Monocyte emigration

Serbina NV, Pamer EG. Monocyte emigration from bone marrow during bacterial infection requires signals mediated by chemokine receptor CCR2. Nat Immunol 2006 7(3) 311-317. 

Much less is understood of the control of eosinophil and monocyte emigration in situ, although similar principles would be applicable to the identification of mechanisms involved in the cessation of their emigration. 

Fig. 1. Organ/cellular pathways in the induction of CD8+ suppressor cells by the injection of antigen into the anterior chamber (AC). he injection of antigen into the AC induces a recruitment of F4/80+ monocytic cells to the iris. Interactions with iris monocytic cells, antigen and GF-p in aqueous humor induces an immunosuppressive phenotype in the recruited cells. hese cells then recirculate from the AC to the thymus and the spleen. In the spleen, F4/80+ cells interact with B cells, peripheral NK cells, recent thymic NK emigrants and CD8+ cells with the generation of CD8+ suppressor cells that effect the suppression of a D FI reaction.

Llodra, J., Angeli, V., Liu, J., Trogan, E., Fisher, E.A., Randolph, G.J. 2004. Emigration of monocyte-derived cells from atherosclerotic lesions characterizes regressive, but not progressive, plaques. Proc. Natl. Acad. Sci. U.S.A. 101 11779-11784. 

The complement system is a potent mechanism for initiating and amplifying inflammation. The cleavage products C3a and C5a (anaphylatoxins) stimulate chemotaxis and activation of leucocytes. They are chemotactic for neutrophils and trigger degranulation of basophils and mast cells, thus liberating vaso-active substances (e.g. histamine). The net result is an increase in vascular permeability and emigration of neutrophils and monocytes from blood vessels. 

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