Abstract
Steadily growing knowledge about pathogenetic mechanisms in autoimmune rheumatic diseases (RDs) has paved the way to different therapeutic approaches. In particular, the availability of biologics on the market has dramatically modified the natural history of rheumatic chronic inflammatory diseases with a meaningful impact on patients’ quality of life. Among the wide spectrum of available biological treatments, rituximab (RTX), initially used in the treatment of non- Hodgkin’s lymphoma, was later approved for rheumatoid arthritis and anti-neutrophil cytoplasmic antibodies-associated vasculitis. Currently, in rheumatology, RTX is also used with off-label indications in patients with systemic sclerosis, Sjögren’s syndrome and systemic lupus erythematosus. RTX is a monoclonal antibody targeted to CD20 molecules expressed on the surface of pre-B and mature B lymphocytes. It acts by causing apoptosis of these cells with antibody- and complement-dependent cytotoxicity. As inflammatory responses to cell-associated immune complexes are key elements in the pathogenesis of several autoimmune RDs, such an approach might be effective in these patients. In fact, RTX promotes a rapid and long-term depletion of circulating and lymphoid tissue-associated B cells, thus leading to a lower recruitment of these effector cells at sites of immune complex deposition, therefore reducing inflammation and tissue damage. RTX is extremely interesting for rheumatologists, as it represents an important additional therapeutic approach. Therefore, the advent in clinical practice of approved RTX biosimilars, such as CT-P10, may help in improving treatment access as well as reducing costs.
Highlights
Rituximab (RTX) is a chimeric monoclonal anti-CD20 antibody that induces B-cell depletion through complement-mediated cytotoxicity, antibody-dependent cellular cytotoxicity (ADCC) and direct signaling
It was firstly approved for the treatment of indolent nonHodgkin’s lymphoma in 1994 and later for the treatment of rheumatoid arthritis (RA). It was approved for remission induction and maintenance therapy of associated vasculitis (AAV).[3,4]
The complex pathogenesis of most systemic autoimmune rheumatic diseases (SARDs) is not yet fully understood, but an essential role of B cells appears to be clear in the autoimmune response to these diseases, providing a rationale for the use of RTX, a B-cell depleting agent
Summary
Rituximab (RTX) is a chimeric monoclonal anti-CD20 antibody that induces B-cell depletion through complement-mediated cytotoxicity, antibody-dependent cellular cytotoxicity (ADCC) and direct signaling. It is presumed to play a central role in the generation of B-cell responses against T-cell independent antigens.[1,2]. It was firstly approved for the treatment of indolent nonHodgkin’s lymphoma in 1994 and later for the treatment of rheumatoid arthritis (RA). It was approved for remission induction and maintenance therapy of associated vasculitis (AAV).[3,4] RTX has been used in the most common systemic autoimmune rheumatic diseases (SARDs), such as, amongst others, systemic lupus erythematosus (SLE), systemic sclerosis (SSc), primary Sjögren syndrome (pSS) and idiopathic inflammatory myopathy (IIM). The complex pathogenesis of most SARDs is not yet fully understood, but an essential role of B cells appears to be clear in the autoimmune response to these diseases, providing a rationale for the use of RTX, a B-cell depleting agent
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