EDITORIAL - What can we learn from treatment-induced changes in RF and anti-CCP antibodies (ACPA)?

[Guest guest]

Journal of Rheumatology

Oct 2008

What Can We Learn from Treatment-Induced Changes in Rheumatoid Factor

and Anti-Citrullinated Peptide Antibodies?

FRANCESCA BOBBIO-PALLAVICINI, MD,

Chair and Division of Rheumatology;

ROBERTO CAPORALI, MD,

Associate Professor,

Chair and Division of Rheumatology;

SERENA BUGATTI, MD,

Chair and Division of Rheumatology;

CARLOMAURIZIO MONTECUCCO, MD,

Full Professor, Director,

Chair and Division of Rheumatology,

University of Pavia, Fondazione IRCCS Policlinico San Matteo,

Pavia, Italy

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Basic and clinical research initiatives on the 2 major autoantibody

systems in rheumatoid arthritis (RA), rheumatoid factor (RF) and

anti-citrullinated peptide antibodies (ACPA), have moved in parallel

in recent years1-3. Indeed, recent works have disclosed some of the

mechanisms underlying the genesis, maintenance, and role of the

humoral autoimmune response in RA, identifying defective B cell

tolerance checkpoints4 and dissecting the interactions among

environment, genes, and adaptive immunity3. On the other hand,

monitoring the autoimmune response in RA through its most accessible

marker, i.e., serum autoantibodies, has gained growing interest as RF

and ACPA are recognized as powerful predictive, diagnostic, and

prognostic tools in RA.

Several studies in recent years have focused on changes in RF and ACPA

levels during different treatment strategies, especially with

biological agents such as tumor necrosis factor-á (TNF-á) inhibitors,

summarized in Table 15, and B cell targeted therapies6. These studies

are welcome for a number of reasons. First, the identification of

different pretreatment values and/or different rates of decline of RF

and ACPA might offer accessible biomarkers of clinical response.

Second, treatment-related changes of serum autoantibodies might

provide insights into the specific immunoregulatory activity of a

single drug or class of drugs. Third, monitoring the serum autoimmune

response in RA might shed new light on mechanisms underlying the

generation and maintenance of autoreactive B cells. Last, assuming

that autoantibodies play a pathogenetic role in RA, treatment-induced

seroconversion could be regarded as one of the goals for true

remission or cure.

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