<p>Immune complexes (ICs) are produced during normal immune responses and facilitate clearance of foreign antigens. ICs not efficiently cleared from the circulation can cause tissue damage. This might happen if ICs are formed with autoantibodies and autoantigens. Well described effects of ICs are neutralization of antigen, classical complement activation or FcR-mediated phagocytosis, whereas cytokine inducing effects of ICs in human clinical settings are less well described. I have investigated cytokine-inducing properties <i>in vitro</i> of ICs from patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and cryoglobulinemia in association with lymphoproliferative diseases. </p><p>Cryoglobulin (CG)-induced cytokine production varied with changes in temperature and ionic strength in parallel to CG precipitation. IgG CG-induced cytokine production was also mediated via FcγIIa on monocytes. Blockade of the complement system, resembling the <i>in vivo</i> situation of complement consumption in CG-associated diseases, increased IgG CG induced IL-10 and decreased TNF-α production. This represents hitherto not described mechanisms for CG-associated inflammation.</p><p>ICs from SLE patients induced IL-10 and IL-6 production from PBMC cultures via FcγRIIa. Occurrence of anti-SSA autoantibodies and signs of <i>in vivo</i> complement activation contributed to increased levels of circulating ICs in SLE patients, corresponding to increased amounts of IC-induced IL-10 <i>in vitro</i>. This represents a possible vicious cycle that might perpetuate antibody dependent pathology in SLE, and put anti-SSA in a new pathological context.</p><p>RF-associated ICs from RA joints and ICs formed with antibodies against collagen type II from RA serum induced pro-inflammatory cytokine production from monocytes via FcγRIIa, showing how specific autoantibodies might induce or perpetuate joint inflammation in RA. </p><p>I have described how ICs can induce significant amounts of pathophysiologically important monocyte-derived cytokines in three major IC-dependent diseases. Blockade of FcγRIIa and suppression of monocytes/macrophages might be a means of reducing pathogenic IC-induced cytokine production in these diseases. </p>

Immune complexes (ICs) are produced during normal immune responses and facilitate clearance of foreign antigens. ICs not efficiently cleared from the circulation can cause tissue damage. This might happen if ICs are formed with autoantibodies and autoantigens. Well described effects of ICs are neutralization of antigen, classical complement activation or FcR-mediated phagocytosis, whereas cytokine inducing effects of ICs in human clinical settings are less well described. I have investigated cytokine-inducing properties in vitro of ICs from patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and cryoglobulinemia in association with lymphoproliferative diseases. Cryoglobulin (CG)-induced cytokine production varied with changes in temperature and ionic strength in parallel to CG precipitation. IgG CG-induced cytokine production was also mediated via FcγIIa on monocytes. Blockade of the complement system, resembling the in vivo situation of complement consumption in CG-associated diseases, increased IgG CG induced IL-10 and decreased TNF-α production. This represents hitherto not described mechanisms for CG-associated inflammation. ICs from SLE patients induced IL-10 and IL-6 production from PBMC cultures via FcγRIIa. Occurrence of anti-SSA autoantibodies and signs of in vivo complement activation contributed to increased levels of circulating ICs in SLE patients, corresponding to increased amounts of IC-induced IL-10 in vitro. This represents a possible vicious cycle that might perpetuate antibody dependent pathology in SLE, and put anti-SSA in a new pathological context. RF-associated ICs from RA joints and ICs formed with antibodies against collagen type II from RA serum induced pro-inflammatory cytokine production from monocytes via FcγRIIa, showing how specific autoantibodies might induce or perpetuate joint inflammation in RA. I have described how ICs can induce significant amounts of pathophysiologically important monocyte-derived cytokines in three major IC-dependent diseases. Blockade of FcγRIIa and suppression of monocytes/macrophages might be a means of reducing pathogenic IC-induced cytokine production in these diseases.

Bakgrund: Reumatoid artrit och ankyloserande spondylit är reumatiska sjukdomar där smärta, stelhet och trötthet är vanliga symptom. Detta kan ge funktionsnedsättningar och påverka livskvalitén negativt hos de drabbade som ofta blir inaktiva, trots att forskning visar att fysisk aktivitet kan lindra funktionshinder orsakade av sjukdomen. Dock finns begränsat med forskning på vilken effekt en period med högfrekvent varierad träning kan ha på diagnosspecifika problem och funktionsnedsättningar hos patienter med reumatiska sjukdomar. Metod: Studien är en interventionsstudie av kvantitativ karaktär. Interventionen bestod av varierad gruppträning 3–4 pass/dag, 5 dagar/vecka i 4 veckor. Datainsamlingsmetoderna som använts i studien är generell upplevd smärta skattad med visuell analog skala (VAS), benstyrka mätt med timed stands test (TST), nackrotation mätt med myrinmätare, greppstyrka mätt med JAMAR och funktionell arbetskapacitet mätt med sex minuters gångtest (6MWT). Testerna utfördes innan och efter interventionen. För VAS redovisas medianvärde, för övriga tester redovisas medelvärde. Resultat: 232 patienter deltog i studien. På samtliga parametrar visades en signifikant förbättring. VAS förbättrades med 2,8, TST med 5,99 sekunder, JAMAR höger med 4,65 kg/vänster med 4,06 kg, 6MWT med 102,58 meter och nackrotation med 20,55°. Konklusion: Studiens deltagare visade en förbättring avseende samtliga parametrar. Mer forskning krävs för att påvisa om något specifikt träningsupplägg har bäst effekt på nämnda parametrar hos personer med reumatisk sjukdom, samt för att utvärdera effekten av kontextuella faktorer. / Background: Rheumatoid arthritis and ankylosing spondylitis are rheumatic diseases with common symptoms as pain, stiffness and fatigue. This can lead to disabilities and have a negative effect on the quality of life. Those affected often become inactive, despite research showing that physical activity can alleviate disabilities caused by the disease. However, there is limited research on what effect a period of high-frequency varied training can have on diagnosis-specific problems and disabilities in patients with rheumatic diseases. Method: This is a quantitative intervention study. The intervention consisted of varied group training 3-4 sessions/day, 5 days/week for 4 weeks. Methods used for collecting data in the study are generally perceived pain estimated with visual analog scale (VAS), leg strength measured with timed stands test (TST), neck rotation measured with myrin goniometer, grip strength measured with JAMAR and functional work capacity measured with six-minute walking test (6MWT). The tests were performed pre- and postintervention. For VAS, median value is reported, for all other tests, mean value is reported. Result: 232 patients participated in the study. A significant improvement was shown on all parameters. VAS improved by 2.8, TST by 5.99 seconds, JAMAR right by 4.65 kg/left by 4.06 kg, 6MWT by 102.58 meters and neck rotation by 20.55°. Conclusion: The participants of this study showed an improvement regarding all parameters. More research is needed to show whether any specific training program has the best effect on the mentioned parameters in people with rheumatic disease, and to evaluate the effect of contextual factors.

Bakgrund: Reumatiska sjukdomar är en vanlig orsak till inaktivitet hos de drabbade, även om fysisk aktivitet och träning enligt flertalet studier påvisats ha positiva effekter för sjukdomsbilden. Fysioterapeuter arbetar mycket med att motivera dessa patienter till beteendeförändring men deras roll i arbetet med motivation är mindre utforskat.  Syfte: Att undersöka fysioterapeuters upplevelser och erfarenheter av att motivera beteendeförändring i form av träning hos patienter med reumatiska sjukdomar.  Metod: En kvalitativ intervjustudie med ett strategiskt urval av fysioterapeuter och sjukgymnaster verksamma inom öppenvården med fokus på reumatologmottagningar. Datamaterialet analyserades enligt kvalitativ innehållsanalys med induktiv ansats. Resultat: Analysen av intervjuerna resulterade i 5 kategorier och 8 underkategorier. Kategorierna var; Tillvägagångssätt för att främja beteendeförändring, Motivationens roll i beteendeförändring, Vidmakthållande av träning, Organisatoriska faktorer och Individuella faktorer   Slutsats: Fysioterapeuterna använder ett individanpassat arbetssätt där man främjar självständighet för att kunna motivera patienter med reumatiska sjukdomar till att träna. De hinder fysioterapeuter upplever som försvårande i sitt arbete med patientgruppen är framförallt smärta och fatigue vid reumatism. Gruppverksamhet är ett viktigt verktyg för att underlätta träning för både fysioterapeuterna och patienterna. / Background: Rheumatic diseases are a common cause behind/to inactivity in afflicted individuals, despite physical activity and exercise having proven positive effects to disease profile, according to several studies. Physiotherapists work a great deal with motivating these patients to behavioural change but their role in motivational work is less explored. Aim: To explore physiotherapists experiences of motivating behavioural change by way of training in patients with rheumatic diseases.  Method: A qualitative descriptive interview study with an strategic selection of physiotherapists working in outpatient departments with focus on rheumatology outpatient clinics. The collected data was analyzed according to a qualitative content analysis with an inductive approach. Result: Analysis of the interviews resulted in 5 categories and 8 subcategories. The categories were; Approaches to promote behaviour change, The role of motivation in behaviour change, Maintenance of exercise, Organizational factors and Individual factors. Conclusion: Physiotherapists should adhere to an individualized approach to work in which they promote independence, in order to motivate patients with rheumatic diseases to exercise. The barriers physiotherapists experience as a hindrance to their work with the patient group is foremost pain and fatigue associated with rheumatism. This serves as a hindrance to physiotherapists with getting patients to start and adhere to an exercise behaviour.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2010.

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Diss. (sammanfattning) Stockholm : Karol. inst., 2005. / Härtill 4 uppsatser.

Thematic Paper (M.C.T.M. (Clinical Tropical Medicine))--Mahidol University, 2006.