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The Research Group of Immunology and Rheumatology

The B cell group

The focus of the B Cell Research Group is consequently B cells (all developmental, transitional and maturation stages/phases), as well as autoantigens, autoantibodies, histopathological signs and changes with reference to B cells and factors influencing the humoral compartment e.g. Th17/IL17, regulatory T cells, follicular T helper cells, and related cytokines and chemokines.

A photo of the B cell group
The B cell group. From left, Jack Panapase (Master student in Pharmacy), Karl Albert Brokstad, PhD (Principal Investigator), Lara Aqrawi (PhD student) Oddgeir Selaas (Master student in Pharmacy) and Linda Kallevik (Master student in Pharmacy

Background

Primary Sjögren’s syndrome (SjS) is a complex autoimmune rheumatic disease characterized by the presence of autoantibodies against the ribonucleoprotein (RNP) particles SS-A/Ro and SS-B/La and mononuclear cell infiltration of exocrine tissues. The salivary and lacrimal glands are the principal targets of a proposed T cell–mediated chronic inflammation, with a resulting glandular atrophy and deficient function. The clinical consequences are dry eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia). Due to progression in multiple organs, there may be a number of systemic features of SjS. One of the enigmas in this directed autoimmune attack has been the mechanisms responsible for the formation of mononuclear cell accumulations in exocrine glands. It has been hypothesized that primary events (e.g., infections) may occur in the glands themselves, followed in a second phase by an autoimmune attack. Whether B cell activation is a primary cause or a secondary effect in SjS is not known. However, the progress in this field has been slow and no clear-cut evidence has been provided. A genetic predisposition to SjS has also been suggested, but the combination with a link to an environmental trigger remains to be defined.

 

Despite the dominance of T cells in the glandular lesions, SjS is considered to be a humoral (B cell)-driven autoimmune disease. The cells of the immune system work in concert with other immune competent cells and surrounding epithelial cells may be involved in the disease mechanism, but still the B cells have a very prominent role in this disease. This view is based on serum hypergammaglobulinaemia, autoantibodies, rheumatoid factor, focal B cell infiltrations, and in some cases (4-5%) the development of B cell lymphoma (non-Hodgkin’s lymphoma).

 

Focus of the B cell Research Group

B cells (all developmental, transitional and maturation stages/phases)

• Autoantigens

• Autoantibodies

• Histopathological signs and changes with reference to B cells

• Factors influencing the Humoral compartment

     o Cells: e.g. Th17/IL17, Treg, Tfhc

     o Molecules: Cytokines, Chemokines and Growth factors