T cell Repertoire Profiling and the Mechanism by which HLA-B27 Causes Ankylosing Spondylitis.
Curr Rheumatol Rep
; 24(12): 398-410, 2022 12.
Article
in En
| MEDLINE
| ID: mdl-36197645
ABSTRACT
PURPOSE OF REVIEW Ankylosing spondylitis (AS) is strongly associated with the HLA-B27 gene. The canonical function of HLA-B27 is to present antigenic peptides to CD8 lymphocytes, leading to adaptive immune responses. The 'arthritogenic peptide' theory as to the mechanism by which HLA-B27 induces ankylosing spondylitis proposes that HLA-B27 presents peptides derived from exogenous sources such as bacteria to CD8 lymphocytes, which subsequently cross-react with antigens at the site of inflammation of the disease, causing inflammation. This review describes findings of studies in AS involving profiling of T cell expansions and discusses future research opportunities based on these findings. RECENT FINDINGS:
Consistent with this theory, there is an expanding body of data showing that expansion of a restricted pool of CD8 lymphocytes is found in most AS patients yet only in a small proportion of healthy HLA-B27 carriers. These exciting findings strongly support the theory that AS is driven by presentation of antigenic peptides to the adaptive immune system by HLA-B27. They point to new potential approaches to identify the exogenous and endogenous antigens involved and to potential therapies for the disease.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Spondylitis, Ankylosing
/
HLA-B27 Antigen
Type of study:
Etiology_studies
/
Prognostic_studies
Limits:
Humans
Language:
En
Journal:
Curr Rheumatol Rep
Journal subject:
REUMATOLOGIA
Year:
2022
Document type:
Article
Affiliation country:
Reino Unido