Abstract:
Cytokines, lymphocytes, platelets and several
biomolecules have long been implicated in the pathology
of rheumatoid arthritis (RA), and the influences of antibody
production and tagging, and cytokine, chemokine
and enzyme production at specific rheumatoid joints were
thought to be exclusive to the advancement of disease
parameters. Another role player in RA is red blood cells
(RBCs) which, of late, have been found to be involved in
RA pathobiology, as there is a positive correlation between
RBC counts and joint pathology, as well as with inflammatory
biomarkers in the disease. There is also an association
between RBC distribution width and the incidence of
myocardial infarction amongst RA patients, and there is a
change in the lipid distribution within RBC membranes.
Of late, certain RBC-associated factors with previously
obscure roles and cell-derived particles thought to be inconsequential
to the other constituents of plasma were found
to be active biomolecular players. Several of these have
been discovered to be present in or originating from RBCs.
Their influences have been shown to involve in membrane
dynamics that cause structural and functional changes
in both platelets and RBCs. RBC-derived microparticles
are emerging entities found to play direct roles in immunomodulation
via interactions with other plasma cells.
These correlations highlight the direct influences of RBCs
on exacerbating RA pathology. This review will attempt
to shed more light on how RBCs, in the true inflammatory milieu of RA, are playing an even greater role than previously
assumed.
