The role of B and T cells in ITP

ITP is an autoimmune disease in which platelets and megakaryocyte destruction
is mediated by autoantibodies. These autoantibodies are produced by plasma
cells, derived from B cells, a process initiated by antigen-specific T cells.
These antigen-specific T cells have been identified in the peripheral blood of
ITP patients, yet it is unknown whether these cells are continuously
maintaining the disease in the chronic phase. Treatments targeting T and B
cells (e.g. rituximab, azathioprine, ciclosporine) are effective in ITP and
therefore point towards a role for these lymphocytes in disease progression.
Our lab has longstanding experience with investigations on antigen-specific
cells.

We hypothesize that ITP disease activity is dependent on helper and regulatory
autoantigen-specific T cells, controlling the B cell to plasma cell transition
and autoantibody production.

Investigate the relationship between disease activity in ITP and the phenotype
and function of autoantigen-specific T cells and B cells.

In this observational cohort study, the blood collection time points and assays
are as follows:
All included patients will be requested to donate 100ml of blood at inclusion
and thereafter once every year for a total duration of five years. The numbers
and function of autoantigen-specific T cells and B cells will be compared
between patient categories defined on the basis of clinical characteristics.

Relapsing or newly diagnosed ITP patients (i.e. with active disease) will be
enrolled for collection of 50 ml of peripheral blood at four pre-defined time
points: at relapse and after 1, 4 and 10 weeks. Autoantigen-specific responses
will be compared between the time points.

Minimal to negligible. 50-100 mL of additional blood drawn per time point.