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. Author manuscript; available in PMC: 2016 Aug 1.
Published in final edited form as: Helicobacter. 2015 Mar 1;20(4):239–251. doi: 10.1111/hel.12200

Figure 2.

Figure 2

Host production of anti-CagA Abs, resulting in ITP. (1) Helicobacter pylori injects CagA (red) into host gastric ECs via T4SS (tan). (2) CagA undergoes intracellular phosphorylation (red and yellow). (3) Two Ags are produced and presented on the cell surface of the infected host cell: one specific for CagA (light blue) and one that shows molecular mimicry to platelet surface glycoproteins (purple). (4) Host Abs recognizing either Ag undergo replication within the host lymph nodes. (5) These Abs are then released into the circulatory system, resulting in a secondary immune-mediated thrombocytopenia. (6) Increased platelet clearance is a result of Ab-Ag recognition in the reticuloendothelial system (R.E.S.), increased immune complex formation, and decreased platelet production in the bone marrow. (pink: platelet; orange: megakaryocyte; blue: mononuclear phagocyte; green: R.E.S.)