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2018 ; 9
(ä): 1489
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It Takes "Guts" to Cause Joint Inflammation: Role of Innate-Like T Cells
#MMPMID30008717
Mortier C
; Govindarajan S
; Venken K
; Elewaut D
Front Immunol
2018[]; 9
(ä): 1489
PMID30008717
show ga
Innate-like T cells such as invariant natural killer T (iNKT) cells and
mucosal-associated T (MAIT) cells, characterized by a semi-invariant T cell
receptor and restriction toward MHC-like molecules (CD1 and MR1 respectively),
are a unique unconventional immune subset acting at the interface of innate and
adaptive immunity. Highly represented at barrier sites and capable of rapidly
producing substantial amounts of cytokines, they serve a pivotal role as
first-line responders against microbial infections. In contrast, it was
demonstrated that innate-like T cells can be skewed toward a predominant
pro-inflammatory state and are consequently involved in a number of autoimmune
and inflammatory diseases like inflammatory bowel diseases and rheumatic
disorders, such as spondyloarthritis (SpA) and rheumatoid arthritis.
Interestingly, there is link between gut and joint disease as they often
co-incide and share certain aspects of the pathogenesis such as established
genetic risk factors, a critical role for pro-inflammatory cytokines, such as
TNF-?, IL-23, and IL-17 and therapeutic susceptibility. In this regard
dysregulated IL-23/IL-17 responses appear to be crucial in both debilitating
pathologies and innate-like T cells likely act as key player. In this review, we
will explore the remarkable features of iNKT cells and MAIT cells, and discuss
their contribution to immunity and combined gut-joint disease.