Examination of the pooled sera from early and late PD patients and controls by Western blot analysis did not show substantial immune reactivity (data not shown), confirming the ELISA results on the lack of immune responses towards oligomers in the vast majority of healthy and PD individuals.
At the end of this infection trial, i.e. 34 weeks p.i., CFT titres ranged between 1 10 to 1 20 for the in-house CFT (see Additional File 3: Examination of Panel 3 sera using in-house CFT), and between 1 5 and 1 160 for the CIRAD CFT (see Additional File 4: Examination of Panel 3 sera using CIRAD CFT).
The increase of the cELISA titres was seen after day 6 post infection (see Additional File 2: Examination of Panel 2 sera using cELISA), with the exception of animal BD091 (beginning at 6 dpi, Figure 1A; see also below).
Test results of the cELISA showed a rise in titres from week 3 to 4 p.i., with levels either remaining positive until to the end of the trial or slowly decreasing to reach the cut-off value of 50% inhibition (see Additional File 5: Examination of Panel 3 sera using cELISA).
Examination of an independent cohort of sera from 18 Sjögren's syndrome patients gave comparable results (J. Browning, data not shown).
Among these systems, efficient monospecific methods – such as ELISAs and line immunoblot assays (LIAs) for single-parameter or profile analysis – have been established in clinical laboratory practice during past years, allowing examination of a large number of sera in a rapid approach at high sensitivity and at high specificity [ 7- 10].
Both jaguarundis were immobilized on February 20 for the collection of sera and further examination.
Examination of our data suggested that sera-derived TGF-β1 was released by platelets during collection procedures.
At termination of the experiment (day 73), bone mineral density (BMD) was analyzed, paws were collected for histological examination, and sera were analyzed for markers of cartilage turnover and pro-inflammatory cytokines.
A unique profile of CD4bs-directed antibodies was observed upon examination of the ability of the immune sera to outcompete binding against mAb b12 (Fig 4C).
