April 3, 2012; Pathogenesis of Rheumatoid Arthritis: From Genes to Joints

April 3, 2012; Pathogenesis of Rheumatoid Arthritis: From Genes to Joints
Gregg J. Silverman, MD, NYU School of Medicine
New York University Langone Medical Center, New York, NY

Table of Contents

Rheumatoid Arthritis

0:02:02

Sero-Positive vs Sero-Negative Disease Characteristics

0:04:52

The Shared Epitope Hypothesis

0:07:42

RA Monozygotic Twin Concordance Correlates with HLA-DR4 and SE1

0:10:00

HLA and Non-HLA Genes are Linked in APCA-Positive Genome-wide Association Studies (GWAS)

0:12:12

GWAS Differences Are Seen in ACPA-Positive But Not -Negative RA

0:14:09

Female Gender is a Risk Factor for RA

0:15:39

Environmental Factors Implicated in RA Predisposition

0:16:10

Diverse autoantibody specificities in Rheumatoid Arthritis

0:17:31

Peptidyl arginine deiminase (PADI)

0:20:36

Design and performance of the prototypic CCP system: Citrullinated filaggrin peptide

0:23:05

Development of ACPA Repertoire Prior to Clinical Onset

0:26:00

Rheumatoid factors

0:26:48

RF-bearing B cells Contribute to Disease Perpetuation by Epitope Spreading

0:29:54

Evidence that ACPA contribute to RA pathogenesis

0:31:50

Immune complexes containing citrullinated proteins may Boost Inflammatory Responses

0:33:15

If SE alleles are common in Caucasian populations, why are anti-CCP antibodies uncommon?

0:33:58

Can human B cells from healthy donors produce ACPA?

0:34:56

T Cells likely important in RA Pathogenesis

0:36:37

Antibodies to citrullinated protein antigens (ACPAs)

0:37:35

ACPA Repertoire spreading with disease progression

0:39:59

Summary

0:45:54

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Dr. Silverman discusses Rheumatoid Arthritis.

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Apr 05, 2012	1103	VA:04:05:7228:2012

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