Arthritis research team - Anca Catrina

Team description

We are a mixed team of basic and clinical scientists performing translational research in the field of rheumatology with a special focus on rheumatoid arthritis. Using a large array of molecular techniques and having access to national registries and clinical samples we are currently exploring the early pathogenic events leading to chronic joint disease. We focus on understanding how interactions between genes and environment lead first to pathogenic events outside the joint (such as in the lungs and the immune system) and only in a second step to local joint inflammation.  We also investigate how hypoxia and antibodies contribute to propagation of chronic joint inflammation and bone destruction.

Team members

Anca Catrina, MD, PhD, group leader

Heidi Wähämaa, PhD, lab coordinator

Meng Sun, PhD

Erik af Klint, MD, PhD

Petra Neregård, MD, PhD

Marianne Engström, Research Engineer

 Aase Eline Haj Hensvold, MD, PhD Student

Gudrun Reynisdottir, MD, PhD Student

Akilan Krishnamurthy, MSc, PhD Student

Vijay Joshua Balasingh, MSc, PhD Student

Pingling Zeng, MSc, PhD Student

Karin Lundvall, Research Nurs

Team publications

Synovial membrane immunohistology in early-untreated rheumatoid arthritis reveals high expression of catabolic bone markers that is modulated by methotrexate.
Revu S, Neregård P, af Klint E, Korotkova M, Catrina A
Arthritis Res. Ther. 2013 ;15(6):R205

Environmental and genetic factors in the development of anticitrullinated protein antibodies (ACPAs) and ACPA-positive rheumatoid arthritis: an epidemiological investigation in twins.
Hensvold A, Magnusson P, Joshua V, Hansson M, Israelsson L, Ferreira R, et al
Ann. Rheum. Dis. 2015 Feb;74(2):375-80

Structural changes and antibody enrichment in the lungs are early features of anti-citrullinated protein antibody-positive rheumatoid arthritis.
Reynisdottir G, Karimi R, Joshua V, Olsen H, Hensvold A, Harju A, et al
2014 Jan;66(1):31-9

Dendritic cell reprogramming by endogenously produced lactic acid.
Nasi A, Fekete T, Krishnamurthy A, Snowden S, Rajnavölgyi E, Catrina A, et al
J. Immunol. 2013 Sep;191(6):3090-9

The cathelicidins LL-37 and rCRAMP are associated with pathogenic events of arthritis in humans and rats.
Hoffmann M, Bruns H, Bäckdahl L, Neregård P, Niederreiter B, Herrmann M, et al
Ann. Rheum. Dis. 2013 Jul;72(7):1239-48

Monoclonal IgG antibodies generated from joint-derived B cells of RA patients have a strong bias toward citrullinated autoantigen recognition.
Amara K, Steen J, Murray F, Morbach H, Fernandez-Rodriguez B, Joshua V, et al
J. Exp. Med. 2013 Mar;210(3):445-55

Local administration of glucocorticoids decreases synovial citrullination in rheumatoid arthritis.
Makrygiannakis D, Revu S, Engström M, af Klint E, Nicholas A, Pruijn G, et al
Arthritis Res. Ther. 2012 Jan;14(1):R20

Rheumatoid arthritis.
Klareskog L, Catrina A, Paget S
Lancet 2009 Feb;373(9664):659-72

Evaluation of arthroscopy and macroscopic scoring.
af Klint E, Catrina A, Matt P, Neregråd P, Lampa J, Ulfgren A, et al
Arthritis Res. Ther. 2009 ;11(3):R81

Monocytes are essential for inhibition of synovial T-cell glucocorticoid-mediated apoptosis in rheumatoid arthritis.
Makrygiannakis D, Revu S, Neregård P, af Klint E, Snir O, Grundtman C, et al
Arthritis Res. Ther. 2008 ;10(6):R147

Smoking increases peptidylarginine deiminase 2 enzyme expression in human lungs and increases citrullination in BAL cells.
Makrygiannakis D, Hermansson M, Ulfgren A, Nicholas A, Zendman A, Eklund A, et al
Ann. Rheum. Dis. 2008 Oct;67(10):1488-92

Intraarticular corticosteroids decrease synovial RANKL expression in inflammatory arthritis.
Makrygiannakis D, af Klint E, Catrina S, Botusan I, Klareskog E, Klareskog L, et al
Arthritis Rheum. 2006 May;54(5):1463-72

Past Members

Petra Neregård, 2013

Link to thesis:

Shankar Revu, 2012

Link to thesis:

Dimitris Makrygiannakis, 2008

Link to thesis: