B O O K - American College of Rheumatology

Session Overview:
The innate immune system can sense “danger” and induce
inflammation and initiate tissue repair. Sensing danger in the
setting of infection or tissue damage is important for normal
host defenses and homeostasis. Moreover, in vaccine adjuvants
can be used to boost immune responses by activating cells of
the innate immune system. However, there are clinical settings
in which innate immunity goes awry triggering unnecessary
inflammation, injury, and disease. Thus, the molecular
mechanism leading from uric acid or calcium pyrophosphate
crystals to gout or pseudogout are similar to those triggered by
infection or tissue necrosis.
Upon completion of this session, participants should be able to:
• describe the inflammasome, how it is activated and how it
induces inflammation
• discuss how crystals, such as urate, calcium pyrophosphate or
even aluminum hydroxide, trigger activation of inflammation
and why IL-1ra works for gout
• explain the importance of innate immunity in resolution of
inflammation
ACR Medical Aspects of Rheumatic
Diseases
9:00 - 10:00 am
Hall A3
Heparin and Antiphospholipid Syndrome-induced
Thrombocytopenia cP ARS
Moderator: Alexandra Villa-Forte, MD, MPH; Cleveland Clinic
Foundation; Cleveland, OH
Speaker: John R. Bartholomew, MD; Cleveland Clinic; Cleveland,
OH
Session Overview:
Heparin-induced thrombocytopenia and the antiphospholipid
syndrome are disorders with distinct pathogenesis; however
they share several clinical features, including thrombocytopenia
and thrombotic events. Evaluation of patients with
thrombocytopenia and thrombosis and distinguishing these two
disorders require careful clinical assessment, as well as focused
laboratory evaluation. An algorithmic approach to the evaluation
and the differential diagnosis of patients with thrombocytopenia
and thrombosis can be helpful to the rheumatologist.
Upon completion of this session, participants should be able to:
• identify the important elements of the clinical features and
appropriate laboratory testing in the diagnosis of heparininduced
thrombocytopenia and antiphospholipid syndrome
• describe the clinical utility and limitations of auto-antibodies
testing in the diagnosis of thrombocytopenia
• discuss treatment options in heparin-induced
thrombocytopenia
Moderator: Kathleen M. O’Neil, MD; Oklahoma University
Health Science Center; Oklahoma City, OK
Speaker: Ann M. Reed, MD; Mayo Clinic; Rochester, MN
Session Overview:
Childhood-onset dermatomyositis shares many features with
adult dermatomyositis, but there are also important differences.
New insights into the pathophysiology of this disease include
the roles played by maternofetal microchimerism, Treg and
B lymphocytes in the inflammatory infiltrates, and new data
from gene expression arrays, giving insights into this perplexing
disease. Data from clinical trials including B cell depletion in
juvenile dermatomyositis will be available in 2010; therefore,
an update on current understanding of relevant pathogenic
pathways in this disease is important.
Upon completion of this session, participants should be able to:
• describe the clinical spectrum of juvenile dermatomyositis and
its multi-organ involvement
• discuss the current knowledge of the pathophysiology of
juvenile dermatomyositis
• assess the efficacy and safety of aggressive treatment
modalities in juvenile dermatomyositis, and the role these
therapies may play in treatment of patients with this disease
Sidney J. Marcus Auditorium
T cell Memory R
Moderators: Keith B. Elkon, MD; University of Washington;
Seattle, WA
Michael Ehrenstein, PhD; University College London School of
Medicine; London, United Kingdom
Speaker: Rafi Ahmed, PhD; Emory University School of Medicine;
Atlanta, GA
Session Overview:
Most autoimmune disorders are driven by T cells. Memory
T cells are expanded and presumably provide a reservoir for
autoreactivity that persists even when biologic therapy is
used to block acute inflammation. It is therefore necessary
to understand how memory T cells are generated and what
strategies may prove effective in selectively impairing their
function in autoimmune diseases.
Upon completion of this session, participants should be able to:
• identify differences between naive and memory T cells
phenotype and function
• determine how T memory cells are generated in virus
infections
• describe which cytokines and ligands influence the function of
memory T cells
ACR Poster Session A and Poster
Tours
9:00 am - 6:00 pm
monday
ACR State-of-the-Art Lectures
9:00 - 10:00 am
Thomas J. Murphy Ballroom
Juvenile Dermatomyositis in 2010 - From Bench to
Bedside P PS
Halls B1 & B2
Poster presenters will be available from 9:00 - 11:00 AM. Poster
tours will be held 9:00 - 9:45 AM, 10:15 - 11:00 AM and 4:30 -
5:30 PM.
2010 Program Book 31