Autoantigen (eng text)

This question relates to why autoimmune disease develops in the first place. Our hypothesis is that the immune system does what it is supposed to – attacks foreign invading microorganisms, but that during this process there is damage to cells and molecules in the vicinity. Such chemical modifications of self proteins lead to them being perceived as being non-self to the immune system, leading to breaking of immune tolerance and iniation of specific autoimmune attack. We therefore believe that autoimmune disease develops as a consequence of unwanted side-effects of a ’normal’ inflammatory process.

MDA-MOG

Structural MDA Modification of MOG

In order to study this phenomenon we chemically modify autoantigens known to be important in inducing autoimmune diseases – insulin and glutamic acid decarboxylase for T1DM, and MOG for MS. We use modifications that are the result of activation of macrophages and neutrophils, the cells that comprise most inflammatory cells infiltrating an inflammatory site. The modifications include oxidation, chlorination, nitrosylation and citrullination and we assess the biochemical, immunological and structural effects of these modifications on the autoantigens.

Click here to view the PTM webinar

CMM Research Groups

NEUROGENETIK OCH PSYKIATRISKA SJUKDOMAR

GENETISKA SJUKDOMAR

INFLAMMATORISKA SJUKDOMAR

KARDIOVASKULÄRA OCH METABOLA SJUKDOMAR