Journal
JOURNAL OF LEUKOCYTE BIOLOGY
Volume 94, Issue 3, Pages 521-529Publisher
OXFORD UNIV PRESS
DOI: 10.1189/jlb.0213074
Keywords
human; T cell activation; rheumatoid arthritis
Categories
Funding
- Ministerio Educacion y Ciencia [BFU06/15063]
- Fondo de Investigaciones Sanitarias [PS09/132]
- Fondo Investigaciones Sanitarias
Ask authors/readers for more resources
Platelet binding is a new regulatory mechanism of T cell function; higher frequency of platelet binding to lymphocytes is associated with low severe inflammatory profile. Expression of the scavenger receptor CD36 on lymphocytes is intriguing. We observed that a minor subpopulation of lymphocytes expressed CD36 on the cell surface. We investigated the source of CD36 and also the proliferation and cytokine production of these CD36(+) CD4(+) lymphocytes. Flow cytometry analysis and immunofluorescence microscopy showed that CD36(+) platelets were responsible for CD36 detection on lymphocytes. CD36 was then used as a tool to characterize lymphocytes with bound platelets. Activation-induced proliferation was lower in CD4(+) lymphocytes with bound platelets than lymphocytes without bound platelets. IL-17 and IFN- production was also reduced in lymphocytes with bound platelets. We then studied the presence of CD36(+) CD4(+) lymphocytes in RA patients. We observed that the percentage of CD4(+) lymphocytes with bound platelets was higher on RA patients than in healthy donors. RA patients with higher titers of anti-CCP, RF levels, and cardiovascular risk index presented a lower percentage of CD4(+) lymphocytes with bound platelets. These patients also had higher IL-17 and IFN- production. These results suggest that platelet-binding modifies lymphocyte function. This binding could be a regulatory mechanism in RA that confers a less severe phenotype.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available