Review highlights the therapeutic potential of targeting BAFF and BAFF-R in autoimmune cytopenias, indicating a promising approach to overcome transient treatment responses.
Key Points
Assess the therapeutic rationale for targeting the B-cell-activating factor (BAFF) and its receptor (BAFF-R) axis to improve long-term outcomes in immune thrombocytopenia and warm autoimmune hemolytic anemia.
Narrative evaluation of B-cell biology, autoreactivity mechanisms, and BAFF/BAFF-R signaling in autoimmune cytopenias.
Review of clinical evidence regarding circulating BAFF concentrations and durability limitations of current standard-of-care therapies.
BAFF engagement with BAFF-R directly drives autoreactive B-cell differentiation, expansion, and survival in both conditions.
Patients with immune thrombocytopenia and warm autoimmune hemolytic anemia exhibit elevated BAFF levels, which are linked to relapse after cessation of conventional therapies.