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Abstract Number: 1946

Effect of Immunosuppressive Treatment On Gene Expression in Patients with Polymyositis and Dermatomyositis

Ingela M. Loell1, Yi-Wen Chen2, Marina Korotkova3, Kanneboyina Nagaraju2 and Ingrid E. Lundberg4, 1Rheumatology Unit, Department of Medicine, Karolinska University Hospital in Solna, Karolinska Institutet, Stockholm, Sweden, 2Center for Genetic Medicine Research, Children's National Medical Center, Washington, DC, 3Department of Medicine, Karolinska Institutet, Stockholm, Sweden, 4Rheumatology Unit, Karolinska University Hospital, Solna, Karolinska Institutet, Stockholm, Sweden

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: glucocorticoids, polymyositis/dermatomyositis (PM/DM) and treatment

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Session Information

Title: Muscle Biology, Myositis and Myopathies: Genetics, Autoantibodies and other Molecular Aspects of Idiopathic Inflammatory Myopathies and Models

Session Type: Abstract Submissions (ACR)

Background/Purpose:

Polymyositis (PM) and dermatomyositis (DM) muscle tissue is characterized by infiltrating T cells, macrophages and dendritic cells, as well as cytokines and chemokines. In addition, the muscle fibers express major histocompatibility complex (MHC) class I. Patients are treated with high doses of glucocorticoids in combination with additional immunosuppressive drugs. However, remaining signs of inflammation in the muscle tissue, such as T cells, MHC class I and cytokines, as well as sustained muscle impairment are common even after prolonged treatment.  Our aim was to investigate how the gene expression in pathways of inflammation and muscle remodeling is affected by immunosuppressive treatment in patients with PM and DM.

Methods:

Six newly diagnosed, untreated patients (2 PM/4 DM, 2 men/4 women) with biopsies from m.vastus lateralis before and after a median of 10 (8-16) months of immunosuppressive treatment were analyzed using microarray. 

Results: Alterations in a number of genes coding for immune responses and muscle tissue remodelling were observed. 

Affy accession #

Gene

Gene ID

Fold

P-value

Immune response

1554519_at

CD80

CD80

-2,2

0,034

210895_s_at

CD86

CD86

-2,6

0,013

222868_s_at

interleukin 18 binding protein

IL18BP

-1,9

0,032

206295_at

interleukin 18

IL18

-2,2

0,041

205992_s_at

interleukin 15

IL15

-1,5

0,027

216598_s_at

chemokine (C-C motif) ligand 2

CCL2

-5,9

0,004

1555759_a_at

chemokine (C-C motif) ligand 5

CCL5

-3,1

0,003

1405_i_at

chemokine (C-C motif) ligand 5

CCL5

-3,0

0,043

206978_at

chemokine (C-C motif) receptor 2

CCR2

-2,3

0,004

206991_s_at

chemokine (C-C motif) receptor 5

CCR5

-2,8

0,027

204533_at

chemokine (C-X-C motif) ligand 10

CXCL10

-5,6

0,020

210163_at

chemokine (C-X-C motif) ligand 11

CXCL11

-6,3

0,005

211122_s_at

chemokine (C-X-C motif) ligand 11

CXCL11

-5,6

0,015

215313_x_at

MHC class I, A

HLA-A

-1,1

0,012

211911_x_at

MHC class I, B

HLA-B

-1,7

0,010

208812_x_at

MHC class I, C

HLA-C

-2,6

0,013

211991_s_at

MHC class II, DP alpha 1

HLA-DPA1

-2,2

0,046

203290_at

MHC class II, DQ alpha 1

HLA-DQA1

-2,8

0,036

211656_x_at

MHC class II, DQ beta 1

HLA-DQB1

-2,2

0,038

209312_x_at

MHC class II, DR beta 3

HLA-DRB3

-1,7

0,027

204806_x_at

MHC class I, F

HLA-F

-2,4

0,018

Muscle structure

206891_at

actinin, alpha 3

ACTN3

3,4

0,037

200930_s_at

vinculin

VCL

1,9

0,022

207145_at

growth differentiation factor 8

MSTN

2,3

0,041

204802_at

Ras-related associated with diabetes

RRAD

-3,4

0,013

204560_at

FK506 binding protein 5

FKBP5

3,2

0,016

206394_at

myosin binding protein C, fast type

MYBPC2

1,9

0,031

206304_at

myosin binding protein H

MYBPH

-6,9

0,036

208148_at

myosin, heavy polypeptide 4

MYH4

2,2

0,020

202724_s_at

forkhead box O1A

FOXO1

2,2

0,033

Conclusion: This data indicates that transcriptional alterations in genes involved in muscle tissue structure are taking place during immunosuppressive treatment.  The treatment down-regulates the muscle inflammation to some extent but the local milieu might be accountable for the preserved expression of inflammatory cells and mediators seen in treated PM/DM patients.


Disclosure:

I. M. Loell,
None;

Y. W. Chen,
None;

M. Korotkova,
None;

K. Nagaraju,
None;

I. E. Lundberg,
None.

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