Complement-dependent mechanisms in immune defence and autoimmune disease
Principal investigator; Truedsson, Lennart, Adjunct Professor, MD/PhD
Clinical speciality: Clinical immunology and transfusion medicine
The complement systems may be regarded as a link between innate and adaptive immunity and is critically involved in the development of some diseases. Complement activation brings about opsonisation, release of chemotactic factors and cytolysis. The lectin activation pathway and the role of C1q in scavenging of apoptotic cells thereby preventing an autoimmune response, provide new perspectives on complement. We have documented novel interactions that play a role in activation of complement and for the functions of complement both in defence against infection and in autoimmunity.
The overarching aim of this project is to understand the biological functions of the complement system in humans. To achieve this aim, we study complement-dependent mechanisms in various diseases. We particularly investigate complement deficiency states to elucidate the importance of the biological functions of complement in relation to disease.
Specific aims are to study:
- Complement-dependent immune defence against bacterial infections.
- The importance of complement in apoptosis induction and elimination of apoptotic cells.
- Polymorphisms and deficiency of complement components in relation to disease.
The various functions of the complement system are studied mainly in blood samples (serum, plasma and cells) from different groups of patients and controls. Within the framework of the proposed project we will utilise well established collaborations which ensure relevant and in some cases unique patient materials to study. We use various immunological and genetic methods, including complement assays developed and described by us. We have an extensive experience in complement research and the methods to be used are well established at the laboratory.
The project may give new and important knowledge about complement-mediated mechanisms in immune defence and in disease pathogenesis. The project is important also by the study of some severe and rare diseases. The findings can be used to establish rational guidelines for diagnosis, prophylaxis and prognostic evaluation in the clinical setting.
Link to project homepage: http://www.med.lu.se/english/labmedlund/mig/research_groups/the_truedsson_group
5 recent original publications
Martini PGV, Powell JL, Cook LC, Alderucci S, Norton AW, Lundberg DM, Fish, SM, Langsetmo K, Zaleski KJ, Saviloi N, Lotterhand J, Jönsson G, Lood C, Gullstrand B, Bedard C, Gill J, Concino MF, Heartlein MW, Truedsson L, Tzianabos AO
Recombinant human complement component C2 restores classical pathway activity in vitro and in vivo: an alternative treatment for C2 deficiency diseases.
BMC Immunology. 2010; 11: 43-
Lood C, Gullstrand B, Truedsson L, Olin A, Alm GV, Rönnblom L, Sturfelt G, Eloranta M-L, Bengtsson AA
Role of C1q in the Regulation of IFNα Production.
Arthritis & Rheumatism. 2009; 260: 3081-3090
Gullstrand Birgitta, Mårtensson Ulla, Sturfelt Gunnar, Bengtsson A A, Truedsson Lennart
Complement classical pathway components are all important in clearance of apoptotic and secondary necrotic cells.
Clinical and experimental immunology. 2009; 156: 303-311
Skattum L, Gullstrand B, Holmström E, Oxelius V-A, Truedsson L
Serum bactericidal activity against Neisseria meningitides in patients with C3 nephritic factors is dependent on IgG allotypes
Clinical Immunology. 2008; 129: 123-131
Selander B, Martensson U, Weintraub A, Holmstrom E, Matsushita M, Thiel S, Jensenius JC, Truedsson L, Sjoholm AG.
Mannan-binding lectin activates C3 and the alternative complement pathway without involvement of C2
J Clin Invest. 2006; 116(5): 1425-1434
Further publications here (new window)
|Total financing:||0.8 MSEK||Gov grant for clinical research ("ALF"):||0.4 MSEK|
|Total external financing:||0.4 MSEK||Natl and intl prioritized grants:||0.0 MSEK|