Monocytes are key cells in innate immunity with their
protection against pathogens and transformation into macrophages, but there has
been research on their potential pathologic role in diseases such as immune
suppression at tumor sites and in the case of this post, a suppressive role in
vaccine immunity. Dr. Steven Dow’s lab
at Colorado State University found that high amounts of vaccine adjuvants were
able to mobilize monocytes from the bone marrow and into the lymph nodes where
they interact with T-cells to affect vaccine immunity. Adjuvants are used to increase the immune
response to a vaccine to speed and increase immunity. They were interested in the effects on normal
healthy mice and knockouts of CCR2 which is a receptor important in monocyte
chemotaxis. To their surprise, they
found that inflammatory monocytes mobilized from the bone marrow after
vaccination actually decreased the immunity gained from the vaccine! In this study they looked at local (site of
injection) inflammation, chemokine release, and monocyte recruitment, but also
utilized monocyte depletion by CCR2 knockout , compounds that block migration
or by providing extracellular cysteine.
Interaction of these monocytes with T-cells was also explored and they
found that after vaccination, inflammatory monocytes potentially sequester
cysteine which is required for activation and proliferation of T-cells and in
doing so decreased the immune response to the vaccine. I thought the role of monocytes was fairly
simple…to travel to a site and differentiate into macrophages, but it seems,
just like in all of immunology, there is a lot more to these cells than
previously thought. This research gives
possible pathways to increase vaccine effectiveness in certain populations or
diseases that were tough to vaccinate against through temporary manipulation of
monocytes or the treatment of cysteine with the vaccine.
Below is the article from Dr. Dow’s Lab.
Michell LA et al. Suppression of vaccine immunity by
inflammatory monocytes. J Immunol. Nov 7 2012.
Macrophages are very powerful, but seem to be quite "mindless". Once activated, they will perform their function until they're told to stop, and their prolonged activity could come at the expense of the host. I suppose that is why there are many other "smarter" cells to control the actions of macrophages, such as T-Regs that suppress Th1 responses (which activate angry M1 macrophages).
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