Figure 1.

A model of the phagocytic uptake and intracellular processing of Borrelia by macrophages. (1,2) Actin-rich uptake structures. (1) Filopodia immobilize motile Borrelia at the host cell surface, with (2) subsequent enwrapment by a coiling pseudopod. (3) Borreliae are taken up into a plasma membrane-derived compartment, the phagosome. The phagosomal membrane loosely follows the spirochete morphology and contacts the endoplasmic reticulum (ER) at multiple sites. (3a–3c) Potential deviations from the regular pathway of internalization and processing. (3a) A subset of borreliae partially extract themselves from the nascent phagosome, resulting in the formation of membrane tunnels. (3b) A subpopulation of borreliae lose the phagosomal membrane and retain their elongated morphology, (3c) leading to increased survival in the host cell. (4) The elongated spirochete is compacted into a globular structure within the phagosome. This is initiated by contact with endocytic vesicles, which leads to local membrane tubulation and thus shrinkage of the phagosomal surface. (5) Borreliae are degraded within mature phagolysosomes. Subsequently, complexes consisting of MHCII and pathogen-derived peptides are exposed on the cell surface for antigen presentation.