**1. Introduction**

18 Rheumatoid Arthritis – Etiology, Consequences and Co-Morbidities

Vol.201, No.6, pp.949-960, ISSN 0022-1007

Sakaguchi, S. (2005). A role for fungal {beta}-glucans and their receptor Dectin-1 in the induction of autoimmune arthritis in genetically susceptible mice. *J Exp Med*,

> Like cells of the adaptive immune system, natural killer T (NKT) cells possess immune recognition receptors formed by germline DNA rearrangement. However, in common with cells of the innate immune system, the repertoire of NKT cell receptors is limited and NKT cells can mount a robust effector response with little capacity for immunological memory, sharing some of the characteristics of other innate-like lymphocytes such as γδ T cells, marginal zone B cells, B1 B cells and NK cells. NKT cells have been shown to play a staggering array of roles in infection, cancer and autoimmunity. Autoimmune diseases in which NKT cells have been implicated include type I diabetes, multiple sclerosis, systemic lupus erythematosus and graft-versus-host disease. In rheumatoid arthritis, much work has been done to characterise the frequency and phenotype of NKT cells. Animal models such as collagen-induced arthritis or the antibody-mediated arthritis in the K/BxN serum transfer model have provided valuable insight into the multi-faceted potential of these remarkable cells and in time, pharmacological manipulation of their immune function may provide us with the prospect of novel therapeutic tools.
