding Site). Both methods for IgG-4 determination showed a significant correlation (r = 0.91); the WHO reference serum 67/97 was used for calibration. The mean range and percentiles for age are given. IgG subclass levels were correlated with the age of the children in the order IgG-2 greater than IgG-1 greater than IgG-4, but this was not the case for IgG-3. The normal ranges of IgG subclasses were in good agreement with those of previous studies. No IgG-4 was detected by RID in only 8.8% of all the children, but in all aged 7 years and above.

Adolescent↗